The lancelet resembles a lancet, a double-bladed surgical knife.

Few people will find delight in the dredge that is hauled from the ocean floor. But for the British biologist Ray Lankester, such hauls represented an unseen world of wonder. In his Diversions of a Naturalist he describes how an encounter with a creature from the bottom of the sea that filled him with so much joy that he completely forgot about his sea-sickness:

“I remember lying very ill on the deck of a slowly lurching ‘lugger’ in a heaving sea off Guernsey, when the dredge came up,and as its contents were turned out near me, a semi-transparent, oblong, flattened thing like a small paper-knife began to hop about on the boards. It was the first specimen I ever saw alive of the lancelet, that strange, fish-like little creature.”
~ Ray Lankester (1915)

Lankester had good reasons to be excited. For him and other naturalists, the lancelet was not merely another bottom dweller; it was a creature with the potential to resolve the ancient origins of the vertebrates, group of animals with a spine. But that’s running ahead of the story. What kind of creature is the lancelet, to begin with? The German zoologist Pallas was the first to describe the lancelet in the scientific literature. He worked with a preserved specimen, and mistakenly classified it as a slug in 1774. Perhaps he would have recognized how un-slug like the lancelet really is if he had seen one alive, wiggling and hopping about.

The 19th century naturalists Costa and Yarrell did have this opportunity. They were also the first to note that the lancelet resembles a vertebrate. Not only does the lancelet have a rudimentary spine that runs from their head to their tail, they also have segmented muscle bundles and a tail that extends past their anus, just like other vertebrates have.

The drawing of the lancelet as it appeared in Yarrell's History of British Fishes.

Lancelets and vertebrates share a similar anatomy, but a lancelet is not a vertebrate quite yet. There is still a huge gap between the complex tissues of vertebrates and the simple organization of their lancelet equivalents. The lancelet’s nerve cord is slightly swollen near its head, but this bulge is not yet a brain. Lancelets have contracting blood vessels that pump around blood, but no central heart. And then there are the organs that they lack entirely, such as a skull or a pair of eyes. Ernst Haeckel was right when he wrote that “the lancelet differs more from the fishes than the fishes do from man”.

As a creature on the border between vertebrate and invertebrate, biologists first regarded the lancelet as a ‘primitive vertebrate’ and later as ‘closest living cousin of vertebrates’ (and other almost-vertebrates, such as hagfish). It was clear to all that these little paper-knives were important creatures for studying the origins of the vertebrate lineage. No one believed that the lancelets were the unchanged descendants of some proto-vertebrate, but biologists reasoned that since all traits shared between lancelets and vertebrates have been inherited from a common ancestor, the lancelet still offered a glimpse of what these distant ancestors might have looked like.

Fossil unearthed in Canada and China show that there is some truth to this logic. The ancient Pikaia already had a flexible proto-spine and segmented muscles, resembles the lancelet in these regards. Pikaia is not a direct ancestor of either vertebrates or lancelets, but palaeontologists agree that they represent some of our earliest relatives.

In short, for more than a century, all the evidence seemed to indicate that the family ties between lancelets and vertebrates were close. Until 2006, when a team of molecular biologists drove a chain-saw into the stem of the vertebrate family tree. Their DNA-analyses revealed that not lancelets, but sea squirts and their ilk (the tunicates) are the closest living relatives of vertebrates. Common zoological sense turned out to be wrong. Somehow these shapeless sacks, hardly recognizable as animals, are closer related to us than the mobile and gracile lancelets.

The sea squirt Ciona intestinalis is a closer relative of yours than the lancelet is.

To be fair, biologists long knew that sea squirts occupy a branch close to the vertebrates in the tree of life. Adult sea squirts might be stationary filter feeding tubes, but their larvae look more like tadpoles than anything else. It was the Russian embryologist Alexander Kowalevsky who first noted that young sea squirts come complete with a head, tail and a proto-spine in 1866.

The lancelet genome, sequenced in 2008, confirmed that tunicates are the sister lineage of vertebrates and that lancelets branched off first. This redrawn family tree opens a whole new can of questions. If sea squirts really are our closest non-vertebrate cousins, how come we look so different from each other as adults?

Our genes hold some clues. The genomes of both tunicates and vertebrates show signs of widespread, but different kinds of, genetic upheaval. The first evidence that the genomes of the first vertebrates differed drastically from those of their forebears came from the observation that some of their gene families are overrepresented, often following a 4:1 ratio.

Sea squirt larvae (bottom) resemble tadpoles (top) in their earliest stages of development.

Take the famous Hox genes. These genes determine the shape of animals by regulating which segments develop into what kind of structure, such as a rib. Hox genes are arranged in clusters and are ‘read’ in a strict order during the development. Humans, mice, and chickens have four of these clusters, whereas invertebrates such as lancelets only have one. Confronted with this pattern again and again, biologists concluded that the entire genome of the ancestral vertebrate must have been duplicated twice, giving rise to a fourfold increase in genes. These two rounds of duplication were followed by massive gene losses where redundant and harmful copies were purged from the genome. Many biologists think that the genes that remained opened up the road to an increase in complexity, as genes acquired new roles and functions. More on this in a later blog post.

The genomes of sea squirts tell a different story. Instead of gaining genes, they have lost many of them over time. Of all the Hox genes that are present in the lancelet genome, 25 are missing from tunicate genomes. The remaining Hox genes have been shuffled around, generating scrambled versions of the traditional Hox clusters. As a cause or consequence, the development sea squirt larvae also proceeds in a way that is different from what we know of lancelet and vertebrate embryos. Their genes and genomes also seem to evolve at a higher rate and accumulating changes faster than the genes of lancelets and vertebrates do.

Vertebrates and tunicates thus seem to have evolved in completely opposite directions. Where the tunicates lost genes, the vertebrates gained them. As tunicates grew more simple and derived, the vertebrates became more complex. It’s thrilling to realize that their starting point was the same: a strange, little fish-like creature, not unlike the humble lancelet. If only it were possible to travel back 500 billion years in time on a lurching lugger, dredging the Cambrian oceans seeing what wonders come up.

Welcome to the sixteenth edition of the MolBio Carnival! Some great blog posts on cellular and molecular biology have been submitted, many of them written by first-time contributors, so I urge you to check them all out. Let’s not waste any time and get this carnival started. It’s time to explore the most intricate machine of all: the living cell.

Welcome to the cell!

Inside the machine

Can you hear the hum? That’s the sound of biochemistry. Inside the cell, thousands of proteins are carrying out their tasks with clockwork precision. Cooperation is key here. Some proteins mesh together like gears: they depend on each other to function. Gemma Atkinson explains how such protein pairs co-evolve, hummingbird and flower as an analogy.

Gears don’t turn themselves. We need a source of energy for our machine. We’re in luck: Christopher Dieni describes an enzyme that delivers sudden bursts of energy to keep the engines running. What’s more, this same enzyme can keep frozen frogs alive and assists in releasing insulin. Multipurpose design indeed!

While the main product of our cellular machine is life, there’s no reason we couldn’t tweak it to produce more. Lab Rat explains how we can let algae produce bioplastics, using a bacterial trick.

Woah.. Did you feel that rumble? Our cell is on the move! It unrolls its sticky proteins along the way to pull itself forward. The Leading Edge would like to study these sticky proteins in his or her test tube, but as it turns out, they prefer to remain attached to the surface instead.

Gremlins!

All machines are plagued by system failures, and sometimes even downright sabotage, and the cell is no exception. Viruses are the most notorious hijackers of cellular machinery. They usually come and go, but sometimes they become part of the machine themselves. EE Georgi describes how this happens.

Some gremlins cause more damage than others. HIV is one virus that certainly has earned its reputation of malevolence. EE Georgi joins in with another post, on whether gene therapy could eradicate this virus.

Bones can tell us about gremlins past. Lesions and pits in ancient bones sometimes represent the traces of ancient infections. Kristina Killgrove writes about palaeopathological evidence that the ancient Romans already suffered from Syphilis.

Connor Bamford continues along this line, and wonders if dinosaurs ever got the measles. Yes, he says! Or measle-like viruses, in any case. How do we know? Some dinosaur vertebra showed classical signs of Paget’s disease: remodeled bone and an increase in the amount of red blood vessels.

That’s it for this month’s edition of The MolBio Carnival. I hope you enjoyed this peek inside the machine, and you are welcomed to submit your best molbio blog articles to the next edition, which will be hosted by Connor (yes, that’s ‘dinosaur measles’ Connor!) from Rule of 6ix.

Images:
Crowded cell by TimVickers.

Summary: Scientists show that vertebrate-specific globins originated in two rounds of genome duplication.

We vertebrates work for our O₂. Whether we’re a fish or antelope, we all have gills and lungs to filter oxygen out of air or water. We also have beating hearts to transport oxygen-rich blood to the most distant corners of our bodies. But not the lancelet. This little fishlike creature breathes directly through its skin. The lancelet does have gills, but it only uses them to filter food particles from the water, not oxygen. It doesn’t even have a heart to direct the flow of its blood.

The way vertebrates and lancelets handle oxygen also differs on a molecular scale. We vertebrates have evolved a whole suite of proteins for carrying and storing oxygen that the lancelets lack. The most well-known member of these proteins is hemoglobin, which makes up 95% our red blood cells. Hemoglobin is a perfect oxygen transporter. It takes up oxygen where its concentration is high (lungs) and releases it where concentrations are low (muscles and other organs). We also have globins that specialize in storing oxygen, such as myoglobin our muscles and cytoglobin in our brains.

The lancelet has neither heart nor hemoglobin.

The origins of all these oxygen-manipulating tools can be traced back to a dramatic event in our evolution. Almost half a billion years ago, not long after the lancelet and vertebrate lineage had parted ways, the entire genome of the vertebrate ancestor was carbon copied by accident. Twice. Our distant ancestor thus had four times as many genes as before. This opened up evolutionary pathways that were closed before. How so? Imagine your Lego collection quadrupled in size. Not only can you now build a larger castle, the extra bricks also bring added flexibility. You can combine them in new ways, while leaving the core of the castle intact. It’s much the same for duplicated genes. Their redundancy allows them to specialize, divide labour and evolve new functions.

In a paper that was published last month, scientists show that our globin genes were born from these two rounds of genome duplication. The team, lead by Jay Storz from the University of Nebraska, first retrieved all the globin sequences of lancelets, sea squirts and fifteen different vertebrates (birds, lizards, fish and mammals) and determined the evolutionary relationships between them.

They found that all vertebrate globins occupied four branches in the globin family tree. They were myoglobin, cytoglobin, hemoglobin and GbY, a globin that has only been found in reptiles and the platypus. These four lineages corresponded to a single lineage of lancelet globins. While such as a 4:1 distribution fits the double genome duplication scenario, the history turned out to be a bit more complex.

The genetic neighbourhoods of the three globins are similar - not identical.

Storz and his colleagues reasoned that if the four globin lineages really arose through genome duplications, their genetic neighbourhoods should look alike. After all, all the genes of our ancestor were copied in one go. As genes tend to retain their relative positions over time, the genetic neighbours of the copied globins families should be similar. Of course they won’t be identical after 500 million years of evolution. Genes are lost, gained and reshuffled all the time time. Nevertheless, the ‘neighborhood signal’ (geneticists call it synteny) is a strong one, and should still be recognizable millions of years later.

The team found three of these globin-containing neighbourhoods, spread out over different chromosomes. They dubbed them Mb (myoglobin), Cygb (cytoglobin) and Hb (hemoglobin). GbY turned out to be a more recent addition to the hemoglobin family rather than the fourth globin type. The researchers discovered that this fourth globin was missing altogether. Its former neighbours are still there, on our nineteenth chromosome, but the globin itself went extinct a long time ago. For want of a globin, the researchers named this region Gb^-.

The researchers show how the initial duplication produced the Mb/Cygb and a Hb/Gb^- cluster. This is an interesting split, as the proto-hemoglobins (the blood globin) evolved to become oxygen transporters while myo- and cytoglobin (the muscle and brain globin) became oxygen storage proteins. The authors write that “the first round of WGD may have initially set the stage for the physiological division of labor between the evolutionary forerunners of [myoglobin] and [hemoglobin] by permitting divergence in the tissue specificity of gene expression.” In other words, it was the genome duplication that allowed these globins to evolve specific functions in separate tissues.

After 500 million years of evolution, lancelets are small, mud-dwelling filter feeders. We vertebrates have evolved into free-roaming grazers, predators and 180 tonne heavy filter feeders. It’s thanks to the combined evolution of a complex circulatory system (our hearts and gills/lungs) and an elaborate oxygen transport system (the globin family) allowed our ancestors to become larger and live a more active lifestyle than our distant cousins. Hemoglobin is the key to a healthy heartbeat indeed.

These are not the best of times for amphibians. All around the world, populations of frogs, salamanders and newts are declining. At least 489 species (7.8% of all known amphibians) are nearing extinction. More than a hundred of these endangered species have not been seen in recent years, and have likely gone extinct already.

Who is to blame for this wave of extinction? While climate change, pollution and habitat destruction certainly play a supporting role in this amphibian drama, biologists now agree that a fungus is the major villain. The fungus in question is chytrid fungus, and bears the name Batrachochytrium dendrobatidis, or Bd for short, and causes a disease called chytridiomycosis.

This Limosa Harlequin Frog has died from chytridiomycosis. Notice the reddening of the skin and the lesions on its belly.

What Bd does to an amphibian’s skin is not pretty. The fungus grows right within the cells of the skin. When it has produced enough spores, they burst out of the cells and re-enter uninfected skin cells. This cycle of growth and infection causes lesions and a premature shedding of the top layer of the skin. Lee Berger, who first identified Bd in sick and dying frogs in 1998, wrote that “these specialized adaptations suggest that B. dendrobatidis has long evolved to live in skin.”

This seems strange. Bd only became a problem somewhere in the second half of the twentieth century. Analyses of museum skins show that Bd was absent from most affected localities prior to the 1970s. It has spread over the world at an alarming rate since then, killing frogs, salamanders and newts wherever it goes. But if Bd has really existed for a long time and kills its hosts with such vigour, shouldn’t it have burned itself out by now?

Biologists have come up with two general explanations for the sudden emergence and spread of Bd in the 20th century. Some have suggested that environmental changes make amphibians more susceptible to Bd. Others have proposed that Bd is a novel disease to which amphibians have no resistance. These two hypotheses are far from exclusive, and come with many flavours in between.

Feeling at home in skin

When the Bd genome was sequenced in 2006, biologists hoped it would reveal how Bd became a slayer of frogs. But without similar genomes to compare the Bd genome to, it was hard to draw conclusions about what makes Bd special. The chytrids, the branch of fungi that Bd belongs to, turned out to be particularly understudied.

Conventional chytrids are quite harmless. They are microscopic fungi that usually live in water or wet soil where they degrade leaves and other organic material. The closest known relative of Bd is Homolaphlyctis polyrhiza (or Hp). This fungus was isolated from leaf litter in Maine by Joyce Longcore. Erica Bree Rosenblum, evolutionary biologist at the University of Idaho, and her colleagues have now sequenced the DNA of this leaf muncher, to see what makes it different from Bd.

Rosenblum discovered several types of genes that are abundant in the Bd genome, but not in the Hp genome. The proteases were on of them. Proteases are like molecular scissors. These enzymes recognize, cut and cleave other proteins. Rosenblum found that three different protease families have expanded in the Bd lineage. They have between between four to ten times as much members as the same families in the Hp genome.

Each of these petri dishes is filled with skin flakes from cane toads. The left dish is untreated, the second dish has been treated with Hp, the third dish has been treated with Bd.

Fungi that infect human skin or nails are known to carry similarly large and diverse sets of protein slicers. They help the fungus to invade tissues and obtain nutrients by breaking down the proteins and cells of its host. It’s likely that the numerous proteases in the Bd genome also play a role in the colonization of amphibian skin.

Another abnormal group of genes in the Bd genome is the crinkler family. Crinklers have never been found in other fungi. They were originally discovered in oomocytes, which are single-celled organisms that infect plants and cause diseases such as late blight and sudden oak death. True to their name, crinklers cause the leaves of the plants they infect to crinkle. It is unknown what these proteins do to amphibian skin and whether they are important for infection, but their presence in the Bd genome is certainly intriguing.

Another group had described these Bd-crinklers earlier. They proposed that crinkler genes hopped from oomycetes to Bd and that this transfer of genes possibly led to the Bd-epidemic. Sophien Kamoun, who works with oomycetes and discovered crinklers in 2003, thinks that this conclusion is premature. “There are 62 crinklers in the Bd genome and they only resemble oomycete crinklers on a general level. If it is true that oomycetes are the source of the crinklers, they must have been transferred a long time ago.”

Rosenblum says the origins of Bd proteases are similarly ancient. “The Bd protease families expanded recently on an evolutionary time scale. This still means that most expansions are a millions years old. They certainly didn’t happen in the last 50 years.” So while the presence of crinklers and proteases might explain how Bd evolved to live in skin, but not why it became a global menace. These proteins loaded the gun, but they didn’t pull the trigger.

Conquering the world

I’ve painted a grim picture of Bd so far, but the truth is that not every strain of Bd is a global killer. In a recent PNAS paper, scientists describe two lineages of Bd from Switzerland and South Africa that are genetically distinct from the globally occurring lineage that is killing amphibians worldwide. They’re also not nearly as lethal. The researchers infected tadpoles with the South African strain and found that more than 7 out of 10 of them survived. Tadpoles that were exposed to global varieties of Bd were much worse off. In the most severe cases, less than 20% survived infection.

Isolated pockets of Bd such as those in South Africa and Switzerland have likely existed for a long time. Geneticists have uncovered some clues as to how a global killer fungus could emerge from such local varieties. To see what they found, we first have to take a short trip into basic Bd genetics. Bd is a diploid fungus, which means that it has two copies of each chromosome, just like humans have. Diploid organisms can thus carry two different versions of any given genetic variant, a situation which is known heterozygosity. When the same genetic variation is present on both chromosomes, this is called homozygosity.

Genomes of sexual organisms are a mixed bag of homozygous and heterozygous variants. But not that of Bd. Its genome is way more heterozygous than is normal. “The simplest explanation for this pattern is that the hypervirulent lineage of Bd is the product of two undiscovered parents”, says Matthew Fisher a geneticist from Imperial College London and co-author of the PNAS paper. In other words, the killer lineage of Bd is a hybrid fungus. It has received two different sets of chromosomes from its parents, which explains the high degree of heterozygosity in its genome. “Sex is rare for this species. But when it happens, a new strain with new properties might emerge”, says Fisher. “We think this is how hypervirulent Bd originated, somewhere in the 20th century.”

Not every frog is susceptible to Bd. Bullfrogs tolerant to the disease, but they can still spread it. Bd was introduced in Kent (UK) from North American bullfrogs.

Fisher thinks the international trade in amphibians is directly responsible for the emergence of Bd. “From the 1950s onwards the African clawed frog (Xenopus laevis) was shipped all over the world, first as a pregnancy test and later as a laboratory animal. This global trade in amphibian increased the possibility that two divergent lineages of Bd come into contact with each other. I’m pretty sure that hypervirulent Bd wouldn’t have evolved without the amphibian trade. We can clearly see the ongoing effects of this trade as it spreads the killer lineage ever more widely.”

Fisher’s team used the genetic relationships between the different lineages to date the emergence of Bd to 35 to 257 years ago, depending on which genome segment they analysed. Rosenblum points out that this analysis depends on a number of assumptions, each of which could affect the outcome. “My suspicion is that our next wave of analyses will suggest these genetic transitions are more ancient than that”, she says. Fisher admits that it is hard to argue what the exact emergence date is. “But since it underwent its spread in the 20th century, we think it is likely that the recombination event took place in recent history.”

A firmer answer to the questions where and when Bd evolved will have to await the sequencing of more genomes, from other lineages of Bd and from additional chytrids. Each genome will provide another piece of the puzzle. There are still corners of this world where Bd hasn’t penetrated yet, such as Madagascar. The sooner we understand this amphibian scourge, the better we can prevent its spread. The frogs will thank us for it.

Deep beneath the waters of Costa Rica, dozens of crabs are waving their claws in unison, in what seems to be a rhythmic performance. It’s almost as if these crabs are locked in a ritual dance. But these charming crabs are not dancing. They are farming.

The hairy claws of these crabs are covered with bacteria. With every swing of their arms, they mix up the water column and provide their homegrown bacteria with additional nutrients. The submersible team that discovered this new species shot this amazing video of the gardening crabs in action:

These white and hairy crabs are a new species of ‘Yeti crab’. The species received the formal name of Kiwa puravida in PLoS ONE article last week, meaning ‘pure life’, which is a common saying in Costa Rica.

The first Yeti crab (Kiwa hirsuta) was discovered in 2006 off the coast of Easter Island. The team that discovered this crab already noticed that its bristled claws were covered with bacteria. They only collected a single specimen however, limiting the opportunities for a thorough investigation of the association between bacteria and crab. The nature of their relationship remained a mystery.

Until now, that is. Not long after these first Yeti crabs were found, more Yeti’s revealed themselves, over 6,500 kilometres away from Easter Island. This new species was discovered thanks to one submersible pilot. “Gavin Eppard is one of the pilots of the ALVIN submersible. He was in the sub when he spotted the new species of Yeti crab, standing on a carbonate block waving their claws back and forth”, says Andrew Thurber, one of the authors of the recent paper. “Gavin was on the original cruise that discovered the first Yeti. He immediately recognized that this was something new to science.”

The new species Yeti crab: Kiwa puravida (missing two walking legs, sadly).

The submersible team returned to collect more dancing crabs after this initial discovery. All the crabs were found waving their arms near cold seeps, where methane and hydrogen sulfide escapes from the ocean floor. You might think such environments are inhospitable places for life, but several species of bacteria thrive near such seeps. They liberate energy from methane and hydrogen sulfide by stripping the electrons from these molecules and passing them on to oxygen.

These species can form dense mats around cold seeps, but they also grow on the Yeti’s claws. Thurber and his colleagues found DNA belonging to two bacterial families that eat methane and hydrogen sulfide, respectively. Thurber thinks that the crabs perform their dance to make sure that the bacteria always have access to both oxygen from the ocean water and methane or sulfide from the seep. If the crabs would stand still, the symbiotic bacteria growing between its bristles could locally deplete either resource. But by waving their arms, Yeti crabs mix water and seepage, keeping bacterial productivity high.

The symbiotic bacteria of the Yeti crab were most similar to bacteria that live near hydrothermal vents and on the creatures that live there, such as the vent shrimp. Hydrothermal vents are similar to cold seeps, so Thurber suggests they disperse through the oceans using vents and seeps as stepping stones.

While these findings indicate that Yeti crabs grow their own food, Thurber and his colleagues also show that the Yeti’s harvest it. Thurber didn’t observe them snacking on bacteria in the wild, but he did film captured crabs that used their mouth parts to feed from their claws. “I initially put them in the aquarium to see if I could get them to dance. They wouldn’t, making me think that they sway their arms in response to the movement of water or a chemical queue. Instead they ended up feeding off their bacteria, which I was lucky enough to catch on film”, he says. Without seepage to farm in, this poor fellow probably went hungry:

The Yeti crabs themselves also contain traces of feeding symbiotic bacteria in the wild. Carbon comes in a heavy (C13) and a lighter (C12) variety. The enzyme that plants and bacteria use to derive energy from sunlight selects the lighter form of carbon slightly more often than the heavy form. However, the enzymes of microbes that consume methane or sulfide have a very strong preference for C12 over C13. As a result the ‘carbon signature’ of methane and sulfide munchers will be lighter than that of bacteria that obtain energy from sunlight. The carbon profile of the Yeti crab matched that of its symbionts, indicating that they are its main food source. The fatty acid distribution of Yeti crabs mirrored that of its bacteria in a similar manner.

All in all Thurber et al have made a compelling case that Yeti crabs grow and harvest their own bacteria. But don’t these crabs ever get tired from dancing? Thurber: “The crabs have to use energy to swing their arms back and forth – so by doing so they must gain more energy through their symbionts than they expend by waving their arms. I don’t think they get tired.”

The dancing yetis also seem to have more than enough energy to engage in some yeti wrestling from time to time. The ALVIN team captured a video of what seems to be two Yeti crabs fighting for a nice spot in the seep. The challenging crabs had recently molted, so perhaps it wanted a good position to regain its bacterial covering. But Thurber points out that this confrontation could also be a mating display, as crabs are known to mate after molting. Strife or love, you decide:

The Yeti crab’s rise to internet fame was swift. Proof: a compilation of crabs dancing to different pieces of music.

This bumblebee bat could be the smallest mammal in the world.

Isolation can be a blessing. I am most productive when I’m not connected to the web. If I’m writing in a train or plane, severed from the thoughts of others, it is easier to capture my own trails of thought and let them expand. Don’t get me wrong, my inner writer loves the internet. It’s where I go to learn about new research and get inspired by scientists and writers from all over the world. With every click I uncover a new idea or story, waiting for a mind to latch onto.

And this is why my inner writer loathes the internet. On the web it seems as if every idea has been thought of before and every story has been retold countless times. In an echo chamber filled with a thousand voices, it can be hard to find your own.

In nature life is not much different. Every animal, from the smallest bat to the largest cat, has to find a niche and voice of its own. Take Kitti’s Hog-nosed Bat, or the bumblebee bat. With a length of just 3 centimetres (1.2 in), this cute creature is a strong contender for the title of ‘smallest mammal of the world’. The bumblebee bat and occurs in two separate populations in Myanmar and Thailand. Its total natural range is restricted to a mere 2,000 square kilometres (770 square miles). For comparison: this is a region half the size of Rhode Island, and a little smaller than Luxembourg.

The natural range of the Myanmar (dark blue) and Thai (green) populations of bumblebee bat.

The Myanmar and Thai bumblebee bats are indistinguishable by eye, but not by ear. The echo calls of Myanmar bats have a somewhat higher pitch. The consequences of this difference extend beyond mere echolocation, because bats also use their echoes in personal communication. In some bat species, bats even prefer to mate with partners with similar echo calls. If the same is true for bumblebee bats, a small difference in echo frequency could have driven a wedge between the two populations in the distant past.

How so? Suppose that by chance, two groups arise within a population that each perceive the world in a slightly different way. If this small difference affects their choice of partners (such as with the bumblebee bats and their echoes, perhaps), these differences and preferences are passed on from generation to generation, become amplified and get locked in, up to the point where members of the two groups no longer recognize each other as potential mates. When they have stopped interbreeding, they have taken the first steps towards becoming different species.

Biologists have come up with several names for this process, such as ‘speciation through sensory drive’, but considering how these species-to-be ignore each other, I think ‘speciation through mutual ignorance’ is a better description. While it this makes for an attractive story, it is not the only explanation for the different echo frequencies of bumblebee bats. After all, these differences could also have evolved after the Thai and Myanmar bat populations became separated.

The Khwae Noi River (Kwai River) is part of the natural habitat of the bumblebee bat.

An international team of biologists, equipped with ultrasound detectors and mist nets, set out for the forests of Myanmar and Thailand to confirm whether bumblebee bats became isolated by ignorance or not. The team caught and released over 700 bats from Myanmar and Thailand, and took punctures of their skin or wings. A DNA analysis of these samples revealed that the smaller Myanmar population split from a larger Thai population around 400.000 years ago so. At such a coarse resolution, it is only possible to take a bat’s eye view of their evolutionary history. The researchers could only conclude that the Myanmar population likely originated from a small number of Thai bats, but not how or why they became isolated.

They therefore decided to ‘zoom in’ on the colonies that make up the Thai population, to see if they could catch isolation on the wing. Even though the Thai colonies form a continuous range, the team did find an abrupt change in echo frequency in the southern colonies. Southern calls had an increased frequency of 3 kHz, compared to the calls of bats from the north. This acoustic boundary was clear and sudden, but it wasn’t reflected in the DNA of the bumblebee bat. On average, colonies on both sides of the boundary did not differ more from each than other neighbouring colonies did.

One piece of DNA formed an exception. Bats from the north side of the echo border carried a different version than bats from the south. This stretch of DNA is located near a gene that is involved in producing hair cells in the bat’s hearing organ, so it might have played a role in the evolution of the different echoes of the Thai and Myanmar bats.

This is a CT scan of a complete skeleton of the bumblebee bat scan, provided by Digimorph.

The skewed distribution of this ‘echo location gene’ suggests that it provides an advantage of some kind. But what? Enter a second species of bat: Himalayan Whiskered Bat, or Myotis siligorensis. This bat is of a similar size and catches similar prey, but more importantly: it emits its echoes along the same bandwidth as the bumblebee bat. This could give problems if a bumblebee bat and whiskered bat would be out hunting and echoing in the same region. Their echo signals would interfere, and they would be unable to determine their distance to their prey.

The bats could avoid jamming each other’s frequencies if one of them would shift the pitch of its echo. Indeed this seems to be what happened to the bumblebee bats in the south of Thailand and in Myanmar. Recordings revealed that their caves were also frequented by whiskered bats, whereas in the north of Thailand not a whisker was seen.

The researchers conclude that it is unlikely that echolocation was the driving force behind the isolation of Myanmar and Thai bats. Given the large distance (for a bumblebee sized bat, at least) between the two populations and that Thai bats are genetically the most diverse, they suggest that a few bats were swept from Thailand to Myanmar by storm, cyclone or typhoon or perhaps one of the strong winter monsoons that occur about once every 100.000 years.

A handful of bumblebee bats, tumbling in the storm. As the winds die down, the creatures find themselves far away from home. From the woods sounds an all too familiar shriek, from an unfamiliar source. The bumblebee bats know what they must do. Time to find a voice of their own.

Remember the dancing Yeti Crabs? They’re back! Check out this amazing illustration of two farming Yeti Crabs by Irene Goede:

So white, so hairy.. I want to pet them!

Irene is a freelance illustrator who has specialized in nature and history. Every week, she draws an animal that has been in the news for the kids section of NRC Handelsblad‘s science supplement. You can find a selection of her illustrations here.

I love how realistic, yet playful and full of character these Yeti Crabs are. Judging from its carapace, the depicted species seems to be Kiwa hirsuta (which is the hot vent variety, not the species that lives near cold seeps).

I fell in love with Yeti Crabs from the moment I learnt about their peculiar existence below the sea. I’m delighted that the first piece of art I bought myself features these weird and wondrous creatures.

Protobalistum imperiale from around 50 million years old of Bolca, Italy.

Like most evolutionary tales, this one could have started on the Galapagos Islands. Instead we find ourselves in an ancient sea, near the end of the Devonian, 360 million years ago. A mass extinction has struck life underwater. The armoured placoderms, once an abundant class of fishes, have gone extinct. Other groups of fishes have been decimated and are struggling to survive. But, as a Dutch saying goes, one man’s death is another man’s breath. For the ray-finned fishes (fishes whose fins are supported by a ray of spines) this time of trouble is a time of opportunity. With their direct competitors out of the way, they are free to evolve into a multitude of shapes and species, from stream-lined hunters to plump grazers. The fish are dead. Long live the fish!

Fast forward to today. With over 23.000 species alive, ray-finned fishes are the largest and most diverse group of vertebrates of this day. Their rapid evolution after the Devonian mass extinction was the turning point that ensured them their evolutionary success. Biologists have come across similar explosive patterns of diversification across the tree of life, and call them ‘adaptive radiation’. Adaptive radiations are evolution’s way of hitting the jackpot. The payout is twofold: a single lineage spins of many new species (speciation) that adapt to diverse ways of life (adaptation).

A species may radiate when it finds itself in an environment where plenty of ecological opportunities await exploitation, such as when it has just colonized an island or lake, or after mass a extinctions. Darwin’s Galapagos finches are the iconic examples of such an adaptive radiation. A single ancestral species arrived to the Galapagos archipelago and split into a dozen species, each one adapted to the local circumstances of its island. The finches with the heaviest beaks eat the largest seeds, whereas those with slender, sharp beaks ones that catch insects.

The beaks of Darwin's finches are adapted to different food sources.

These little finches have been studied in great detail ever since Darwin first set foot on the Galapagos, but biologists still know little about how adaptive radiations unfold. Some think that species and their different shapes evolve in a single burst. This explosive diversity is then followed by periods of relative stability. Others disagree, and think that radiations occur in stages. They argue that new species first adapt to their environment or habitat, by changing their body shape and size, before they adapt to a specific diet or way of life, by changing their skulls and jaws. In this model, wings evolve before beaks, fins before mouths and legs before teeth.

Biologists have argued both ways, but neither side has delivered convincing evidence so far. This is where fossils of ray-finned fish come in. The biggest advantage dead fish have over living finches is that we know both their past and future. This makes it possible to track their radiation through time and see whether their different shapes evolved in steps or not. The fossil record of ray-finned fish is rich, and they underwent multiple adaptive radiations. For the first time after the Devonian mass extinction, and a second time at the end of the Cretaceous period (around 65 million years ago), when a massive asteroid struck earth and killed off many species of animals, including the dinosaurs.

Lauren Sallan and Matt Friedman investigated both these radiations by digitalizing the shapes of 69 Devonian fish and 304 fish from the Cretaceous. They first mapped several landmarks onto their skulls and skeletons, such as the positions of their jaw joints and fins. In the next step they determined which axes of these landmark maps explain the major differences between fish. They then analyzed how these differences changed through time.

Ray-finned fish evolved their heads before tails. Skull diversity starts to increase right after the Devonian (orange range), in the Tournaisian (darkest green). The diversity of body shapes lags behind.

Sallan and Friedman found that for fish from both era, heads evolved before tails. The heads of Devonian fish started to diversify right in the aftermath of the mass extinction. Some skulls became longer and flatter, while skeletons lagged behind. Only after a couple of million years did some evolve the shape of flat spades, in addition to the classical torpedo-shape. The Cretaceous fish also went through a head-first phase. Their skulls grew more elongated and streamlined before the main extinction event at the end of the Cretaceous, and long before their bodies followed suit.

This head-first trend in the evolution of ray-finned fish contradicts the biological big bang model of adaptive radiations, and it is a direct reversal of the idea that radiating species first adapt to their habitats. So why would fish evolve their skulls before anything else? The answer seems simple: to bite, crush, rip, nibble and suck. Certain niches might have been left vacant after the Devonian and Cretaceous mass extinctions, and ray-finned fishes evolved the jaws to exploit them. Large predatory fish died out after the Cretaceous extinction for example, making room for creatures such as the sword-fish like Blochius to evolve.

But skulls did not only evolve earlier, they also reached their peak diversity in a shorter span of time than body shapes did. This suggests that it’s also easier to evolve most variations on a skull than it is to evolve most body forms.

Blochius was a swordfish that lived 56 to 34 million years ago, in what is now Italy.

Friedman and Sallan are careful to generalize their findings to other adaptive radiations. “The real world is more complicated than any model”, is what they write in their final paragraph. A lot more studies need to be done before either theory can be discounted. That said, Sallan thinks the head-first model has the potential to explain a large portion of adaptive radiations. “There’s anecdotal evidence for many groups: lungfishes, sharks, birds, mammals, insects and even worm lizards“, she says. “And in a way it makes sense. When an animal is faced with limited food relative to the total population size, which is likely in a successful group, it has two choices. It can either find a new resource, or move to a new habitat and hope the same resource is there. Changing diets in probably easier and more likely to be successful.”

Do these findings mean that shifts in behaviour are the ultimate drivers of adaptive radiations? A bird first has to change its diet before it can change its beak, after all. Sallan thinks this might be the case. “Animals can be plastic in what they eat”, she says. “You hear about deer eating squirrels, squirrels eating birds, etcetera. Marginal dietary behaviors could turn out to be beneficial and some individuals might be better at exploiting a new food source than others, due to variation already present in the population. Directional selection then takes hold. So basically, you never know until you try!”

Happy belated new year everyone! 2011 was a wonderful year for me. Not only did my blog move to its shiny new abode at Scientific American, I also joined the science desk of NRC Handelsblad, a daily Dutch newspaper. I started out as an intern and was later hired as a staff writer. Since I’m organizing the discussion session ‘Going from blogging to MSM: selling out or gateway drug?’ together with Hannah Waters for this year’s Science Online conference, this seems a good time to share some of my personal experiences of being an on- and offline science writer.

The newspaper scrap above is an excerpt of my very first article that ran in NRC, on the 2nd of December in 2010. In NRC newsroom jargon, this is a ‘shortie’. Shorties range from 80 to 150 words in length and contain a short description of a single research paper’s results and findings. This one is about how oxytocin, a chemical often branded as the ‘love hormone’, can also induce negative memories. I remember spending a good 5 to 6 hours reading the paper and writing this piece.

So did it feel good to have made the newspaper for the first time? While I was relieved that my writing was deemed good enough for print (after several rounds of editing and rewriting – the first blow is never half the battle), the blogger inside me felt betrayed. As a blogger I was used to wrote long stories on subjects I was deeply familiar with. Here I was writing about oxytocin, a hormone I knew nothing about, in the tersest way possible. This is how science blogger extraordinaire Ed Yong covered the same research, using over 820 words. My 130 words looked stale in comparison. They were missing depth, context and nuance.

But before judging the shortie for what it isn’t, I should have realized that NRC Handelsblad is not the internet. Unlike Ed, a newspaper doesn’t have the luxury of unlimited white space. NRC publishes five science pages a week (and a larger science supplement in the weekend), so every inch of paper should be an inch well spent. A column full of shorties contains a diverse mix of science news in a short amount of space. They’re like chocolate sprinkles on a daily science dessert. And in a sense, their brevity is their forte (‘it’s not a bug. it’s a feature!’). Its length reflects its importance, relative to the other articles of that day. This kind of hierarchy is hard to come by on a blog, where every post seems as important as the next.

That said, short articles still make me uncomfortable. My biggest worry is that they contain enough information to pique a reader’s interest, yet not enough to satisfy her curiosity. Often I get questions from readers that were covered in the original research, but which didn’t fit into my story. And there’s always the danger of oversimplification. It’s impossible to trim down a research paper of 6 pages full of details and caveats to a hundred words without cutting some corners. Therefore, in my ideal newspaper, the last line of each short piece would read ‘click here to read more’.

If short stories made the blogger inside of me cringe, he should feel comfortable with the large feature articles that I’ve written, right? Yeah, that’s not true either. I’ve found that even in 2,300 words, there are always opportunities missed, details left out and ground left uncovered. A paper I mention might be a single part a much larger body of research. A person I interviewed might feel misquoted because I highlight key quotes from an hour long interview. Online, I could have linked to papers, additional sources, graphs and transcripts. Offline, the article is the article.

Forward-looking mainstream media organizations should recognize the potential of online reporting. I try to sneak in links into the newspaper whenever I can, but I’d like to see the integration of offline articles and online resources carried much further. And while I’ve been dipping my toes in this cross pollination already, with some of my blog posts becoming newspaper articles, and vice versa, I hope there’s a bigger role for me and other young bloggers to play in this transition in the future.

The story of a frog-killing fungus also became a story in NRC Handelsblad. Photo by Brian Gratwicke

Online-offline discussions aside, I am glad I had the opportunity to work in MSM. I acquired journalistic skills that I didn’t even know existed when I was a rogue blogger. The first time I called a scientist to interview them about his research, I was nervous. The interviews went horrible. In hindsight, I was trying to impress my conversation partner more than I was asking relevant questions. ‘Hey, I have a MSc degree in biology, I know what you’re talking about’. It took some time before I realized that it’s all right to ask basic questions.

This is but one example of many, and there is still much left to learn. Blogging made me a writer, but it is thanks to editors and colleagues, who were honest enough to criticize and give advice when it was necessary and kind enough to guide me as I stumbled onwards, that I became a better one.

Next week I’ll return to regular evolution blogging. Here’s to another year of genes, Neandertals, dinosaurs, Yeti crabs, ecology and evolution!

The bald uakari has a distinctive, but simple, face. Photo by Ipaat

Specks. Stripes. Red fur. Black fur. Eye masks. Bald spots. Beards. Moustaches. New World monkeys are nature’s motley crew. Their faces display an extraordinary range of colours and patterns. Some are simple and straightforward, others intricate and complex. Take the bald uakari. Its hypervascularized, red skin is striking, but uniform. The uakari’s nose is just as red as its forehead. Other species have more complex facial patterns, such as the marmosets. Large tufts of hair extend from around their ears. Specks of white and brown are islands in a sea of grey.

Evolutionary biologist Sharlene Santana was struck by this diversity. She wanted to know what evolutionary forces shape the colours and patterns on a primate’s face. Why is the marmoset’s face so much more complex than the uakari’s?

For us primates, faces are an important source of information. We are visual and social animals, reading faces is what we do. A face can tell to which group or species a primate belongs (species recognition), or reveal the identity of a fellow group member (individual recognition). Santana came up with two hypotheses to explain how these two modes of recognition affect the evolution of the colours and patterns on primate faces.

Wied's marmosets have intricate facial patterns. Photo by grendelkahn.

Santana’s first hypothesis is that a complex face aids in the recognition individuals. A face that consists of multiple distinct components also has more potential variations and combinations. If Mico has longer hair tufts and a darker eye mask than Sue, it’s easier to tell them apart. According to this scenario, primates living in large, social groups should have the most complex faces. Seeing who’s who at a glance is more important for them than it is for solitary animals.

In Santana’s second hypothesis, species recognition is the main driver of facial complexity. The roles are reversed in this explanation: solitary primates or primates living in small groups should now have the most complex faces. They only meet others of their kind sporadically, so they have to be able to rapidly identify that potential mate or territorial aggressor when they see one. This is easier when faces are distinctive and intricate.

To test these hypotheses, Santana collected photo’s of 129 different primate species, together with colleagues from the University of California. She scored all these faces on their facial complexity. She first divided the faces in 14 different regions and then tallied how many different colours occurred across these regions. A simple approach, but it is the first time that the facial colours and patterns of so many different species have been measured and compared. “Past work has been mostly focused on particular species or one feature of the face”, Santana says.

Emperor Tamarins have massive moustaches. Photo by Mila Zinkova.

Sure enough, Santana found a correlation between facial complexity and sociality: primates living in smaller groups have more complex facial patterning. This is in line with Santana’s second scenario, where species that rarely interact with others of their kind have to identify and classify other primates as quick as possible. When species live in the same habitat as a high number of closely related species, they also tended to have more complex faces. A distinctive and recognizable face is even more important when things get crowded.

The New World monkeys that live in large groups must have other means to recognize their fellow group members. Perhaps they can distinguish between subtle differences in shape and structure of noses, lips and eyes, or on differences in colour intensity, rather than the shape of facial patterns. Social primates also display a wider range of expressions on their faces. Perhaps there’s a trade-off between the evolution of complex facial musculature and of complex facial patterning. No one can see your grin if it is covered by a massive moustache, after all. These are interesting ideas, but they cannot be resolved until more primatologists have gathered more data on the expressions and facial musculature of New World monkeys.

When Santana compared the facial complexity of primates with their geographical distribution, she identified several other drivers of facial evolution, aside from sociality. Eye masks become darker towards the Equator and the east, to shield eyes from glare in open and sunny surroundings. In more temperate regions, beards, moustaches and hairs grow longer. In the forested west, monkeys have darker noses, to aid in camouflage. None of these ecological rules are absolute: a primate’s face is shaped by the combination of behavioural, ecological and social pressures.

It’s interesting that Santana never set foot in the Amazon rainforest or the Brazilian Caatinga for her research. She collected the primate pictures came from databases like All The World’s Primates and Arkive, she mined the information on average group size came from scientific publications and literature, and the data on their geographical ranges came from the database InfoNatura. All the data was there, but it Santana and her colleagues connected all the dots. “I think we are coming to an interesting point at which there is a ‘critical mass’ of data and resources for many species, all of which is allowing us to conduct these broad comparative and integrative studies. These would have been virtually impossible in the past”, Santana says.

Ever since Humboldt travelled Latin America, and Darwin described the emotions of man and animals, our collective scientific knowledge has increased. There are ever more dots to draw lines between and unforeseen patterns to uncover. Data-driven biology is the next chapter in study of life.

This stuffed coelacanth, described by Smith in 1939, achieved worldwide fame. Source.

It was supposed to be extinct. Yet here it lay, with fins round and fleshy, scales as hard as bone and a tail unlike any living fish. “Lass, this discovery will be on the lips of every scientist in the world”, James Smith said to Marjorie Courtenay-Latimer, curator of the East London Museum. Smith had good reasons to make such a grand claim. This was a coelacanth.

Naturalists had known about coelacanths for a long time – but only as fossils. It was Louis Agassiz who first described the group in 1839. Paleontologists had found dozens of different coelacanth species since then, but always in rocks older than 70 million years. The lack of coelacanth fossils in younger strata led them to conclude that coelacanths had gone extinct a long time ago. But the fish that now lay before Smith was no fossil. This creature had been caught only weeks ago, as bycatch by a fishing trawler off the coast of South Africa.

It was 1939, and the discovery of the first living coelacanth was on the lips of scientists around the world. The press heralded the fish as a ‘missing link‘, ‘prehistoric fish’ and ‘living fossil’. In doing so, they branded the coelacanths as a backwards fish for years to come.

The same stereotypes have haunted the coelacanth to this very day. In most popular accounts, the coelacanth is portrayed as a a forgotten survivor that has been left at the evolutionary wayside. In this modern fable, coelacanths had been trapped in a private bubble of time for millions of years until they re-emerged in the 20th century.

Axelrodichthys araripensis, an extinct coelacanth from South America. Photo by Ghedoghedo.

But the truth is that evolution leaves no fish behind. Coelacanths are as much affected by evolution as finches, ferns and flying lemurs. They have their own evolutionary history – we only need to look for it. This is what Japanese and African coelacanth researchers did not long ago when they took stock of the genetic diversity amongst coelacanths in the Indian Ocean. Through their research, they uncovered a small part of the coelacanth’s history of change.

Coelacanths have popped up in many places along the East African coast. Figure from first reference.

Coelacanths have popped up in several places in the Indian Ocean over the years, but the majority of them has been found in the Comoros archipelago. In the late eighties, Hans Fricke filmed how coelacanths inhabit rocky crevices and caves around the Comoros. At night he saw them drifting along the up- and downwelling currents, using their fins as stabilizers, to sneak up on unsuspecting fish. A short stroke with its fan-like tail, a sudden and forceful bite and its prey is gone.

Other coelacanths have been captured off the coast of Madagascar, South Africa, Mozambique and Kenya, but these fish have been dismissed as strays. Biologists reasoned that coelacanths would not be able to survive on the flat and sandy sea floors near Mozambique and South Africa. They presumed that strong ocean currents had swept the creatures away from the Comoros. These dead-end drifters were destined for death.

But there’s evidence that these stragglers represent distinct coelacanth populations. Geologists have identified several marine canyons near South Africa and Mozambique in which coelacanths could live. A dozen coelacanths have been caught near Tanzania every year since 2003. It’s unlikely that these are all strays. Indeed – when marine biologists let a remotely operated submersible descend in Tanzanian waters, they were able to capture footage of nine living coelacanths. Could this be the second home of coelacanths in the Indian Ocean?

In the paper that was published a few months ago, researchers have compare the DNA of Tanzanian and Comoran coelacanths. They found that some Tanzanian fish carry unique genetic variants. These variants were not found in any Comoran fish or anywhere else. This was especially true for coelacanths captured off northern Tanzania. The team believe their results indicate that coelacanths from northern Tanzania form a separate breeding population from the coelacanths from the South and the Comoros. These last two populations are much closer to each other genetically.

The researchers think the last common ancestor of the Tanzanian and Comaran coelacanths lived at least 200,000 years ago. For your sense of time: this was around the same time when the first modern human walked the earth. The researchers arrived at this estimate with a simple technique, known as the molecular clock: the more genetic differences exist between two lineages, the longer ago they diverged. But calibrating the clock can be tricky. Using a different calibration point, the researchers dated the split between the two populations to a few millions years ago.

Whatever the exact figure is, fact is that the Indian Ocean harbours distinct populations of coelacanths. If the Comoros Archipelago is the ancestral home of coelacanths, some fish have packed their things and settled somewhere else. Given enough time these populations might evolve into distinct species. We know this has happened in the past, for there are two species of coelacanth alive today. Aside from the West Indian Coelacanth, there exists a second species of coelacanth that was discovered at a local fish market two decades ago, near Indonesia.

Scientists have just started to collect and sequence coelacanth DNA. The amount of DNA analyzed in genetic studies (including this one) has been tiny so far. As more sequences will become available, more evidence of the continued evolution of the coelacanth will come to light.

Let’s leave the silly concept of ‘living fossils’ behind. Watch the movie above, and see the coelacanth sail the currents with subtle movements of its fins. Marvel at the mysterious headstand these creatures perform. Peer into its eyes, and see how the light is reflected back at you. These creatures are no fossils. They are very much alive.

As Smith wrote in the paper that announced the discovery of a second specimen:

“Numbers of successful modern fishes appear less well equipped for survival than the coelacanth. [..] Coelacanths can scarcely be regarded as degenerate fish. They are apparently full of vigour.”

These are good times to have tentacles. Thanks to the internet, even the most ordinary of octopuses can be catapulted to worldwide fame. Exceptional skills or abilities are not required. A simple coconut hiding act or a short crawl over land are more than enough to break the internet headlines. But as this new generation of octopus idols rises in the ranks of popular culture, we tend to ignore the cephalopod celebrities that came before them. This is the sad tale of a Victorian pioneer, lest we forget the tragedies that can befall our most beloved octopuses.

Henry Lee (1826-1888) adored octopuses. As the resident naturalist at the Brighton aquarium he wrote regular columns about these creatures, which he bundled in the short but delightful book “The Octopus”. Lee shared his fascination for all things tentacles with the Victorian gentry. In the chapter ‘Octopods I have Known’ he describes how the aquarium’s public had grown bored with the exotic fish that had been on display for so long. In those days, in the words of Henry Lee, “an aquarium without an octopus was like a plum-pudding without plums”. So when the Brighton aquarium obtained its first octopus in October 1872, the public rejoiced.

“The new octopus became “the rage.” Visitors jostled each other, and waited their turn to obtain a peep at him – often a tantalizing exercise of patience, for the picturesque rock-work in the tanks provided so many hiding places, that the popular favourite only occasionally condescended to show himself.”

In the winter of 1873, disaster struck the Brighton Aquarium.

“[It] became necessary to clean out a tank in which were some “Nurse-hounds”, or “Larger spotted dog-fishes”, Scyllium stellare. No hostility between them and the octopus being anticipated by their attendant, they were temporarily placed with it, and, for a while, they seemed to dwell together as peaceably as a ‘happy family’ of animals.”

A predator and prey, in one happy family. Splendid!

“But one fatal day – the 7th of January, 1873 – the “devil-fish” was missing, and it was seen that one of the “companions of his solitude” was inordinately distended. A thrill of horror ran through the corridors. There was suspicion of crime and dire disaster. The corpulent nurse-hound was taken into custody, lynched and disembowelled, and his guilt made manifest. For there, within his capacious stomach, unmutilated and entire, lay the poor octopus who had delighted thousands during the Christmas holidays. It had been swallowed whole, and very recently, but life was extinct.”

A nursehound swallowed the Brighton octopus whole.

Needless to say, Lee was shocked by this untimely death. At least there was some consolation to be found in the ‘brilliantly written’ and ‘kindly sympathetic’ articles that appeared in the newspapers. One of the daily papers of London reported on the tragic death of the Brighton octopus as follows:

“Thus was an end put to a most distinguished and useful life. Octopuses doubtless die every day, but seldom has there been an octopus who will be so much missed as the octopus at Brighton.”

It took almost two months before the aquarium had found a suitable replacement for the popular star. But the novelty had faded, and the public lost its interest in the shy creatures. Not before the invention of embeddable video clips would octopuses rise to fame again.

Geothermal pond near the Mutnovsky volcano, Kamtchatka. Copyright Anna S. Karyagina

“But if (and oh what a big if) we could conceive in some warm little pond with all sorts of ammonia and phosphoric salts, light, heat, electricity etcetera present, that a protein compound was chemically formed, ready to undergo still more complex changes [..] ”
~Charles Darwin, in a letter to Joseph Hooker (1871)

All life on earth is related. Trace back the separate lines of descent of all organisms that ever lived, and they will converge to a single point of origin – the beginning of life. Charles Darwin was reluctant to publish his views on life’s origin. His only speculations on the subject are known from a private letter to his friend and colleague Joseph Hooker, in which he speaks of a ‘warm little pond’ in which the first molecules of life could have formed.

A new and controversial study suggests Darwin’s stab in the dark hit close to truth. In the article that was published earlier this week, researchers claim that the first cells evolved in volcanic pools. This new hypothesis brings the origin of life debate back from the depths of the oceans to the surface of the earth – other scientists believe hydrothermal vents in the deep sea are the most conducive environments for nascent life.

The researchers, led by Armen Mulkidjanian, presume that the chemistry of modern cells mirror the original environment in which life first evolved. Since oceans and cells are chemically dissimilar, they think it is unlikely life evolved there. The chemical nature of volcanic pools, or ‘warm little ponds’, resembles the cell’s composition of its cytoplasm much more closely.

The researchers invented the term ‘chemistry conservation principle’ for their idea that organisms retain their chemical traits throughout time. They reason that the membranes of the first cells must have been simple and leaky. Metal ions could have flowed in and out unhindered, leading to a equilibrium between environment and protocell. As the cells adapted to the ion levels in their surroundings, they came to depend on them. Circumstance became necessity. Cells evolved ion pumps and iontight membranes to maintain the ion balance that was initially forced upon them – hence the assumption that cells themselves are reflections of their ancestral environment.

The occurrence of some key ions in oceans and cells.

This is not a new approach. The Canadian biochemist Archibald Macallum applied it as early as 1926, when he noted that ion levels were similar between blood and sea water and concluded that animals must have evolved in the sea. “Maccallum was also the first to measure the concentrations of ions within cells”, says Mulkidjanian. “He discovered that all modern cells contain more potassium than sodium.”

This century old observation is one of the cornerstones of Mulkidjanian’s argument: potassium outnumbers sodium in living cells, yet in oceans and lakes, sodium dominates. Other ions, like zinc, magnesium and phosphate are also present in much higher concentrations in modern cells than they are in oceans of past and present.

The same small set of ions is built into the core machinery of the cell, inherited from the last common ancestor of life. The backbone of DNA is made of phosphate, many ancient proteins require zinc, and the cell needs potassium ions to solder amino acids together in the manufacture proteins, one of the most important chemical reactions in life.

From these observations, Mulkidjanian and his colleagues conclude that it is unlikely life evolved in the sea. They think terrestrial springs, like those in Yellowstone Park, are much better candidate environments for the earliest evolution of life. They argue that geothermally active pools are the only places on earth where potassium, zinc, magnesium and phosphate are found in high enough quantities to explain the ionic content of cells.

Aside from containing the right mix of ions, the researchers list several other features that make volcanic pools suitable cradles for early life, borrowing heavily from the theories that were developed to explain how life could have formed in hydrothermal vents. “In water that flows through hot rock, organic molecules are spontaneously produced through a process called serpentinization“, says Mulkidjanian. “Michael Russell was the one who first brought this reaction under the attention of origin of life researchers. He also noted that hydrothermal vents are not solid, but porous. He suggested these pores could serve as hatcheries for the first cells.”

Mulkidjanian incorporated both these ideas in the volcanic pond model. “Serpentinization can also proceed in continental rocks. Indeed geochemists find organic molecules in the vapour that escapes from the surface. And our geochemical analyses show that in the past, porous minerals would have been deposited on the bottom of geothermic pools rather than mud, because of the lower acidity at the time. Cells could have used these honeycomb structures to survive. In a sense we took these ideas that were developed by Russell for the origin of life in the deep sea, and brought them to the surface.”

In their paper, the researchers write that ‘the terrestrial scenario outlined here incorporates all the features of the hydrothermal vents that favour the origin and early evolution of life, and adds more.’ But not everyone is convinced.

Heated vapour escapes the earht near the Mutnovsky volcano. Copyright Anna S. Karyagina

“The ‘principle of chemistry conservation’ is a postulate rather than a proven principle”, says Jim Cleaves from the Carnegie Institution of Washington. “It may be true on short time scales, but who can say what has happened since the origin of life?”

“Overall, I think it is questionable that organisms would have kept their original composition, given the variability observed in present cells. Is it not at least equally likely that they have modified their cytosolic composition once they had control over this process? Any modern environment which matches this composition would then be purely coincidental. In summary, I don’t get much from this paper that I would hang my hat on.”

Jack Szostak, professor at Harvard Medical School and 2009 winner of the Nobel Prize, has similar doubts about the chemical conservation principle, but he does not dismiss volcanic pools entirely. ” If there is a reason that a high potassium/sodium ratio is biochemically a good thing, then a prebiotic scenario that provided such a ratio might have been more favorable for the origin or early evolution of life”, says Szostak. “But we can’t rule out an origin in a low potassium environment followed by selection for high internal potassium.”

“Independent of these arguments, I do not think the oceans were a favorable environment for the origin of life. Fresh water ponds seem more favorable due to the lower salt and ion concentrations, which would allow for fatty acid based membranes to form. The accumulation of organic compounds in ponds is also easier to imagine than in the ocean, and geothermally active areas provide numerous advantages, as expressed by the authors.”

Michael Russell, one of the pioneers of the hydrothermal vent hypothesis, did not want to comment on the study.

Do I think life began in volcanic waters myself? I don’t know. What I do know, is that the origin of life has always been a topic that has divided scientists and poisoned debates. This is not surprising. The questions about who we are and where we come from incite controversy, precisely because they are dear to us all. Still I think it’s important to not dismiss new ideas outright, especially if they have been thought through. The wider our gaze, the higher our chance that we will one day find our warm, little pond.

Larva of a crocodile icefish. Photo by Uwe Kils.

Few fish would survive a swim in Antartica’s ice-covered waters. Temperatures can drop to -1.9 ℃, whereas a typical fish starts to freeze at -0.8 ℃. If the water is colder, microscopic ice crystals will soon infiltrate the fish through gills and skin and start growing from within. Nerves are severed, tissues damaged, and the fish dies within minutes.

But crystals don’t bother Antarctic icefish. These cold-adapted creatures carry antifreeze proteins in their blood and body fluids. The antifreeze proteins bind ice crystals and smother them by dividing the long and growing crystal fronts into many small and curved fronts. This inhibits crystal growth just enough to prevent the icefish from freezing.

The Antarctic Icefish rule the seas that lie over Antarctica’s continental shelf. Here, more than 90% of all fish are icefish. There are over 132 different species of Antarctic icefish known to science. Some are native to the coastal waters of Australia and South-America, but the majority of them dwell near Antarctica.

Many biologists assume that the antifreeze proteins were the key to the icefish’s evolutionary success. Antarctica went through a major period of cooling around 24 million years ago. Ice sheets formed and glaciers scoured over the continent. In a study that was published last year, German biologists found that the onset of this cooling event coincided with the origin icefish and the evolution of antifreeze proteins. Their conclusion was simple: the antifreeze proteins were the evolutionary innovation that triggered the diversification of icefish. With their newly acquired cold resistance, the ancestral icefish and their descendants invaded the frigid waters of the Antarctic and multiplied.

These ancestors were bottom dwellers. When they first spread out over the Antarctic shelf, a world of plenty awaited above their heads, full of tasty krill and opportunities. But this world was out of reach: icefish don’t have a swim bladder. To rise up from the sea floor, ice fish evolved other tricks. Some replaced bone with cartilage, others store fatty molecules in sacs between their muscles and under their skin, as a kind of visceral floating devices.

But now a team of ecologists and biologists suggests there’s more to this simple two-stage model. Their DNA analyses confirm that the last common ancestor of all Antarctic Icefish lived 22.4 million years ago, but also reveal that the majority of icefish diversity evolved 10 million years after these first origins. The Trematomus family originated 9 million years ago, the crocodile icefish 6 million years ago, and the Artedidraconidae 3 million years ago. These additional pulses of speciation occurred long after the first antifreeze proteins evolved.

Many icefish lineages diverged long after antifreeze proteins evolved.

The evolutionary path towards buoyancy was not straightforward either. In general, closely related species share similar ways of life. For example, one icefish family could have dominated the sea floor, whereas another lineage inhabits the upper waters. But when the biologists compared the buoyancy measurements of different icefish, they found a different pattern. Within each icefish family there were many species that had adapted to life at different depths. For icefish, there exists no link between niche and lineage.

Antarctica’s harsh and erratic climate might explain this lack of direction in icefish evolution. While Antarctica has been a cool place for millions of years, the degree to which the continent and its surrounding waters have been covered by ice has varied. Sometimes the ice expanded as far as the edges of the continental shelf, wiping out the animal communities that lived there, only to suddenly retreat again, leaving a few isolated ice caps behind.

In 2008, polar researchers describe how Antarctic life might have ‘hung by a thread‘ during such glacial periods. Fish and other creatures might have persisted in so-called ‘polynyas‘, areas of open water surrounded by sea ice. Or in this case, oases in a desert of ice. Once the ice retreated again, the survivors had an empty sea floor all for themselves. The cycle of creation and destruction of ice would have brought in new waves of colonists every time, explaining why the different lineages of Icefish repeatedly colonized the different layers of the Antarctic Ocean.

The Emerald rockcod, or Trematomus bernachii. Photo by Zureks

This goes to show that nothing in evolution is as simple as it might first seem. ‘Antifreeze proteins triggered icefish diversification’ makes for a simple story, but it does not hold up once we take a closer, deeper look. Even with antifreeze, Antarctic life has treated icefish harshly.

For creatures so familiar with extreme cold, it remains to be seen how they will cope with a warming world. The authors conclude: “In a tragic twist of fate, the development of polar climatic conditions that shaped the radiation of Antarctic icefish is now reversing, and the increasing temperature of the Southern Ocean, with the associated potential for the arrival of invasive species and disruption of foodwebs, is the greatest threat to the survival of this unparalleled radiation of fish.”

Climate change could be more than the icefish can take. There might be no icy oases this time.

A wild eel in the Grevelingenmeer. Photo shot by Arne Kuilman, all rights reserved.

Few animals travel so far to have sex as the European eel. When autumn comes, these eels leave their lakes and rivers and embark on an arduous journey towards the Sargasso sea. Most fish perish in the first leg. Some are crushed in the turbines of hydroelectricity plants, others are caught in basket traps. For those that do manage to exchange sweet for salt water, the journey has only just begun. Their spawning grounds are still 5,000 kilometres (3,000 miles) away. The eels swim for months, without resting or eating. When they arrive in the Sargasso sea, worn-out and exhausted, there is but one task left: to mate, then die.

As one life cycle comes to an end, another one begins. The first major stage in the life of a newborn eel is that of the leptocephalus, meaning ‘slender head’. At this stage the eel larvae resemble tiny leaves of glass. Their bodies are completely transparent and flat as a nickel. The leptocephali might look delicate, but make no mistake: these youngsters can fend for themselves. They grow much larger than average fish larvae and are competent swimmers. They have to be, for their first goal in life is to return to the homelands of their parents. Even when they catch the Gulf Stream and other currents in their tails, it can take them up to a year to reach Europe’s shores.

When the leptocephali near the coast, they transform into tube-like glass eels. The body plan of a glass eel is much closer to that of a mature eel, although it is still transparent. The miniature eels might hang about in the coastal waters for a while, but eventually they migrate upstream and colonize creaks and streams. Continental waters will be home for the next decade. As they increase in size, the eels climb the rungs of the food chain until they have reached the very top. Before long, the Sargasso calls again.

The life cycle of the European eel.

This might seem like an awfully complicated way to grow up and propagate, and it is. The life cycle of eels and their close relatives (mainly tarpons and bonefish) is one of the most complex known in fish. No other fish go through a leptocephalus stage, for example. These larvae are so different from adult eels that they were seen as a separate species until the end of the 19th century.

Dutch researchers have now found a clue in the eel’s genome as to how this complex life cycle arose. Unlike other fish, eels have retained eight complete Hox clusters in their genome. Hox genes are the master controllers of embryonal development. By switching other genes on and off, they shape the lay-out of the future animal. Amongst other things, the location and timing of Hox activity determines where limbs will sprout and how the brain is patterned.

Most vertebrates (including us) have four Hox clusters. The lancelet, one of the closest living vertebrate cousins, gets by with only one. Our extra hox clusters originated during two ancient genome duplications in our distant ancestor. One cluster became two, two became four. The protovertebrates put these additional Hox clusters to good use – they evolved brains, skull and jaws. The lancelets remained brain-, skull- and jawless.

This double duplication wasn’t enough for fish. The genes of the ancestor of teleosts went through a third round of duplication, creating 8 Hox clusters. But this time around, the expanded genetic toolkit did not give rise to new organs and bones. On the contrary: most fish got rid of their extra Hox genes and clusters. Zebrafish lost their 8th cluster entirely for example, whereas killifish lost the 6th. Except for the eels, of course. They just kept them all.

The Dutch researchers suggest that this high Hox cluster count allows the eels to unite two vastly different body plans into one life cycle. The transition from leptocephalus to glass eel is certainly dramatic. The gelatinous skeleton of the leptocephalus is absorbed and replaced by bone, the larvae shrink to half their size and the ribbon-shaped body becomes cylindrical. It seems likely that the larvae have to tap into the developmental potential of their extra Hox genes to pull this of, although the researchers haven’t tested this yet (they only studied Hox activity in the early embryo).

Of course the mere number of hox genes is not a direct measure of complexity. The slight shifts in timing and location of their activity are what make the difference for a developing larva. Yet there exist a second example of a creature with additional Hox genes and a life cycle that matches that of the European eel in its complexity. The salmon. It might not be a coincidence that the salmon’s genome has been duplicated a fourth time.

Charting the long and winded life cycle of the European Eel has taken centuries so far, but time might be running out. Long generation times make the creatures vulnerable to overfishing and habitat destruction. Eel populations have collapsed in recent years, up to the point where the IUCN has redlisted the species. It’s a small tragedy that fishermen are still allowed to catch eels young and old. Glass eels looking to return to Europe are harvested in Great Britain, Spain and France. Adult silver eels are caught as they leave for the Sargasso sea in countries like the Netherlands.

Fort Europe. Unreachable, inescapable.

The robotic submarine Hercules explores Lost City, a hydrothermal vent system in the center of the Atlantic Ocean. Image courtesy Deborah Kelley (University of Washington), Institute for Exploration, URI-IAO, and NOAA.

“Have you ever read Ulysses?”

The question catches me off guard. I am interviewing Michael Russell, a geochemist working at NASA’s Jet Propulsion Laboratory. Russell was originally trained as an ore prospector, but several twists and turns in his scientific career brought him where geology, chemistry and biology intersect: the origin of life. Decades of research on ancient rocks and modern biochemistry culminated into the hypothesis that life emerged as a self sustaining web of chemical reactions, in hydrothermal vents on the ocean floor. According to Russell and others, life was breathed into these carbonate chimneys by simple molecules seeping from the ocean floor.

We have only covered a handful of molecules and minerals when Russell brings up Ulysses. Confused, I admit there exists a James Joyce shaped gap in my literary knowledge. “Sorry”, I say, “I haven’t.” Russell laughs. “That’s all right, I mean who has? But I’ve finally finished it, and the one thing I got out of it was the word ineluctable. So we now have a paper out that is called ‘On the Ineluctable Requirement for Molybdenum in the Origin of Life’.”

Ineluctable. There’s no time to let the word sink in; the conversation is moving forward at a dizzying speed. We skirt past supernovas, the problems with primordial soup and endless stacks of turtles. Not until the dust has settled do I look up the relevant passage in Ulysses. None the wiser, I turn to the dictionary. Inevitable. Essential. Unavoidable. Words rarely used to describe molybdenum. Why, of all obscure elements known to man, would molybdenum be necessary for life?

Molybdenum was 'ineluctable' for the origin of life. Photo courtesy Alcehmist-hp.

The answer lies with the electrons that whirl around the molybdenum core. Like many other metals, molybdenum is eager to take an extra electron under its wings or give a spare one away. Life has eagerly exploited this ability to juggle electrons around. Cells not only incorporate molybdenum ions into their enzymes, but also zinc, copper, iron and nickel. Many of these metal containing proteins shuttle electrons between molecules, as if they are playing a massive game of hot potato, changing, breaking and building molecules along the way. Electrons truly are what makes life go round. Or, as the Hungarian Nobel prize winner Albert Szent-Györgyi put it: “Life is nothing but an electron looking for a place to rest”.

Some electrons find cold and empty beds in their search. Take the methanogens. These bacteria and archaea make a living by stripping electrons from hydrogen (H₂) and attaching them onto carbon dioxide (CO₂) in several steps, generating methane (CH₄) and water (H₂O) in the process. That might sound easy enough, but carbon dioxide is not a thankful molecule: it’s stable as it is, and very reluctant to accept additional electrons.

This is where molybdenum comes in. Or rather could come in, for while molybdenum plays a role in the conversion of carbon dioxide to methane, the mechanism that Russell proposes has not yet been proven for this particular reaction. Russell’s argument boils down to a single point: molybdenum can ease difficult electron transfers because it usually has not one, but two electrons to give away. There’s nothing stopping molybdenum from donating these electrons to two different molecules. In this way, the molybdenum ion could compensate for the effort of imposing one electron onto a stubborn naysayer (such as carbon dioxide), by donating the other one to a more willing recipient.

Two molybdenum enzymes, superimposed. Image from reference.

The forking of electrons works because the electron that rolls ‘downhill’ releases energy that is channelled into pushing the other electron ‘up the slope’. Some molybdenum enzymes are known to perform this trick, but no one really knows how widespread such crossed electron transfers really are in biochemistry. In an article published last year, Russell and Wolfgang Nitschke write that electron bifurcation ‘is an old, but almost forgotten friend of research’.

How old? In Russell’s most recent paper (the one with ‘ineluctable’ in the title), he and his team suggest as old as life itself. Previous investigations into the age of the molybdenum family were based on genetic sequences alone, and pointed towards a more recent origin. But comparisons between bare genes can paint a misleading picture. Genetic sequences are to proteins what recipes are to cooking: shallow descriptions that lack the finer subtleties of texture and form. This is why Russell and his colleagues compared the three dimensional structure of different molybdenum proteins instead. Structure is more conserved than sequence, which is perfect for exploring ancient relationships.

They found that the roots of molybdenum enzymes run deep. According to structure, most molybdenum proteins can be sorted into two piles: those of archaea and bacteria. The oldest divide in life. Archaea are microorganisms, just like bacteria, but their biochemistry differs like day and night. According to Russell, the presence of molybdenum proteins in both archaea and bacteria means they were also present in the last common ancestor of all life on earth. His conclusion: to master the molecules of metabolism, including both electron lovers and haters, life needed molybdenum (and tungsten, which is chemically similar).

Does the ancient origin of molybdenum enzymes really prove that electron bifurcation by molybdenum was ‘ineluctable’ for the origin of life? No. When it comes to life’s earliest beginnings, some degree of speculation is inevitable. “Some of the time, you’re just going to be wrong”, says Russell. “We try to approach the truth, but we have to face up with the fact that we cannot be right all the time.” While molybdenum might not be the key to our origins, it still holds a clue to the larger riddle, a tiny puzzle all in itself.

Russell has one more argument to persuade me that molybdenum really does hold the answer to life, the universe and everything. Near the end of our conversation, he asks whether I have read the Hitchhiker’s Guide to the Galaxy. “The atomic number of Molybdenum is 42.” I can almost hear the grin on the other end of the line.

Aurochs were the ancestors of domestic cattle. Photo Marcus Sümnick

Animals were wilder then. Horns were longer, temperaments fiercer. These wild things had forever been free when humans took control of their flocks and herds, 10.000 years ago. Through careful breeding and rearing, the first pastoralists of the Near East moulded the beasts into more docile versions of their former selves. Over time, Bezoar became goat and auroch became cow. But it weren’t just the beasts that changed. Somewhere deep inside their lungs, invisible to the human eye, a wild bacterium became livestock disease.

Meet Mycoplasma mycoides. This bacterium has left a long and bloody trail through livestock history. Virulent strains of Mycoplasma raged around the world in the 19th century, killing millions of goats and cows. But the roots of Mycoplasma mycoides run deeper. In their paper, Anne Fischer and her colleagues show that the entire Mycoplasma mycoides cluster arose 10,000 years ago. Mycoplasma mycoides is as old as the livestock it kills.

A severe Mycoplasma infection begins with a cough, followed by a groan, a grunt and more coughing. Breathing becomes difficult and painful. Eventually, the cow or goat becomes listless and, in the terminal stage of disease, stops moving altogether. It just stands there, oozing mucus and saliva from its nose and mouth, until it dies. Untreated, the most deadly of Mycoplasma strains can slaughter herds within days.

Mycoplasma mycoides travels in the droplets that are released with every cough and breath. A goat or cow has to be to be in direct contact with the droplets from a diseased animal in order to contract the disease. This is not as rare of a occurrence as it sounds. All it takes to infect an entire herd is one infected animal in a tightly packed truck, stable or kraal. After a major outbreak amongst goats in South Africa, veterinary surgeon Duncan Hutcheon recalled the extraordinary speed at which the disease spread and animals died:

On 4 March 1881, the main flock began to show evidence of lung disease which spread rapidly. Some 700 goats died in the next 14 days. I was not sure at first that the disease could be contagious. I had no knowledge of any disease which could cause the death of so many goats so quickly.

The nineteenth century Hutcheon lived in was a golden age, as far as Mycoplasma mycoides was concerned. The livestock trade became global, while vaccination programmes were still in their infancy. Entire countries could be infected by a single animal. 50 years before Hutcheon described the outbreak amongst goats, a handful of cows in his country became infected by a Friesian bull, imported from the Netherlands. The disease soon swept through South Africa, killing 100.000 cows and oxen along the way.

A young Navajo woman tending to her sheep and goats.

To be fair, not every strain of Mycoplasma mycoides is a killer, and not every infection ends in death. The Mycoplasma family is large and most strains are not as lethal as Mycoplasma mycoides mycoides (for cows) and Mycoplasma capricolum capripneumoniae (for goats), the two strains that cause the contagious pneumonia described above.

Over the past few years, scientists have realized that the Mycoplasma mycoides family extends beyond its two most infamous members, but have so far failed to chart all the relationships between the different strains. To figure out who is related to whom, Anne Fischer and her colleagues collected 118 different strains from all over the world, and sequenced 7 of their genes. The collection features bacteria from all times and places, including strains isolated from African cattle in 1931, Rocky Mountain goats and Mouflons from Qatar.

Using the genetic differences between strains as a measure for their kinship, Fischer’s team reconstructed the entire Mycoplasma mycoides family tree. From this tree, the team concludes that the founding father of all Mycoplasma mycoides lived 10,000 years ago – around the same time pastoralists domesticated cattle, goats and sheep in the Near East. It’s easy to see how a lung disease would thrive better in a dense, human controlled herd, compared to a wild one. Animals are brought together in kraals, stables and around watering troughs, and if the herd is mixed, they are exposed to bacteria and viruses they haven’t encountered before.

No bacterial family is born out of thin air, not even a lung disease like Mycoplasma mycoides, so who where its ancestors? Was it indeed a wild bacterium, lurking in the lungs of the first wild beasts herded by man, as I suggested in the introduction? Fischer and her colleagues might have found a clue to that points in this direction. In their extensive collection of bacteria, they identified an unknown relative of the Mycoplasma cluster in several wild goats. This new species was isolated from Alpine ibexes in zoos and from a wild Rocky Mountain goat. The researchers are already sequencing its genome and characterizing its biochemical traits, to see what secrets about Mycoplasma mycoides‘ ancestry it holds.

The family tree of the Mycoplasma mycoides cluster. Horizontal axis represents time, in years. The entire cluster is 10,000 years old, but the two most virulent strains (M caprcicolum subsp capripneumoniae and M mycoides subsp mycoides) are much younger.

Mycoplasma leachii, a member of the Mycoplasma family that causes inflammation in the joints and udders of cows rather than pneumonia, has another interesting story to tell. Most strains formed distinct genetic populations. Not Mycoplasma leachii. The researchers discovered that this bug is of hybrid origin. Almost a third of its genes come from Mycoplasma that cause contagious pneumonia in cows, whereas the remaining two-thirds are from goat-specific strains. Since no Mycoplasma can survive without a host, the hybridization must have taken place within a single a single animal. Animals in mixed herds run the most risk of becoming infected by multiple strains. They are what the authors call “hybridization ovens”, baking new Mycoplasma mycoides variants in their co-infected bodies.

While Mycoplasma mycoides as a family might be as ancient as livestock itself, the two most contagious and deadly strains are much younger. The common ancestors of the strains that cause contagious pneumonia in cows and goats lived between 91 and 414 and between 56 and 490 years ago, respectively. I’m surprised that the authors make little note of this in their paper and wonder what could have favoured the origin and survival of these hypervirulent bugs in recent centuries. Herding made Mycoplasma mycoides – but what turned it into a killer?

Evolution has a knack for confronting us with strange and unexpected questions. One of them echoed through the halls of the Collections Centre of the National Museum of Scotland, not too long ago:

“Why does a fish need a sacrum!?”

Lauren Sallan was peering through her microscope, studying a fossil specimen of Tarrasius, when she noticed something odd. Its spine was divided into five sections, as it is in every tetrapod, the group of four-limbed, land-dwelling animals that includes humans. The only problem: Tarrasius was a fish.

Modern fish don’t have a sacrum, nor do they have a neck or thorax. Their vertebral column is a monotonous series of vertebrae strung together, with only minor modifications from head to tail. For us tetrapods it’s a different story. Travel down our spine and you will encounter five distinct types of vertebrae, each with their own place, function and shape. First up are the cervical vertebrae of the neck, followed by the thoraic vertebrae that carry our ribs, the lumbar vertebrae, the sacral vertebrae wedged between our hip bones and finally the caudal vertebrae of the tail, for those of us that have one.

Since segmented backbones evolved in the early tetrapods that exchanged water for land, paleontologists assumed it was a specific adaptation to a terrestrial life. The enigmatic Ichthyostega, an ancient amphibian that lived between 375 and 360 million years ago, was amongst the first to waddle around with such a fully ‘regionalized axial column’. Ahlberg, who reconstructed the Ichthyostegaskeleton in 2005, pointed out that Ichthyostega could probably flex the lumbar region of its spine up and down. This was a departure from the side-to-side wrenching that is so typical of fish. Ahlberg speculated Ichthyostega could walk, or at least crawl.

Update: computer models indicate Ichthyostega could not walk. Like the Tarrasius paper, this research was published today.

Case closed, but not quite. Tarrasius tells a rather different story: not all animals with necks and sacrums were landlubbers. Far from it, Tarrasius was a small and slender eel-like fish. It lived between 359 and 318 million years ago, in the shallow waters of what is now Scotland. Here it stalked the reefs, crushing the shells and carapaces of its prey with its molars, just like modern wolf eels do.

Tarrasius crushed its prey with its molars, just like modern wolf eels do. Photo Dan Hershman.

While Tarrasius might have looked and lived like a modern eel, it certainly didn’t swim like one. Its lumbar vertebrae were compact, its sacral vertebrae huge and locked into each other, whereas the vertebrae in its tail were tiny, thin and scattered. Sallan think this unusual anatomy allowed Tarrasius to thrust through the water like a giant tadpole, sweeping its flexible tail from side to side. The rigid trunk would have controlled the forces generated by the beating tail. This is why this fish needs a sacrum.

Put this way, it makes perfect sense for a fish to have a segmented vertebral column. Yet this particular arrangement of vertebrae only evolved in Tarrasius and in tetrapods. How did two distantly related lineages stumble upon the same solution? Was there a common template, an ancient developmental program that unfurled in Tarrasius and tetrapod, but was ignored in others? Or did similar selection pressures shape their backbones in similar ways? In other words, is homology or convergence to blame?

There are signs pointing in both directions. For example, even though dogfish have no segmented spine, regulatory Hox genes in the vertebral column of developing dogfish embryos are activated in the same order as they are in tetrapod embryos, where they demarcate the boundaries of the segments in the tetrapod spine. Perhaps the recipe for a segmented spine was already present in the common ancestor of cartilaginous and bony fish^.*Tarrasius and tetrapods could both have drawn upon this developmental potential, an axial patterning system more ancient than themselves. Now might be too early to verify or reject this possibility: developmental biologists have only just begun to chart the diversity of Hox gene activity in the animal kingdom. At the moment, Hox gene expression data is only available for a handful of creatures, few of them fish.

Acanthostega, one of the first tetrapods with limbs.

Regardless how deep the roots of these genes run, the segmented spine evolved twice, on independent occasions. What made Tarrasius and tetrapods converge on this particular body plan? Sallan suggests it was their similar way of lifen. Both the first tetrapods and Tarrasius united a short torso and heavy skeleton with a broad an strong tail. Tarrasius propelled itself forward with its paddle-shaped pectoral fins, tetrapods used their webbed limbs for the same purpose. And finally, both were bottom dwellers, navigating reefs and floodplains.

If this scenario is true, our distant ancestors evolved a segmented spine to be adept swimmers in shallow waters. Only later did their swimming rod modified to bear our limbs on land and make walking possible. This would not be the first trait our ancestors coopted and repurposed. The gait we think is so typical of land-dwelling animals evolved underwater. Lungfish can walk too.

Whether these speculations will hold up in the future is up to science, but I can tell you I find this more complex and detailed explanation immensely more satisfying than any simple story in which our ancestors ‘crawled on land’. There is no direction in evolution, no creature with the foresight to realize that opportunities await outside of the water. The first tetrapods were animals in their own right, with adaptations for their own sake and an uncertain future ahead of them. Their path was never clear-cut. The segmented spine that was vital to the terrestrial success of our ancestors, turned out to be a dead end for Tarrasius. Wrong place, wrong spine. Rest in science, little buddy.

*: Confusingly, tetrapods are bony fish. Blame the taxonomy.

Terrestrial hermit crabs love peanut snacks, but can only smell them when it's wet. Illustration Irene Goede. Used with permission.

The Caribbean hermit crabs in Anna-Sara Krång’s laboratory are no picky eaters. They are eager to gobble down any fruit, nuts, fish or coconut flakes that comes their way. But above all else, these culinary connoisseurs prefer peanut flips. These snacks are always the first to disappear down their gullets when feeding time comes around.

The hermit crab’s refined taste is matched by its sense of smell, which is renowned amongst the biologists that study them. Robber crabs, close relatives of terrestrial hermit crabs, can locate coconuts from great distance by smell alone for example. Some hermit crab species can even smell death. When one crabs dies, others will track down its cadaverous scent in a macabre race to claim the shell it left behind.

Hermit crabs don’t have a single nose, like us. They have hundreds. Their inner antenna are covered by scores of thin and short hairs (called aesthetascs) with which they smell. The crabs flick these hairy antenna back and forth to sniff the air, or tap them on the ground to sample the dirt. A large part of the hermit crab’s brain is dedicated to processing the scents and tastes that their antenna pick up.

Consider Krång’s surprise when she discovered, through a simple experiment, that her crabs could not smell the peanut snacks they seem to savour so much. This is what Krång did: she placed a hungry hermit crab in a plastic box wit an upturned flower pot for shelter and two pitfalls on either side. A tasty snack awaited in one pitfall, whereas the other remained empty. Krång would leave the crabs to their own devices for the night (hermit crabs are nocturnal creatures) and noted in which pitfall the creatures had scuttled by the next morning. If hermit crabs could pick up the scent, most of the crabs should end up in the pitfall that contained the food.

But the crabs failed the sniffing test. Hard. Sure, half of the hermit crabs were lucky to find a tasty piece of salmon or some peanut crisps, but the other half went hungry for a night. The hermit crabs stumbled into the pitfalls at random, oblivious of the odours that could have led them in the right direction. Only the freshly diced bananas and apples could coax the crabs: between 80 and 90 percent of the crabs managed to find these treats.

In parallel to these choice experiments, Krång and her colleagues measured whether the crab’s antenna could detect a battery of different odours directly. She removed the antenna from euthanized crabs and placed them between electrical wires. She then applied puffs of different odours to the amputated antenna, to see whether they would elicit an electrical response. In total, Krång tested 140 different compounds this way.

By fixing antenna between electrical wires, it is possible to make an 'antennogram': a recording of the antenna's electrical response to certain odours. Image Joby Joseph

Krång found that the hermit crab’s odour palette most resembles that of their aquatic relatives. It certainly wasn’t as rich as that of insects, or robber crabs for that matter. “They did not respond to esters, lactones and ketones, which we know are typical terrestrial odourants. The limited set of compounds they did respond to were soluble in water, such as acids and amines”, Krång writes in an e-mail.

Then it hit Krång. What if the crabs depend on water to smell the world around them? This would explain why the crabs were able to find moist fruits, whereas the dry peanut crisps escaped detection by their probing antenna. To test this hypothesis, Krång repeated the pitfall experiments, with a cup of water right next to the dry peanuts. As if by magic, the crabs now homed in on their beloved snacks. Around 75 percent of the creatures chose the correct pitfall. It must have been the peanut odours that lured them: the crabs were not attracted to a cup of water by itself.

Krång also repeated the antenna experiments, but this time she made sure the air was moist before she released the odorous puffs. Bingo. The electrical response to certain odourants was three to ten times higher in humid air than it was in normal conditions. Krång does not know for certain how water vapour affects the transmission of odours, but she thinks that the water helps them to diffuse through the thin walls of the aesthetascs.

It seems the hermit crabs are still struggling with their aquatic heritage. The ancestors of terrestrial hermit crabs crawled out of the water not too long ago. The oldest fossils of land dwelling hermit crabs are about 20 million years old. A blink of an eye, or a flick of an antenna, in the grand scale of things. The terrestrial track record of insects stretches as far back as 400 million years ago.

Caribbean hermit crabs are also called soldier crabs.

Trading water for land takes more than lungs and legs. The world smells different up here. Under water, molecules that are soluble in water carry farthest, whereas gaseous molecules are the most stable and reliable signals in the air. Krång’s research shows that have not quite made the switch. The scents they perceive occupy the interface between water and land. Yes, they can smell food from great distance, but only when the air is moist.

Credit where credit is due: the hermit crabs cope perfectly well with their limited sense of smell. They live near coasts and on tropical islands, where the sea is always near. But how will they proceed from here? Will they continue to adapt to life on land? And if so, will their aesthetascs ever be tickled by the spicy scent of pine? Will they ever savour a whiff of sweet cinnamon, or enjoy the smells of freshly roasted peanuts in the morning?

Perhaps. The insects have done it before. Their ancestor evolved an entire new suite of genes that is dedicated to sensing terrestrial odourants, like esters and ketones. A new gene family for new smells. That sounds like a sensible solution, but it’s impossible to say whether hermit crabs will follow the same path.

For now, the peanut-loving hermit crabs have plenty of mysteries to divulge, says Krång:

“Why do hermit crabs have such enormous olfactory lobes, while they can only sense such a limited number of odours? We still don’t know the answer to this. Also, their close relative, the robber crab (Birgus latro) seems to detect and also be attracted to insoluble odourants. We don’t yet know why this difference exists.”

Images:
Caribbean Hermit Crab crawling towards peanuts by Irene Goede. Website.
Antennogram by Joby Joseph
References:
Krång AS, Knaden M, Steck K, & Hansson BS (2012). Transition from sea to land: olfactory function and constraints in the terrestrial hermit crab Coenobita clypeatus. Proceedings. Biological sciences / The Royal Society PMID: 22673356

Carving blog posts one by one. Photo theangryblender

Today, the Scientific American blogging network celebrates its very first birthday. It has been a tremendous ride so far, and I would really like to thank you for reading along so far, but there’s one little question I wanted to get out of the way first:

Who are you?

You see, writing this blog is fun. Loads of fun. I get to cover science I am interested in, and there are no editors hacking and slashing my writings to pieces. Here, there’s only one person with full editorial control, and I like his style.

That said, I have no idea whether you like this blog. I can see how many of you click, like, stumble and tweet, but I haven’t the faintest clue who you are or why you read this blog. So I want to follow Ed Yong’s excellent example, and ask you some questions to get a better idea of who you are and why you come here. Are you a scientist yourself, or ? How did you find this blog? Do you like what you read, or are there other topics I should cover more?

It doesn’t matter if you’ve never commented before or don’t want to say much, but please take the stage and leave a comment behind.

Thank you!

Photo by redwood1

Somewhere deep in my grandmother’s veins, a blood clot breaks free. Her blood carries the clot past her heart, to her lungs, where it becomes stuck in a pulmonary artery. This is when my grandmother feels a sudden sting in her chest and loses her breath. She is suffering a pulmonary embolism.

My grandmother is tired. She wants to go home, but understands that she has to stay in the hospital for another while. Outside, the autumn sun colours the treetops a golden red. “At least the view is wonderful.” My grandmother manages a faint smile. We eat some of the strawberries that I brought, careful not to stain the sheets. Visiting hours are almost over.

As I drive back home, an old plan wrests itself free from the back of my mind. I know it is a selfish plan, driven by my own curiosity and of no immediate benefit to my grandmother. I want to have her DNA analyzed. Before time runs out.

I’ve never discussed genetic testing with my grandmother. I’m not even sure my grandmother would know what a gene is. After all, she was just an 18 year old girl in a war-torn country when Avery, MacLeod, and McCarty concluded for the first time that strands of DNA, and not proteins, carry our hereditary information. Later, when scientists cracked the genetic code and learned how to sequence genes, she was still a young woman, raising two young boys. The boys grew up and became fathers. DNA sequencing became faster, cheaper and more robust by the year. Now my grandmother has grown old and grey. Now she has a grandson with a plan.

Stomach duel

Curious to peek behind the curtains of me, I ordered a testing kit from 23andMe two years ago. I filled a tube filled with some of my finest spit, sent it back to Los Angeles and before long, I received an e-mail informing me that my results were ready. I still remember the duel held by excitement and anxiety in my stomach that evening. Here I was, just a few clicks away from my genes. What if one betrayed me, revealing itself as a harbinger of some untreatable or life-threatening disease?

I surfed to 23andMe’s website and there they were. All the SNPs that are me (SNPs – say ‘snips’ – are the one letter variations in our DNA that companies like 23andMe genotype and interpret). There were SNPs for my brown eyes, curly hair and wet earwax. And for dozens of different diseases and conditions, all numbered in red, green or grey.

Rheumatoid arthritis was red. 3.5% of the European men with my SNPs get this joint disease, compared to 2.9% on average. A significantly higher risk, yes, but not something to lose sleep over. After unlocking the report, Alzheimer’s disease turned out green. The average risk for a man of European ancestry is 7.2%, but my SNPs lower my risk to 4.9%.

There were no betrayals. Instead, their were small victories and defeats all across my genome. For every SNP that protected me from disease X, there was SNP that increased my risk for disease Y. In the disease lottery, I pulled more migraines and tremors, but less back pain and restless legs. It was hard to make sense of it all. Was I healthy, sick or something in between?

This is when I thought of my grandmother. There is no way for me to know which predictions will come true, except to sit around and wait until old age and disease come knock on my door. But for my grandmother, a predicted embolism would be old news. Her life could be the benchmark for a genetic test.

The conductor

A few weeks after my grandmother is discharged from the hospital, I look her up. She’s still short of breath. As we sip our tea, I try my best to explain her how a DNA test works. “You have to spit into a small tube. I will send that tube to a lab in the US for your, where they will isolate your DNA from the cells in your saliva that normally line the inside of your mouth.”

“And then they will know everything about my spit?” Okay. One step back. “Much more than that”, I begin. “You inherited your DNA from your parents, and they got it from their parents. I got mine partly from you, through papa. Your DNA says something about who you are on the most fundamental level. Whether you have brown or blue eyes, where you come from, but also whether you are predisposed to get cancer.” My grandmother nods thoughtfully.

A relief. She’s willing to have her DNA tested, as long as I walk her through the results once they’re in.

It is Sunday, a few months after the embolism. The frilled, purple blouse my grandmother is wearing seems too chic for the task at hand. Carefully, she spits into the tube that I brought. And again. And again. The saliva level barely rises. Between spitting, my grandmother tells stories of relatives and acquaintances I barely know. “I’m only halfway,” my grandmother sighs after half an hour.

Grandma gets there, eventually, and three weeks later the email arrives: ‘Your results are ready.’ I log in and start scrolling through the list of diseases and conditions. Colorectal cancer, 5 percent. Diabetes, 15.6 percent. Prediction after prediction, as if my grandmother has her whole life ahead of her. She hasn’t.

Click here to see what a typical 23andMe health report looks like

Armchair genetics

Armed with a printout of her test results, I go visit my grandmother. I move the wooden stool besides her comfortable armchair, so that we can run through the results together.

We start with the diseases for which my grandmother is at increased risk. Age-related macular degeneration (AMD), an eye condition in which the light-sensitive patch in the center of the retina slowly degrades, is at the top. AMD is the most common cause of blindness amongst the elderly: over 15 percent of white women over 80 in the US have it.

“It says here that with the genetic variants you carry, your risk for AMD is 9.3 percent”, I explain. “The average risk is seven percent. But your eyes are still OK, right?” “Yes, yes. But I know my father did have AMD. He even went to Nijmegen for treatment. And some of my sisters have it too. A very nasty disease.”

Next up is rheumatoid arthritis. Like me, my grandmother is unlucky when it comes to this joint disease: thanks to her SNPs, she is almost twice as likely to suffer from RA. Four out of hundred European woman get rheumatoid arthritis on average, compared to eight out of hundred women with my grandmother’s genotype. I don’t need to ask whether my grandmother has RA. I know she has it.

Onto the good news: diseases my grandmother is less likely to have. Diabetes is on the top of this list. The average risk of getting diabetes is 20.7 percent, whereas my grandmother has a chance of 15.7 percent. “But I do have diabetes”, my grandmother objects. “It’s not severe though, I don’t ever need to inject insulin.” I don’t say it out loud, but I suspect my grandmother’s lifestyle overshadows her genes here. The heritability of diabetes is only 26%, as 23andMe mentions. Environment does the rest. And truth be told, my grandmother has been overweight for as long as I remember.

We reach the end of the list. My grandmother is impressed by the predictions 23andMe has distilled from her DNA, but I’m not so sure. With the benefit of 85 years of hindsight, the predictions seem haphazard and irrelevant, a mixed bag of near hits and misses. Only when I ignore half of the health reports, and stare at the other half through eyes half closed do the contours of genetic destiny become visible.

Against all odds

Disease prediction is tough. Correlations between certain SNPs and diseases are often weak and difficult to interpret, despite what roaring headlines (‘Scientists discover genes for X’, with X ranging from diabetes to coffee addiction) would make us believe. This uncertainty, inherent to science, stands at odds with the desire of companies like 23andMe to present disease risk as clear, single digits.

Genome-wide association studies (GWAS) make up the scientific fuel on which 23andMe runs. Look past the intimidating name, and you’ll find GWAS are relatively straightforward as far as scientific studies go. Most follow a simple, three-step recipe: geneticists divide test subjects into a patient and control group, genotype their DNA and fish out the SNPs that are overrepresented in the patient group. These overrepresented SNPs contribute to the onset or progression of disease, is the assumption.

Geneticists quantify this contribution in the odds ratio: the proportion of people in the patient group with a certain SNP, divided by the proportion of people in the control group with that same SNP. Suppose 12 percent of your patients carry SNP A, compared to only 8 percent of people in the control group, then the odds ratio for SNP A is 1.5.

This is where things get interesting, and tricky. To calculate disease risk, 23andMe multiplies the odds ratios of someone’s SNPs with the average risk of disease. Ideally, the odds ratios in such a calculation should be well established and reproducible. The only problem: they’re not. On the contrary. Most are preliminary and prone to change. In a recent review of AMD genetics, the reviewer didn’t bother to list the odds ratio’s of all the SNPs that have been associated with AMD, because “these values are constantly shifting and vary based on the population that is studied as well as the (phenotypic) features of the AMD”.

As science progresses, the number of SNPs known to be associated with a certain disease is bound to increase. 23andMe’s currently calculates AMD risk using five different SNPs, yet many more have already been discovered. In a recent screening of common SNPs associated with AMD, geneticists identified almost twenty different variants.

Now I do think it is right for 23andMe to not include every SNP and odds ratio it can lay its hands on right away, because these numbers can be so fickle. But the continuous discovery of new SNPs does make clear that no prediction is final. If 23andMe decides to include additional SNPs for its calculation of prostate cancer risk tomorrow, your risk will change, for better or worse.

Problems arise elsewhere in the equation too. As a white woman over 80, my grandmother’s baseline risk for AMD should be up to at least ten, and maybe even twenty percent. 23andMe only lists the risk for women between the age of 43 and 79, which stands at 7 percent. Unfortunately, it’s not clear why data for other age ranges is lacking, or even where these figures come from. Whereas 23andMe’s geneticists meticulously cite the GWAS they have plucked odds ratios from, they remain silent when it comes to the population studies that is the source for this baseline risk. This is more than a sloppy omission. There is as much potential for error here as there is with the odds ratios. Only this time, 23andMe keeps its customers in the dark.

The contribution of environmental factors to disease risk, on the other hand, is something that 23andMe covers well. For every disease, the company lists how much of the risk can be attributed to genetics, and how much to the environment. Note: for a geneticist, the environment encompasses almost everything we do and experience that’s not genetically determined, from smoking, to physical activity and diet.

A hundred flips

But let’s just suppose for a minute that environmental factors contribute nothing to disease risk at all. And suppose that 23andMe’s prediction are infallible, and that my risk for rheumatoid arthritis really is 3.5%. In the end, whether I get the disease or not is still a chance event, no different than the flip of an unfair coin. In our lives, we have to make hundreds such flips. Most will come up in our favour. A few of them won’t. Chances are that the long list of predictions includes the disease that will be the end of me, in red, grey or green. But which one?

Two months ago my grandmother was hospitalized again. It was a stroke this time, in the middle of the night. The view isn’t as great as it was one year ago. My grandmother is asleep when I enter room 1D. She looks even more brittle than she did before. When I get home, I search through her test results until I find the health report I was looking for: ‘Typical risk of having a stroke.’

Disclaimer: this blog post is an adaptation and partial translation from an article that appeared in the Dutch newspapers nrc.next (08.16.2012) and NRC Handelsblad (08.23.2012). Major parts have been deleted and rewritten. The events described took place from November 2010 to August 2012.

Satin bowerbirds decorate their bowers with all things blue. Picture by thinboyfatter.

Sometimes all you have to do to make me buy your book, is think of a good title. Survival of the Beautiful by David Rothenberg definitely did the trick. “No one ever mentions the beautiful”, I thought when I took the book from its shelf in a London book store. Not when it comes to evolution at least, where the fittest are always said to come out on top.

I took the bait, bought the book and began reading that same afternoon. Then, a few pages in, I put the book aside, irritated. “There is only one animal who makes physical, constructed works of art .. whose complexity and elaboration seem to suggest art for art’s sake”. When I first read that paragraph, I thought Rothenberg was referring to humans. He wasn’t. Rothenberg had bowerbirds on his mind.

As you might know, Australian bowerbirds don’t court their females with plumage, dance or song, but with a decorative structure made from twigs and sticks, called the bower. Male bowerbirds labour on their bowers for months, putting twigs in place and hunting for decorations, sometimes even stealing them from other bowers. The list of materials bowerbirds collect and put up on display is long. Flowers, feathers, fruits, shells, beetle carapaces, butterfly wings and even waste items such as bottle caps, coins and pieces of glass may all end up as part of a bower.

The bowerbird’s courtship ritual is certainly impressive, unique and complex, you could even call it beautiful if you’re into sticks and blues, but is it art? I thought not. Art is created with intention and care, by an artist who can later reflect upon her work. Bowerbirds don’t have this capacity. If bowerbirds are creating art, then chimpanzees banging two rocks together are doing science.

In world war I and II, navy ships were painted in camouflage that was not meant to hide, but to dazzle. This is the USS Charles S. Sperry in 1944. Image public domain

I read on. Rothenberg left his artistic bowerbirds behind, and embarked on a wild exploration of science and beauty. He skirted past colour-shifting cuttlefish and cubist camouflage, and dipped his toes into the fractal nature of Pollock paintings and bubbles that emit light when they are bombarded by sound. All these examples serve to illustrate Rothenberg’s main point, that a deeper consideration of art can enhance and improve our understanding of science. But nowhere was that message more clear and more convincing than in chapter three.

In this chapter, It could be anything, Rothenberg interviews Richard Prum, a professor of ornithology at Yale University. You might know Prum from his work on the colouration of dinosaurs. His team was the first to ever reconstruct the colour patterns of a dinosaur, using pigment-carrying microstructures in its fossil feathers. Or perhaps you have heard of Prum’s infamous research on the sex life of ducks, starring ballistic penises and corkscrew vaginas (I strongly recommend you click that link, just remember to come back aftewards!).

Prum studied bird song, until he lost his hearing after a viral infection. Forced to switch tracks, Prum turned his investigations to the colour of birds the underlying genetics instead. But whether it is in song or colour, Prum finds beauty. And not just from our lofty human perspective: he argues female birds too experience are delighted by beauty. The female peacock appreciates the gaudy feathers of her mate for what they are: beautiful.

This might seem obvious or even trivial to you, but to many biologists, it’s not. Most of Prum’s colleagues see function where he sees beauty. They argue that the traits females of a certain species prefer are indicators of male quality. By flaunting his unwieldy tail, a peacock male really is showing the ladies what a tough and fit guy he is, their reasoning goes. And when the nightingale sings his nightly song, he really is praising the quality of his sperm. By losing most of their body hair, even our own ancestors have played the quality game, according to some. In an interview with Slate Richard Dawkins once said that ‘hairlessness advertises your health to potential mates. The less hair you have on your body, the less real estate you make available to lice and other ectoparasites.’

These biologists are blinded by Darwin’s theory of natural selection, Prum tells Rothenberg, and ignore Darwin’s second theory of evolution, of sexual selection. Soon after publishing On the Origin of Species, Charles Darwin wrote to his friend Asa Gray that “The sight of a feather in a peacock’s tail, whenever I gaze at it, makes me sick!” Darwin had realized that natural selection would never explain the evolution of such ludicrous and extravagant features as the peacock’s tail. For that, he needed another mechanism altogether.

It took more than a decade after publishing the Origin, before Darwin formalized his thoughts and introduced the concept of sexual selection in a new book, The Descent of Man, and Selection in Relation to Sex. In this book, Darwin argues that when females prefer certain traits in males, and if enough generations of males face this preference, they will evolve the colourful frills, feathers or dewlaps that females appreciate. For some traits not nature, but females select. Not the fittest, but the beautiful survive.

Prum thinks biologists should take Darwin’s ideas about sexual selection at face value, and not dress it up as yet another variation of natural selection. He stresses that the sexually selected trait is arbitrary. It can literally be anything. Maybe it’s a wild mane or a complex song, but as long as the laws of physics, chemistry and function allow it, beauty will evolve in unexpected ways and places.

Still Life with Shells, by Adriaen Coorte (1697)

It is in this arbitrariness that the art world of animals and humans converge. Human art ranges from the realistic paintings of Dutch masters to upturned urinals. What survives and what not, what is beautiful and what not, depends on the back story, on culture and on history. The appreciation of the art or trait is what matters, whether that appreciation has cultural or genetic roots. Sexual selection and aesthetic selection are two sides of the same coin.

This quote from Richard Prum really nailed it down for me:

“Evolutionary biology is not about form and function exclusively, but about historicity, development and structure. These are exactly the kinds of concerns that somebody who studies Dickens should have: what was Dickens like as a boy and how did that affect his work. [...] Not about, ‘Oh, Dickens wrote this book so he could have more money so he could attract hotter chicks and have more fitness.’ That is a nonexplanation of his output. It’s ridiculous for literature, and it’s as ridiculous for life itself!”

And so Rothenberg comes back to the bowerbird. His bower is a sculpture devoid of utility. Its architecture and decorations have but one purpose: to be seen. To be beautiful. To be judged by a critical, female audience. Their work is as much embedded in an evolutionary history of bower makers, and cannot be understood without that history. L’art pour l’art, the bowerbirds just got there first.

Now let’s suppose Rothenberg and Prum are right. Suppose the human and animal art worlds really do evolve along similar trajectories, towards arbitrary beauty, what would this view bring us? For one, it would expose adaptive just-so-stories for what they are: stories. Not function, but beauty should be the null hypothesis, the baseline assumption, for testing any hypothesis about the evolution of a sexually selected trait. Bowers are beautiful until proven functional.

Survival of the Beautiful contains many more tantalizing dialogues and crossovers between art and science, but I found the argument outlined above to be the most compelling and persuasive. It was also the easiest for me to follow, coming from a scientific background. The chapters about aesthetics, abstraction, rhythm and form bigger posed a bigger challenge, whereas I felt Rothenberg strays on the lighter side of science a little too often.

“I am a bad explainer, mediocre storyteller, but an enthusiastic reveler”, Rothenberg confesses in the final chapter of his book. But revel he did. While Survival of the Beautiful might not be the definitive book about art and science, it is certainly one of the most pleasant and inviting. And what I appreciate above all else: Survival of the Beautiful made me think.

Why is that birds seem so much more attuned to beauty than us mammals? What happens when beauty crosses the species barrier, and we suddenly find ourselves enjoying a whale song? I sense there’s science out there that needs doing. There must be more revelers with enquiring minds out there. Get to it!

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All animal eyes and eye-spots contain opsin, a protein that captures light. This is the compound eye of Antarctic krill. Photo by Gerd Alberti and Uwe Kills

Gaze deep into any animal eye and you will find opsin, the protein through which we see the world. Every ray of light that you perceive was caught by an opsin first. Without opsin there would be no blue, no red, no green. The entire visible spectrum would be.. just another spectrum.

But opsins haven’t always been the sensitive light detectors that they are today. There is one critter, obscure and small, carries opsins that are blind to light. These opsins aren’t broken, like they are in some cave dwelling species. They never worked to begin with. They are the relics of a distant past, a time in which our ancestors still dwelt in darkness.

Opsin is a member of large family of detector proteins, called the ‘G-protein coupled receptors’ (GPCRs). Like a needle and thread, all GPCRs wind themselves through the outer membrane of the cell seven times. Halfway between cell and outside world, these tiny sensors are perfectly positioned to monitor the surroundings of the cell. Most GPCRs detect the presence of certain molecules. When a certain hormone or neurotransmitter docks their outward facing side they become activated and release signalling molecules on the inside of the cell. But opsin is different. It doesn’t bind molecules physically. Instead, it senses the presence of a more delicate and ephemeral particle: the photon itself, the particles (and waves) that light is made of.

Opsins trap photons with a small molecule in the heart of their architecture, called retinal. In its resting state retinal has a bent and twisted tail. But as soon as light strikes retinal, its tail unbends. This molecular stretching exercise forces the opsin to change shape as well. The opsin is now activated and eventually will cause a nearby nerve to fire, which will relay its message to the brain: light!.

Opsins lie embedded in the outer membrane of the cell, where retinal (grey molecule in the middle) can trap photons.

Scientists have known about the existence of opsins (or rhodopsin, as the retinal-bound form is also called) ever since the 19th century. The German physiologists Wilhelm Kühne and Franz Boll first discovered and isolated rhodopsin in 1876 and 1878, respectively. It took another fifty years before the American biochemist would George Wald discover retinal in 1933.

Since these early days of visual chemistry, scientists have uncovered opsin’s light detecting tricks and resolved its molecular structure in atomic detail. It is safe to say that the physical and chemical nature of opsin are better understood than its history. Many questions about the evolution of opsins have remained unanswered in the past 130 years of opsin research. In which of our many ancestors did opsins evolve? How old is opsin? How old is vision?

The short answer is ‘ancient’. Since almost every animal carries opsins of some sort, these proteins must have appeared early in our evolution. The long and more more precise answer involves an evolutionary reconstruction of opsin’s earliest history, such as the one that was published by Roberto Feuda and others in PNAS three weeks ago. Feuda and his colleagues gathered opsin sequences from all corners of the animal kingdom, hairy, scaly and squishy, and calculated how related these genes were to each other.

First of all, Feuda confirmed the existence of three distinct opsin types within bilateria (bilaterians are animals with left-right symmetry). These three opsin types are called R-opsins, C-opsins and RGR-opsins. For a long time biologists thought C-opsins were exclusively found in animals with a spine (the vertebrates) and that R-opsins were limited to protostomes, a diverse group of animals that includes mollusks and arthropods. (The third type of opsin, the RGR-opsin, is a bit odd compared to the other opsins. Instead of detecting light, they play a role in regenerating ‘spent’ retinal molecules.)

The division was so stark and neat that vertebrates and protostomes must each have evolved their own light detecting opsins from an ancestral template. Or so scientists thought. The tidy story unraveled once opsins started to pop up in unsuspected places. The brain of the ragworm Platynereis dunerlii, a protostome, was found to contain C-opsins. R-opsins were identified in nerve cells in the human retina. These discoveries forced opsin biologists back to the evolutionary drawing board. In their new scenario, the common ancestor of vertebrates and protostomes, the ur-bilaterian, already had three types of opsin. The two lineages later recruited C-opsins or R-opsins for their visual systems, respectively.

Now, Feuda and his colleagues push back the origin of this opsin cluster farther still. The first animal to carry three opsins was not the bilaterian ancestor, but the last common ancestor of Bilateria and Cnidaria (jellyfish, anemones, corals and their kin). Feuda found all cnidarian opsins belong to one of three different groups, each of which correspond to the three basic opsin types in Bilateria.

Cnidarians are plain weird, from a bilaterian perspective. Their anatomy differs radically from our symmetrical bauplan. Cnidaria don’t have brains for example; their thoughts and decisions are born in a decentralized net of nerves instead. For hundreds of millions of years, our evolution and development have followed vastly different path. We became jaguar, they became jellyfish. They are coral, we are crab. Yet Feuda’s results bear one mind-boggling implication: the c-opsins in your cones and rods are more closely related to the corresponding opsins in the eye-spots of a jellyfish, than either of them is to the r-opsin in your retinal nerves. The roots of animal vision run deep indeed.

To see how deep, Feuda’s team leapt to another branch of the family tree, and scoured the genomes of two sponges, Oscarella and Amphimedon, for opsin sequences. No dice. Apparently, opsins only evolved after sponges had diverged from other animals, but before the split between Bilateria and Cnidaria. Fortunately for Feuda, there exists one animal lineage in this sweet spot between sponges on one side and cnidarians/bilaterians on the other. Meet the placozoans. Small, simple and flat, placozoans resemble shapeshifting pancakes more than anything else. They drift along the sea floor, searching for detritus to scavenge. Below, you can see how one Trichoplax (the only defined placozoan species) becomes two:

Sure enough, the placozoan genome harbours two opsins. But here’s the catch: these opsins cannot detect light. Remember retinal, the molecule that changes shape when it is struck by light? The placozoan opsins cannot bind retinal, because they lack the amino acid to which retinal binds (amino acids are the building blocks of proteins). Without ‘lysine-296′, it is unlikely that the placozoan opsins can detect light. But if not light sensors, what then? “Surely placozoans use these opsins. How? I cannot tell. Your answer would be as good as mine I am afraid”, David Pisani, the lead author of the study, writes in an e-mail.

Feuda and colleagues are not the first to notice these placozoan opsins. On this wiki about opsin evolution, a UCSC researcher wrote that “these [placozoan] genes retain uncanny similarities to opsins in otherwise rapidly changing regions. Perhaps these genes should be considered opsins in spite of lacking [lysine-296].” However, Feuda’s team is the first to investigate how these ‘uncanny opsins’ relate to the other opsins. This is how they visualized the scenario they came up with:

Pondering this figure, it hit me that our opsins really had two origins. One is the birth of opsin itself, the other is the mutation that turned opsin into a light sensing protein. The opsin lineage itself arose between 755 and 711 million years ago, from the duplication of a single GPCR. The last common ancestor of Bilateria and Cnidaria lived between 711 and 700 million years ago. This leaves a short window of time (evolutionary speaking) in which opsin acquired the light sensing mutation and split into the three opsin families we still carry today.

This probably won’t be the final word on opsin evolution. Branches will shift as more opsin sequences become available and researcher probe further into the earliest history of animals. Also remember that a single light sensing protein does not make a functional eye or eye-spot. The roads that animals took towards vision are myriad, with each eye and eyelet evolving along its own trajectory, towards splendid colour or dreary monochrome, eagle-eye vision or simple on/off light detection.

But although the differences are many, the starting point was the same. A single opsin. A flash. Then there was light.

The Pink Lakes in Australia are coloured pink by salt-loving microbes. Photo by Neilsphotography.

Most cells would shrivel to death in a salt lake. But not the Halobacteria. These microbes thrive in brine, painting waters a gentle pink or crimson red wherever they bloom. The Halobacteria live in every salt lake on this planet, from the Dead Sea of Israel to the vast salt flats at the feet of the Sierra Nevada. But these hardy microbes haven’t always called the salty depths their home. Their genomes reveal a tale of a dramatic transformation through genetic plunder.

Organisms that can survive in waters of extreme salinity are called ‘halophiles’ – or salt lovers. There exist salt-tolerant algae, fungi and even shrimp. But of all the salt lovers in the world, the pink Halobacteria are the most passionate. They don’t just cope with brine. They embrace it.

Most halophiles do their best to keep their cells clear of salt. But the Halobacteria just don’t care. The insides of their cells are as salty as the lakes they live in. Through this strategy, the Halobacteria have made themselves utterly dependent on salt, up to the point were fresh water is as deadly for them as salt water is for others. Placed in a freshwater lake, their cells would swell and pop like bloated water balloons.

Confusing enough, Halobacteria are not bacteria, but archaea, which have a completely different biochemistry. As a general rule, archaea are more hardy and robust than their bacterial counterparts, living in a wider range of extreme environments.

Microbiologists have long noted something odd about the Halobacteria. In all their evolutionary analyses, they found that Halobacteria are part of a branch of archaea called the ‘methanogens’. What bothers microbiologists is that as microbes, methanogens and Halobacteria couldn’t be more different. In every scheme ever devised to differentiate among micro-organisms, methanogens and Halobacteria end up on opposing sides of the divide. If microbes were spices, methanogens would be the pepper to the halobacterial salt.

Methanogens are the self-reliant survivalists, able to liberate energy from the most basic of molecules. A pinch of hydrogen (H₂), a dash of carbon dioxide (CO₂) and a spoonful of minerals is all a methanogen needs to carve out a living. This sober lifestyle has earned them the moniker of ‘rock eaters’ (lithotrophs).

Halobacteria, on the other hand, fancy their molecules ready-to-eat. They are scavengers, scrounging the salty waters for carbon compounds that they burn using oxygen (methanogens loathe oxygen). As an alternative energy supply, halobacteria are also able to harvest energy from sunlight.

Two types of microbes with radically different life strategies, yet one evolved from the other. So how did the Halobacteria cross the line?

Shijulal Nelson-Sathi thinks he has found the answer. In their latest paper, he and his colleagues show that the ancestor of all Halobacteria acquired as much as a thousand genes from another microbe, a bacterium. And through this act of plunder, the microbiologists write, the Halobacteria left their methanogenic ways behind, becoming salt-loving scavengers in the process.

Picking up extra genes from other species is nigh impossible for animals like us, but for many microbes it is second nature. So when Halobacteria were first found to share some genes with some bacteria some years ago, no one batted an eyelid. Amongst the first foreign genes to be identified in the halobacterial genome were the genes that keep them afloat – literally.

But the massive transfer of genes that Nelson-Sathi and his colleagues have now laid bare goes far beyond occasional theft. The halobacterial ancestor acquired a thousand genes in one big gulp, from a single donor microbe. For your: the entire genome of Halobacterium contains about 2.630 protein-coding genes. Nelson-Sathi found genes for breaking down sugars among the annexed genes, as well as genes for scavenging carbon compounds, breathing oxygen and pumping ions of salt into and out of the cell. Genes, in short, for everything that make salt-loving scavengers out of Halobacteria.

The Halobacteria acquired a thousand genes from a bacterial donor. Figure from reference.

Nelson-Sathi thinks the Halobacteria acquired their genes through a deep and intense cooperation with another microbe. Methanogens sometimes live and work together with other bacteria and archaea that produce hydrogen and carbon dioxide that they consume. It’s not difficult to imagine a next step, in which one of the two symbiotic partners is taken up by the other and gets stripped of its genes.

Examples of such a dramatic transformation through massive gene transfer are few and far between. In its normal mode evolution is a marathon runner, not a pole vaulter. But when it does take the jump, and microbes get mashed up, the outcomes can be wild, exciting and unique. This was the case when two microbes fused to give rise to us, the eukaryotes.

The eukaryotes form the third and youngest domain of life. Eukaryotes can be recognized by several complex structures in their cells, such as the mitochondria that supply our cells with energy. Before they became our personal power plants, mitochondria were free-living microbes. A small amount of DNA still remains in the deepest core of mitochondria, a relic of the days they were wild and free. Most of their genes have since been scuttled from the mitochondrial genome, and ferried over to the main genome. This makes our genomes as much a mix-up of genomes as those of Halobacteria are.

So we are like the pink Halobacteria, yet different. “If similar processes underlie the origin of Halobacteria and eukaryotes”, Nelson-Sathi and his colleagues wonder, then why did eukaryotes grow large and complex, whereas Halobacteria remained small and simple? That’s because Halobacteria failed to retain their endosymbiont, the microbiologists argue, whereas we have carried our mitochondria with us to this very day.

Mitochondria supply our cells produce with vast amounts of energy. They do this by pumping protons across their inner membrane against a steep gradient, and letting them flow in again, powering a tiny molecular turbine along the way. Because this takes place within single compartments, carefully controlled by mitochondrial DNA, the entire process is immensely efficient.

Halobacteria pump protons too. But lacking mitochondria, they pump them across their own membrane into the vast and salty outside world, before they stream back in. Without dedicated compartments to play the protein pumping game, the Halobacteria have to make do with a fraction of the energy that eukaryotic mitochondria can deliver, which limits the genetic and cellular complexity they can attain.

The Halobacteria came close. If they could have coaxed their symbiotic partner to stay, these pink, little buggers could have stumbled upon the same energy-efficient solutions as our distant ancestors did. If there’s any lesson the salt-lovers can teach us, it is this one. In their pink and salty waters, they give us a rare glimpse of how our past could have unfolded, but didn’t.

Homotherium was a sabercat that survived until the last Ice Age. This skull is from the Muséum national d'Histoire naturelle in Paris.

Many sabertooths have stalked this world. The first sabertoothed mammals appeared over 50 million years ago. The last sabercats, such as Smilodon and Homotherium, went extinct only 10.000 years ago. All in all, five different lineages of carnivorous mammals evolved sabertooth dentition: the ancient creodonts, marsupials and three different lineages of true cats and cat-like carnivores. These creatures were unrelated and lived millions of years apart, yet somehow all evolved canines that were similarly massive and grotesque.

This independent and repeated evolution of saberteeth in different mammalian carnivores seems, at first glance, a testament to the power of natural selection. We assume canines long and slender have evolved to subdue and kill, to slash veins and pierce flesh, to bring down the most powerful of prey. Larger canines equal more carnage, or so our intuition tells us.

But Marcela Randau isn’t so sure. In her latest paper, she and her colleagues propose that saberteeth did not evolve because they were deadly, but because they were sexy.

That’s not as far-fetched an idea as it might first appear. Many modern animals bear exaggerated canines and tusks as sexual ornaments, like walruses, baboons, narwhals and several species of deer (yes, quite a scary sight). It are mostly the males that develop such impressive dental weaponry and use them in competitions with other males, in displays of social dominance or in actual fights. The victors usually secure the right to mate with a female or even entire harem. Since the males with the largest and most elaborate tusks win access to more females, evolution can drive the runaway development of longer and longer canines.

Perhaps this is how sabertoothed carnivores evolved their teeth. Modern cats, like lions, raise their lips and expose their canines when they feel threatened or challenged. Cats are visual creatures that pay much attention to the face and expressions of others. Through their canines, they advertise their strength and aggressive intent: back away, because I have the teeth to back up my threats. Could it be that sabertooths simply took such toothed communication to the extreme? A sabertooth snarl would certainly have sent a clear message to male competitors.

Lions communicate aggressive intent by snarling and growling.

But just because this scenario sounds plausible or imaginable, doesn’t mean it’s true. Comparisons with modern animals that bear their tusks in sexual display can be misleading, especially since none of them are carnivorous hunters, like sabertooths were. It’s evident that a deer won’t use its canines for killing (one hopes), but the same can’t be said for a sabertooth. How then does one investigate whether saberteeth evolved for the hunt or for sexual conflict?

Randau’s argument is based on proportions. As an animal matures and grows, most of its body parts will grow with it in a steady, lockstep fashion. But the rules are different for sexually selected ornaments and weapons. In this case, bigger means much better. The larger a buck can grow its antlers, or the more elaborate the peacock tail becomes, the more likely it is to find a mate. Males therefore tend to devote a disproportionate amount of energy in the development of sexual features, with the largest males displaying the most eye-catching tails, frills and feathers. Such patterns of lopsided growth, what biologists call ‘allometrical growth‘, can therefore be a sign of sexual selection at work.

To see whether sabertooth canines display allometrical growth, Randau and her colleagues investigated how canine size of sabertoothed carnivores scaled with the length of their skulls. If larger skulled sabertooths have much larger canines than smaller animals, this could mean they were partly shaped by sexual selection. The research team made the same comparison for extinct and modern cats without sabertooth dentition. And as a sanity check, Randau made the same calculations for the shearing teeth scale, which are used for slicing meat and lie just behind the canines. Since they aren’t visible, they’re unlikely to have a role in display and should therefore grow at the same rate as the skull and rest of the body.

As sabertooths grew, their canines grew disproportionally large. Figure from reference.

Randau found that both sabertoothed carnivores and non-sabertoothed cats develop disproportionally large canines as they grow, but it were the sabertooth canines that were the most extreme. The proportion of the shearing teeth, did not change for skulls of differing lengths, indicating they evolved under a regime of natural selection. Randau’s team concluded that saberteeth were honed, at least in part, by sexual selection.

Of course that doesn’t mean that saberteeth had no role in killing or wounding prey. A sharp and slender tooth can still be a potent weapon. Longer teeth bite deeper and inflict more damage, at the risk of breaking as the prey struggles. However, body parts that are ‘merely’ functional don’t grow progressively larger in larger animals. According to Randau, sexual selection can explain why saberteeth grew as large as they did, whereas natural selection constrained how large they could become while still remaining (somewhat) practical.

Julie Meachen, a sabertooth researcher who was not involved with the study, thinks Randau’s hypothesis is plausible. Meachen herself has investigated the differences between the prey killing arsenal of two different types of sabertoothed carnivorns: dirk-tooths with canines long and slender, and scimitar-tooths, which had shorter and more serrated canines. Meachen found that the sabertooth with larger canines, are also the ones that have the strongest fore-limbs. In her paper makes the case that since slender canines are more prone to break, these creatures needed robust limbs to grapple and hold down prey as they made the kill.

“Originally, it was a chicken or egg problem which came first: the long canines or the robust forelimbs”, says Meachen. “But I see the ideas as being compatible in this way: sexual selection drove the canine length to get longer, but in order for the long canines to remain functional, they also needed their forelimbs to be robust and strong.” Fangs before paws, in other words.

Skulls can’t talk, so answers to the question how sabertoothed carnivores hunted and bred will never be definitive. It’s also clear that a single answer will never suffice for a group as large and varied as sabertooths. But the patterns that sabertooth researchers like Randau and Meachen have uncovered are real. And if their interpretations are correct, sabertooths were every bit as menacing as sexy.