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!

claimtoken-50a2b1c691a93

claimtoken-50a2b22cc5316

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.