When a blue whale opens its mouth, tonnes of water surge in. The whale then forces the water back out with its tongue, in such a way that it flows through the baleen combs in the front of its mouth. These baleen plates can filter up to half a million calories worth of plankton, krill and small fish out of the water. That’s almost 1,000 hamburgers in one gulp. No wonder whales get so big.
The earliest ancestors of the blue whale fed themselves differently. They still had teeth, and no baleen. Some modern whales still have teeth (the Odontoceti – literally ‘toothed whales’), but they form a separate group from the baleen whales (Mysticeti) who have replaced all their teeth with baleen. This transition to toothlessness is documented by multiple fossil whales. Each of these fossils provides a snapshot of what must have been gradual change.
Several early baleen whales such as Janjucetus and Mammalodon still had fully developed, enamel-covered teeth. Eomysticetus had already exchanged its teeth for baleen plates. But it is Aetiocetus, that captures this evolutionary change in its entirety. This was a whale that still had teeth, but that also carried baleen, as small modifications in its skull reveal.
Whale embryos also contains hints that their distant ancestors once bore teeth. They still grow tooth buds that disappear before the young whale is born. Charles Darwin must have had the toothed ancestors of whales on his mind when he wrote the following sentence in the Origin of Species:
What can be more curious than the presence of teeth in foetal whales, which when grown up have not a tooth in their heads; or the teeth, which never cut through the gums, in the upper jaws of unborn calves?
~Charles Darwin, On the origin of species.
Reconstruction of Aeitocetus that lived 25 million years ago. This wale had both teeth and baleen.
Aside from the evidence from fossils and whale embryos, the loss of enamel-capped teeth also left traces in the genomes of modern whales. All reptiles and mammals have genes that produce proteins that mineralize the enamel of teeth. Since baleen whales have no teeth as adults, they have no need for these proteins. Over time such unnecessary genes tend to acquire mutations that impair the protein. This is exactly what happened in baleen whales. In all species of baleen whale, up to three tooth genes turned into pseudogenes (remnants of genes that can no longer produce a functional protein, but are still recognizable as former genes).
But there is something strange about how these mutations are distributed: every species of whale has a different set of mutations. Humpback whales have a mutated enamelin gene, for example. Blue whales carry a different mutation in enamelin. And sei whales have a mutation in a different tooth gene altogether.
Such an uneven distribution of mutations can mean a couple of things. One explanation could be that all the baleen whales lost their enamel independently from each other, due to different mutations in each lineage. Another possibility is that an hitherto unknown mutation that can be found in all baleen whales is responsible for the loss of enamel. Enamel-covered teeth would have been only lost once by the common ancestor of baleen whales. The fossil evidence supports this scenario: the distribution of toothed baleen whales is not nearly as patchy as the distribution of tooth gene mutations.
Scientists from the University of California suspected a gene called MMP20 might contain the mutation that had been overlooked so far. This gene seemed to be a good candidate, because the MMP20 protein is involved in processing tooth proteins such as enamelin and ameloblastin. A mutation in MMP20 could affect multiple enamel proteins downstream. Moreover, humans and mice that have a defective MMP20 gene develop bad and brittle enamel (amelogenesis imperfecta).
The family tree of whales, including extinct relatives. Baleen whales (top) and some pygmy sperm whales (bottom) have mutations in their tooth genes. Every orange symbol denotes a mutation; different letters represent different genes.
The team initially screened four different species of baleen whales for mutations in MMP20. They hit the jackpot right away. In all four whales, a stretch of DNA (a SINE) had inserted itself right inside MMP20, splitting the gene in two. When they extended their search to other species, they found that whale after whale had the same DNA insertion inside MMP20. This ubiquity gives a clear message: it is this insertion that rung the death knell for the whale’s teeth.
But the researchers discovered that some pygmy sperm whales (Kogia), that belong to the branch of toothed whales, also carry mutations in their MMP20 genes. These pygmy sperm whales are also known to have enamel-less teeth. But whereas baleen whales first lost MMP20 before the other tooth genes mutated, these sperm whales seem to have lost the tooth protein enamelin first, with MMP20 now having mutated secondarily in some individuals.
So here are two lineages of whales, caught in the act of evolving on different, but similar paths. Evolution is sometimes criticized for not being amenable to experimental scrutiny in the lab, but the pygmy sperm whales prove these critics wrong. As the authors note, “mammalian diversity presents a unique laboratory, complete with replicated experiments.” Life herself presents us with a multitude of ingenious experiments. It is up to us to interpret them. Personally, I couldn’t imagine a more exciting science.
Reconstruction of Aetiocetus by the great paleoartist Carl Buell. Check out his website here. Image used with his permission.
Whale phylogeny from reference, whales also drawn by Carl Buell.
Meredith RW, Gatesy J, Cheng J, & Springer MS (2011). Pseudogenization of the tooth gene enamelysin (MMP20) in the common ancestor of extant baleen whales. Proceedings. Biological sciences / The Royal Society, 278 (1708), 993-1002 PMID: 20861053
Welcome to the eight issue of the MolBio Carnival! Some great blog posts on molecular and cellular biology have been submitted to this edition. So let’s not waste any time and get this carnival started, because there’s much to read and learn.
Molecular biologists study life at its tiniest scale. Their world is both fascinating and mysterious, but I never regarded it as beautiful. Beauty is the domain of those fields of biology that study exotic creatures and ancient fossils, and not that of those who study nature with a microscope and a pipette. Or so I thought. My view changed when, at the end of my second year in college, one of my teachers showed the following video to our class:
Suddenly, the cell came to life. It became a bustling city where proteins and molecules were doing their jobs, and through their collective actions sustain a complex, living machine. Thanks to the great writers that contributed blog posts for this edition, I can present you a taste of all the wonderful things that happen within our cells.
Imagine a cell. Today, an animal cell will do. Our imagined cell is not floating in empty space. It is embedded into a matrix of proteins and sugars. This matrix provides support, but is also flexible enough to bend and stretch when needed. Michael Scott Long from phasedwrites how deforming this elastic matrix can make it easier for cancer cells to grow deeper into tissues.
Between the tangled proteins of the extracellular matrix, we find our cell. The lipids of its cellular membrane are bobbing up and down. Before we enter our cell, we’d better ring the bell. Not only would it be impolite to barge in – it would also be nigh impossible. The lipid membrane is a formidable barrier to all kinds of ions, proteins and other molecules. The cell’s doorbells are its signalling receptors that raft on the lipid sea. When a molecule binds this receptor, the word of its arrival gets spread on the other side of the membrane via signal molecules that are released. Lab Rat wrote a post on these signal molecules, which appear to be more complex and versatile than was previously known.
Some molecules, such as the hormones estradiol and testosterone, have no need for doorbells: they can pass the membrane on their own. Once they are in the cell, a protein ferry picks them up and brings them straight to the cell’s core, where all the DNA is located. Once it is there, the molecule switches on certain genes and turns off others. But why use the ferry boat at all? Why don’t the molecules bind the DNA themselves? Over at the It Takes 30 blog, Becky Ward gives the answer in a blog post on the signalling networks. There you will also read that the entire mechanism is way more complex than I just summarized (over 100 molecules are involved in the entire process!).
While we’re in the cell’s nucleus, we might as well look around us and see what’s going on here. Katie Pratt explains: the information that lies in the DNA is read and converted into RNA. These RNA molecules contain the instructions for making functional proteins. But some RNAs lack these instructions. Their sole purpose is to regulate the activity of other genes. Scientists use these RNAs to silence the genes they want to study. They even think about using them to repress the genes of virusses such as HIV, as a potential therapy. Head over to Katie’s blog to find out more.
Our imagined cell is not infected by HIV, luckily. We can safely follow a messenger RNA molecule as it squeezes through the nuclear pore on its way to the ribosome. There, its encoded message is translated into an enzyme. Enzymes are pipelines of our cell. By catalyzing chemical reactions, they can direct the flow of small molecules within the cell. Christopher Dieni on Bitesizebio tells you everything you want to know about enzymes. Seriously, it’s a great overview of all the things that enzymes do and don’t do, so go check it out!
That’s it for this month’s edition of The MolBio Carnival. I hope you enjoyed the journey. You can check future hosts and past editions on the Carnival’s home page. Be sure to subscribe to the RSS feed to receive notifications and summaries when new editions of the Carnival are posted. Also, you are welcomed to submit your best molbio blog articles to the next edition of The MolBio Carnival, which will be hosted by Alex from Alles was lebt.
Nineteenth century biologists had a point when they divided the ringed worms into free-living hunters and sessile filter feeders. Their classification was dismissed in the 1970s, but a closer look at the genes of many different worms now shows that they were closer to the truth than their later colleagues.
The classification of worms got off to a false start thanks to Carl Linnaeus, the great-grandfather of taxonomy. After he had given mammals, reptiles, birds and fishes their own groups, he divided the remaining invertebrates (animals without a spine) into just two categories: insects and Vermes, or worms. Anything that was not an insect therefore was, by necessity, a worm. In this way Linnaeus lumped a diverse group of creatures was together into a single class. Corals, jellyfish, squids, worms themselves and other soft-bodied animals were all members of the bloated Vermes. Stephen Jay Gould famously described the Linnaean class of Vermes as a taxonomic wastebucket.1
The taxonomists that came after the Linnaeus spent a lot of time cleaning out this wastebucket. One of the first biologists to study worms in detail was Jean-Baptiste Lamarck. He liberated the ringed worms, or annelids, from the Vermes and placed them into their own, unique group. He recognized that their segmented body plan, gut, nerve cord and blood vessels make them different from other worm-like creatures without these features, such as snails and flatworms.
Tomopteris, a free-living worm belonging to the Errantia. When they are disturbed, they release glowing particles from their parapodia.
Later, in 1866, the French naturalist Quatrefages further divided the ringed worms into the Sedentaria and the Errantia. Not only do these two groups differ in their way of life, with the Errantia being free-living predators and the Sedentaria immobile filter feeders, they also differ in the way they look. The parapodia (little worm legs) of Sedentaria are smaller and less pronounced than those of Errantia for example.
This classification was used for over a century, but it was dismissed as an ‘arbitrary grouping’ that was used only for ‘practical purposes’ by biologists in the 1970s2. They argued that the similarities of Sedentaria and Errantia arose due to convergence, rather than reflecting a deep evolutionary split. In other words, they argued that some worms look the same because they have a similar way of life, and not because they are closely related. Just like the wings of a bird and and bat wings look similar even though the common ancestor of birds and bats had no wings. The revisionists came up with a new classification that featured a split between the bristled worms (polychaetes) and the collared worms (clitellates, which includes the famous and noble earthworm).
But when Torsten Struck and his colleagues analyzed hundreds of genes of 34 different species of ringed worms, they didn’t find this split. Instead, they found that most worms belonged to two groups that mirror the nineteenth century groupings of Errantia and Sedentaria3. The different lifestyles of the two groups aren’t arbitrary. On the contrary, they are the reflections of an ancient crossroads in the evolution history of ringed worms!
The new family tree of Annelids (red), showing that Sedentaria (blue) and Errantia (green) are distinct groups.
This means the end for the bristled worms as taxonomic group. Earlier studies already hinted that something was amiss, but Torsten Struck was surprised to see the revised classification from the 70s rejected with such confidence. This makes clear what the biggest problem is of classifying life solely on the way it looks: you cannot distinguish whether a certain feature was never there in the first place, or whether it became lost during evolution later on. Genes, if you look at enough of them, don’t have this problem, .
Take the collared worms, who adapted to a life in freshwater and in the earth. They lost the parapodia and bristles of their marine ancestors and evolved many changes in the way they reproduce. If you would classify earthworms based on these characteristics, they would appear to be more distantly related to other bristled worms than they really are.
With the new family tree in hand, Torsten Struck could reconstruct what the ancestors looked like (apparently, they were really cute!). The reconstruction of the ancestor of Errantia shows that it was already well adapted to a mobile and predatory way of life. It had well-developed antennae, two pairs of eyes (“‘all the better to see you with, my dear”) and parapodia which it used to move around quickly. The evolution of Sedentaria show the opposite trend. Their ancestor had no antennae and reduced parapodia. Other sensory organs were lost in different lineages of Sedentaria.
Meet the really cute ancestors of annelids, Errantia and Sedentaria
Scientists who use worms as model organisms should pay close attention to these results. The marine ragworm, or Platynereis dumerilii, has recently come in vogue for studying how eyes and organs evolved in animals. Many of its characteristics, like its large antennae and sensory palps, seem to be more characteristic of the family of Errantia, and not for the ringed worms as a group. Torsten Struck writes: “None of the model organisms alone will reveal the ancestral conditions which were present in Annelida. You can only achieve this with a comparative approach that includes several organisms.”
Tomopteris picture by Uwe Kilis.
Annelid phylogeny from reference 3.
Ancestral reconstruction adapted from reference 3
1 Gould, SJ (2001). A Tree Grows in Paris: Lamarck’s Division of Worms and Revision of Nature, The Lying Stones of Marrakech 2. FAUCHALD, K., & ROUSE, G. (1997). Polychaete systematics: Past and present Zoologica Scripta, 26 (2), 71-138 DOI: 10.1111/j.1463-6409.1997.tb00411.x 3. Torsten H. Struck, Christiane Paul, Natascha Hill, Stefanie Hartmann, Christoph Hösel (2010). Phylogenomic analyses unravel annelid evolution Nature
In the arid shrublands of the Australian outback, an orchid grows. Hundreds of small flowers are blooming within its lilac leaves. It is unlikely you have ever seen this rare and endangered orchid. In the thirty years after its discovery in 1928, the orchid was seen just six times. Even if you had the luck to wander near this beautiful orchid (Rhizanthella gardneri) you still wouldn’t notice it, because it lives several centimetres below the ground. Its maroon flowers never see the light of day.
The rare, subterranean orchid Rhizanthella gardneri.
By living underground, the remarkable Rhizanthella is somewhat protected from drought and desiccation. The orchid had to make a Faustian deal to receive this protection: without the light of the sun to nourish it, the orchid became a parasite.
Rhizanthella parasitizes a species of fungus, which lives on the roots of the broom bush Melaleuca uncinata. The relationship between the fungus and broom bush is harmonious. They both produce something that the other needs. The bush captures sunlight and converts it to sugars, which it exchanges for minerals that the fungus takes up from the soil. But the orchid? It grows near the roots of the broom bush, so that it can exploit its fair trade agreement by stealing nutrients from the fungus.
This subterranean and parasitic lifestyle is a big change from normal plant life. Other plants use their green chloroplasts to obtain energy from the sun via photosynthesis. But underground, Rhizanthella no longer needed its chloroplasts. Its leaves turned purple instead of green.
Still, the chloroplasts endured. They might no longer be green, but they have other functions that prevented Rhizanthella from doing them away entirely. Photosynthesis normally overshadows these other roles, but a parasitic plant like Rhizanthella presents the perfect opportunity to peek at this hidden, far side of the chloroplast.
A recent census of the genes inside Rhizantella‘s chloroplasts turned 37 genes. This a big drop from the more than hundred genes that chloroplasts normally have. In fact, with only three dozen genes, Rhizantella‘s chloroplasts are some of the most gene-poor chloroplasts known. The genes that were no longer necessary in the chloroplast were purged from its genome or moved to the cell’s nucleus. All its photosynthesis genes went missing, for example.
Parasites like Rhizanthella are perfect for peering at the far side of the chloroplast, which are the organelles that are responsible for photosynthesis in other plants.
More interesting than the genes that are no longer there, are the genes that remain. The majority of them are somehow involved in manufacturing proteins. Nine chloroplast genes code for RNAs that carry amino acids, and two genes are responsible for stringing these amino acids together into proteins, for example.
Another gene, with the poetic name accD, codes for a part of a protein that produces fatty acids that are part of cellular membranes. The other parts of this protein are coded for by genes that are located in the cell’s nucleus, but the entire protein has to be put together inside the chloroplast. This could be the reason why accD managed to keep its spot inside the chloroplast: as long as at least one part is represented by a gene inside the chloroplast, the larger protein can still be assembled.
A deep incorporation into the cellular infrastructure seems to have been the ticket to survival for the 37 genes that remained. For now, at least. But getting rid of these superfluous genes also means that there is no way back for Rhizanthella and other parasites. It will never be able to absorb the light of the sun again. This can be a dangerous strategy, because a parasite’s fate will always be in the hands of other species. For Rhizantella the dependency on the fungus and broom bush comes on top of its dependence on termites for pollination of its flowers and mammals for the dispersal of its seeds. With so many delicate interactions with other species, no wonder it’s so rare.
Rhizanthella picture by Jean Hort.
Picture of rain on a castor oil plant by Fozzeee.
Delannoy E, Fujii S, des Francs CC, Brundrett M, & Small I (2011). Rampant Gene Loss in the Underground Orchid Rhizanthella gardneri Highlights Evolutionary Constraints on Plastid Genomes. Molecular biology and evolution PMID: 21289370
Milk comes from cows. Most of us know that. More urban readers are forgiven for thinking milk comes from supermarkets. But the the question where milk comes from has the potential to reach beyond dairy farms and breakfast tables. It could be about the origins of milk itself, millions of years ago. “Where does milk come from?” becomes “how did milk evolve?”
Milk is essential for the survival of pups, cubs and calves around the world. Young mammals can gain weight and grow on a diet of milk alone because it is rich in proteins, vitamins, calcium and saturated fats. But milk has not always been this nutritious.
A hatching corn snake. Notice the leathery texture of the egg.
Our mammalian ancestors started giving milk when they were still laying yolky eggs. The shells of these eggs weren’t hard and calcified like the eggs of birds. They were soft and had a parchment-like eggshell instead, much like the eggs of lizards and snakes. If you would study such eggshells under a microscope, you would see that their surface is covered with millions of narrow pores. If it is too hot or dry, water evaporates through these pores, putting the eggs at risk of drying out.
Snakes and lizards prevent this from happening by laying their eggs in a moist soil. But early mammals solved this problem in a different way, Olav Oftendal thinks. He suggests that lactation didn’t evolve to nourish, but to drench. Fluids secreted through the skin of ancestral mammals could have protected the eggs from drought and desiccation. If true, the first ‘milk’ was not that milky at all: think twice before mixing Triassic milk with your cornflakes.
The eggshell pores forced the ancient mammals to look for answers. When these answers were found, the advantages of an passable eggshell could begin to be exploited. Through the pores, extra nutrients added to the moistening fluid reached the developing hatchling inside the egg. New opportunities awaited in this twilight zone between moist and milk. Eggs could grow smaller, because the yolk no longer need to provide every single nutrient the embryo needed. Young animals could delay their development, since they no longer needed to hatch as miniature adults.
But that’s running ahead of the story. There are genes that can tell us more about how our ancestors switched from yolk to milk.
Electron microscope picture of a milk micelle.
Caseins Caseins are the most abundant proteins in milk. They come in two forms. One type binds calcium, the other one is insensitive to calcium. When you bring thousands of these caseins together, they self-assemble into a soluble micelle. Micelles look a bit like little balls of hair. The ‘hairs’ are really the tails of caseins that are sticking outwards. The calcium-insensitive caseins stabilize the micelle, but it is thanks to the calcium-binding caseins that micelles are loaded with calcium. If milk contained the same concentration of calcium without the micelles, the calcium wouldn’t remain soluble and precipitate.
From cows to kangaroos, all mammals have casein genes. And in every mammalian genome, the caseins are surrounded by closely related genes. The technical name for this family of genes is ‘secretory calcium-binding phosphoprotein family’. Or SCPP family, for friends. As the family name implies – most of the SCPP family members can bind calcium. The SCPP family is old. One of its oldest family members, SPARCL1, uses calcium to mineralize our bones. It evolved more than 400 million years ago and can be found in all creatures with a calcified skeleton, such as bony fish, reptiles, birds and mammals.
The SPARCL1 gene was duplicated again and again. These carbon copies of SPARCL1 were free to evolve new functions. Some copies now mineralize other tissues, such as the enamel of our teeth. Kazuhiko Kawasaki and his colleagues from Penn State University have shown that milk caseins evolved from such tooth mineralizing SCPPs. One of the recent reconstructions by Kawasaki revealed that the different types of caseins also evolved from different types of tooth mineralizing SCPPs.
The evolution of the SCPP proteins, from the earliest tetrapods to the almost-mammalian synapsids. The SCPP family has been evolving fast: genes were duplicated and lost many times. The calcium-binding caseins are CSN1/2, the calcium-insensitive casein is CSN 3.
When something is gained, something else is lost. A recurring pattern in evolution. While caseins were born from tooth genes, the vitellogenin family became extinct.
Vitellogenins are the defining proteins of egg yolk. In all species that lay eggs (from insects to amphibians), vitellogenins provide the nourishment that developing embryos inside an egg need. Ancient mammals were no exception to this rule. They had three different vitellogenin genes, like modern birds and reptiles do.
But as milk became more nutritious, the egg yolk of pre-mammalian eggs became less and less important. When they were no longer needed, the vitellogenin genes were inactivated one by one. The remnants of these vitellogenins can still be found in our genomes today. They are the broken relics of a time when our distant ancestors still laid eggs. Still recognizable, but without a function for many millions of years.
While the birth and death of families of genes make for good dramatic narrative, it is important to realize that milk evolved gradually. There is no single point in time when milk, or mammals for that matter, sprung into existence. From pelycosaurs, to therapsids, to cynodonts: mammal-like creatures have around for millions of years.
Oftedal OT (2002). The origin of lactation as a water source for parchment-shelled eggs. Journal of mammary gland biology and neoplasia, 7 (3), 253-66 PMID: 12751890
DALGLEISH, D. (2004). A possible structure of the casein micelle based on high-resolution field-emission scanning electron microscopy International Dairy Journal, 14 (12), 1025-1031 DOI: 10.1016/j.idairyj.2004.04.008
Kawasaki K, Lafont AG, & Sire JY (2011). The evolution of milk casein genes from tooth genes before the origin of mammals. Molecular biology and evolution PMID: 21245413
Brawand D, Wahli W, & Kaessmann H (2008). Loss of egg yolk genes in mammals and the origin of lactation and placentation. PLoS biology, 6 (3) PMID: 18351802
It is the year 2092. Nemo Nobody is the last mortal on our planet. At 117 years old, the brittle Nemo is almost at the end of his life. Everyone around him will live forever, whereas he will be the last one to die. Nemo spends his last days in a hospital where he features in a reality show and is interviewed by a journalist every day. But the journalist finds reconstructing Nemo’s past difficult, as many of his memories seem to contradict one another. For example, when his parents got separated, Nemo either had to stay with his father in England, or move to the United States with his mother. But Nemo never really made that choice. He remembers both living with his mother and taking care of his sick father. Later he remembers being married to three different wives, in varying degrees of happiness. It is as if Nemo never makes a decision. When he is confronted with a fork in the road, he walks both paths. Looking back at his life it as if he is peering through a kaleidoscope – seeing all the possible lives he could have lived at once.
The movie Mr. Nobody raises some mind-boggling questions about choice and consequence. How many different lives could you have lead? What if your parents had moved to a different town when you were young? What if you had studied medicine, instead of psychology? What if you had missed that bus and never met your current partner? Change just a few critical details of your personal history, and you would end up leading a different life altogether. You are where you are know, because a long chain of improbable events brought you there. This dependency on the past is called contingency. Sometimes the dependency is obvious. If you choose not to attend high school, you cannot attend college for example. Other dependencies, such as the launch of your company after bumping into your future business partner at the airport 5 years ago, seem insignificant at first, but can cause a cascade of consequences later on.
But not everything that happens in our life is the result of contingency. I don’t often say this – but some things are ‘destined to happen’. I am not talking about finding Mr. Perfect or Mrs. Right. I am referring to a different kind of destiny. A destiny that is shaped by our biology or environment, for example. A caterpillar in a cocoon will always emerge as a butterfly, not as a bumblebee or as a beetle. Whatever happened in its life as a caterpillar, this particular outcome cannot be changed. Similarly, someone born with one faulty copy of the haemoglobin gene will develop sickle cell anaemia. And whichever life I would have lived, I’d probably be great at growing a beard. Some tendencies are inevitable.
A butterfly emerges from its cocoon. No butterfly can change this outcome.
There is a tension between these two forces. Contingency is a random process. Yes – the future depends on the past, that past is full of ‘historical accidents’. All possible outcomes are rooted in random events. Inevitabilities, on the other hand, are non-random. They have a direction and impose limits on what is possible and what is not. This tension between random and non-random not only affects the course of our own lives, but also that of evolution itself. As a historical process, evolution should be subject to contingency. But we also know that evolution follows certain rules and laws – like natural selection. So how do these two forces play out in nature? To what extent is evolution random? This might look like a simple question, but it has divided some biologists deeply.
One of the most passionate advocates for a contingent view of evolution was Stephen Jay Gould. In his book Wonderful Life he describes a famous thought experiment, where he imagines what would have happened if the asteroid that struck the earth 65 million years ago had missed it instead. The asteroid impact lead to the extinction of thousands of plants and animals, including all large dinosaurs. If the asteroid had flown by our planet, dinosaurs could have continued their rule over the earth. Mammals would never have flourished like they did after the original catastrophe. Perhaps they would have remained small and nocturnal creatures, destined to scrape by in a reptilian world. Gould thinks it is unlikely that humans, or human-like intelligence, would ever evolve in this alternate reality.
Devastating asteroids are historical events that are not part of any theory of evolution. Still such events have the power to change evolution’s course. Even the simplest mutation in a gene is historical event, because they are unpredictable and not predetermined. While biologists may now know some of the laws and forces that drive evolution, historical contingency prevents them from predicting its future. A biologist studying sauropods (‘long-neck dinosaurs’) 66 million years ago could never suspect that these successful, lumbering giants would become extinct one million years later for example. Just a small change in life’s history is enough change the world into one that is very different from the one we see today. Gould said this best himself:
We came this close (put your thumb about a millimetre away from your index finger), thousands and thousands of times, to erasure by the veering of history down another sensible channel. Replay the tape of evolution a million times from a Burgess beginning, and I doubt that anything like Homo Sapiens would ever evolve again. It is, indeed, a wonderful life.
~Stephen Jay Gould, Wonderful Life
The Burgess Shale that Gould mentions is a fossil bed from the Cambrian and forms the main inspiration for Gould’s argument. The creatures in the Burgess Shale were buried in an undersea mudslide around 500 million years ago. This sudden burial lead to the perfect preservation of these animals – even their soft tissues are immortalized in the rocks. The palaeontologists Simon Conway Morris, David Briggs and Harry Whittington reanalyzed and reconstructed many of the Cambrian fossils of the Burgess Shale. They found that many of the Burgess animals had bizarre designs. Animals like Opabinia, Aysheaia and Hallucigenia al have body plans that are so unfamiliar that they appear to be unrelated to animals of today. Even the not-too-spectacular Marrella doesn’t fit into any modern group. Marella has similarities to crustaceans and trilobites, but belongs to neither family.
The bizarre Opabinia, grabbing an Amiskwia with its proboscis.
Although they turned to stone a long time ago, these strange Burgess creatures still pose a burning question: why did they go extinct? Why can’t we buy a pet Opabinia in our pet stores? I’m sure aquarium hobbyists would love to get there hands on Opabinia – it would add some unique diversity to their aquariums, for the millions different species that are alive today only represent a handful of different body plans. A million different beetles are still a million variations on a common theme. From the ~20 different Cambrian arthropod designs present in the Burgess Shale, only four survived. Why only these four, and not another set? Gould thinks that it was sheer luck. We can’t really say why some species went extinct, he says. Their bauplan wasn’t ‘less adapted’ or ‘more primitive’ than that of their more lucky relatives. They were just different. It’s as if their fate was decided in a cruel lottery. But if you would pick a different set of lucky survivors, and marrelloids instead of crustaceans would have crawled around the floors of the sea. A small change in Cambrian times, but a radically different outcome.
Why can't we buy a pet Opabinia in our pet stores?
Gould’s interpretation of the Burgess Shale is not uncontroversial. Two of the heroes in Gould’s book, David Briggs and Simon Conway Morris, criticized the theories of their admirer. David Briggs published a couple of papers that aimed to show that the Burgess creatures weren’t that morphologically diverse at all. But it was Conway Morris who challenged Gould’s claims on contingency in his book the Crucible of Creation.
When Simon Conway Morris looks back at the history of life, he doesn’t see randomness and contingency. He sees direction and convergence. Convergence is the observation that evolution tends to come up with similar answers when it is faced with similar problems. All animal lineages evolved eyes, for example. From the compound eyes of insects to the lens-bearing eyes of squids and vertebrates, each animal has found its own way to see the world around it. The form of the eye might vary, but having eyes seems to be a good rule of design. According to Conway Morris, evolution converges on a limited set of solutions time and time again.
Similar environmental selection pressures, acting on differing anatomies, can create convergent or parallel adaptations. [..] History is constrained, and not all things are possible. To understand how creatures that are descended from very different groups can evolve similar forms and functions, consider that dolphins, which evolved from doglike mammals, are shaped like fish because there exists an optimal shape for moving through water—a classic example of convergent evolution.
~Simon Conway Morris, “Showdown on the Burgess Shale,” Natural History magazine, 107 (10): 48-55.
There are only so many ways of moving around in water so dolphins are restricted in their options. Conway Morris doesn’t say that the specific from of a dolphin is inevitable. There are numerous differences between fish, ichtyosaurs and dolphins. Fish have gills, whereas dolphins breathe through a blowhole. Yet it is obvious that all these different creatures are shaped like a fish. Maybe ‘the form of the fish’ is the only logical endpoint for marine creatures with a spine. He argues that replaying the tape of life will give us a different, but very similar outcome. Yes – Marella could certainly have become the ancestor of a successful lineage of marine arthropods. But they would have filled the same niches as trilobites or crustaceans.
So where do we go from these two conflicting views? Is evolution guided by contingency, or convergence? It is important to remember that this is not an ‘either-or’ issue at all. Contingency and convergence are not mutually incompatible. It would be silly to say that evolution is free of constraints or predictable patterns. It would be equally silly to say that history plays no role in evolution. Contingency and convergence both shape the possibilities and impossibilities of evolution. Figuring how these forces are together weave the tapestry of evolution should be an exciting enterprise (and provide enough fuel for another blogpost).
Why then, do these questions incite so much debate? This is because deep down, they are not about dolphins and Opabinia. The question all of us want to find an answer for is whether the evolution of human conciousness was somehow inevitable. Many, including Conway Morris, think it was. I most recently came across this view in Kevin Kelly’s latest book, What Technology Wants. In this book, technology enthusiast Kevin Kelly goes as far as reversing Gould’s statement that ‘humans are an entity, not a tendency’ into the exact opposite statement ‘humans are a tendency, not an entity’. Convergence, Kelly says, drives life to become more complex and yes, more conscious. Twelve years ago, Gould already pointed out the weak point in this argument:
Evidence for convergence requires multiple cases of independent evolution, while the example that we all carry closest to our hearts (and that engenders the emotional oomph in this debate)—the evolution of consciousness in Homo sapiens—remains an outstanding singleton in the only history of life we know: the story of our own planet.
~Stephen Jay Gould, “Showdown on the Burgess Shale,” Natural History magazine, 107 (10): 48-55.
I have to agree with Gould here. In contrast to the repeated evolution of fishlike creatures, we have only know one example of a conscious creature evolving. It is impossible to claim that the evolution of consciousness is a something that has occurred repeatedly in the history of life. We should be open to the idea that we are here partly because of the inevitabilities that constrain evolution, and partly because we have been lucky enough that history unfolded as it did.
Many find this idea that mankind is not the inevitable outcome of evolution offensive. It rubs against our collective, human pride. Copernicus, Galileo and Kepler already showed us that earth is not in the centre of the universe. Darwin removed mankind from the centre of creation. The last retreat of our feeling of human superiority seems to be the thought that somehow, everything is meant to be this way. It is comforting to believe that the evolution of human consciousness is the fulfilment of a promise made 4,6 billion years ago. Because what would we be left with, if mankind turned out to be a fortunate accident?
I think we would be left with an even greater appreciation of the wonderful world in which we live. The unlikeliness of a conscious species arising to start talking and reflecting on its own place in this universe, doesn’t make evolution any less stunning or interesting. It makes it more so. Nemo Nobody said this better than me. When the journalist asks Nemo which of his conflicting memories represent the ‘right’ story of his life, he replies “Each of these lives is the right one. Every path is the right path. Everything could have been everything else and it would have had just as much meaning.”
This is a science blog, where I will be writing about interesting papers on evolution in an understandable fashion. I like science that's on the intersection of molecular, evolutionary and computational biology. Leave a comment behind if you're amazed, baffled or offended by what I wrote!