Let’s talk about evo-devo and evolutionary novelties on Friday

It’ll be a casual science convo on Friday at 3pm Central. I’m not going to do a lot of prep work because I don’t have the time, but I can talk about new evolutionary features off the top of my head. How about mammary glands? You like mammary glands?

If you’re one of my patrons (only a dollar a month, cheap), you can also join in the Zoom call. If you hate long-winded livestreams, I’ll also pluck out one of the more interesting excerpts and post that on Saturday.

What a pretty tree!

If you’re bored and feel like exploring all of life, try the One Zoom explorer. It’s a graphical interface to a collection of data about phylogeny.

It’s interesting and useful at the top level, but as you dig down into the twigs and leaves, it starts to fall apart, lacking in detail. That’s what you’d expect if you’re trying to track about 1.5 million documented species (somewhere over 10 million species total). It does help communicate the diversity and complexity of life, though.

However, aggressive, forthright opposition also works

OK, so atheists shouldn’t take credit for a decline in religion, but I think science communicators and educators (which is not synonymous with atheism, I’m sure you know) have accomplished something: the gradual decline of creationism. More people are accepting evolution!

In the early years of this blog, way back in the 2000s, I felt a bit of frustration and despair because when I looked at the surveys, all I saw then was a flat line: less than half the population accepted a well-supported scientific fact, and 40% openly rejected it in favor of nonsense contradicted by all the evidence. And the statistics were flat-lined back into the 1960s, when the surveys began! It was all very discouraging, but also motivated a lot of us to get out there and do public science communication. It seems to have worked.

At least, I think educating the public helped. Another factor is that evolution has also become a tribal marker. If you’re a True Republican, you believe in bullshit and the American way; if you’re a True Democrat, you believe in evolution and science. Part of the reason for the growing disparity is simply growing polarization.

Antievolutionism remains a political force. The Republican party often panders to religious fundamentalism, and attitudes toward evolution are politicized as a result. Miller and his collaborators found that 34% of conservative Republicans accepted evolution in 2019, as compared to 83% of liberal Democrats. There is evidence that the politicization is increasing: in 2009, 54% of Republicans and 64% of Democrats accepted human evolution, but by 2013, the ten-point gap widened to a twenty-four-point gap, according to the Pew Research Center.

That tells me it’s just as important as ever to work to make sure citizens accept evolution for the right reasons. Because that’s what the evidence supports.

My synapsid family

Nice image to illustrate a basic cladistic principle. I still get whines from creationists complaining that I said we humans are fish — but that’s just a bigger circle enclosing everyone in this image.

I have no illusions that this will ever sink into the brains of the people who deny it.

…cut off their tails with a CRISPR knife…

Brachyury (Greek for “short tail”) is an important protein in animal development — it’s found in all chordates and is expressed along the midline, and sets up the anterior-posterior axis. It seems to play an essential role in defining tissues along the length of the animal, and many mutations have been found in the gene TBXT for it that cause defects in the spinal cord. In addition to the short tail phenotype it’s named for, different variants affect other regions as well. For instance, you probably know that almost all mammals have precisely 7 cervical vertebrae, but there is a mutation in TBXT that reduces that number to 6.

So, basically, if you want to profoundly muck up the developing vertebrae and spinal cord, mutating TBXT is a way to do it, as long as you don’t mind inducing neural tube defects, like say, spina bifida. It’s a dangerously significant gene to tinker with, and most of the outcomes would not be good. But note — humans and other hominoids have an inherited, ubiquitous spinal cord defect. We don’t have tails, unlike other mammals. Could we be carrying a mutation in our TBXT gene? Could that be what caused all us apes to lose our tails? Maybe we should look and compare our TBXT to that of other animals. Huh, what do you know…we do have a curiously broken TBXT.

A little background first. Eukaryotic genes are broken up into segments called exons alternating with other segments called introns. To make a functional gene product, like Brachyury, the cell has enzymes that cut out the introns from the RNA and splice together the exons. The intronic RNA is then generally allowed to be broken down and recycled. So TBXT has 7 exons, E1, E2, E3, E4, E5, E6, and E7, with intervening introns which must be snipped out and the exons spliced together to make a final, complete RNA, E1-E2-E3-E4-E5-E6-E7, which will be translated to make the Brachyury protein.

Another complication: there are these short bits of selfish DNA called Alus which are scattered throughout the genome. We have over a million Alu elements sprinkled throughout, and usually they do nothing, although if an Alu gets inserted into an exon of a gene, it can disrupt the function of that gene. The good news: there is no Alu stuck in the exons of TBXT. There are a couple of them in the introns of TBXT, but remember, the introns get chopped out and thrown away, so they shouldn’t matter. Except that in this case, they do.

In us hominoids, there is one Alu, AluSx1, in intron 5. There is another Alu, AluY, in intron 6. They happen to complement each other in reverse, so in the TBXT RNA, before the introns are edited out, the RNA folds over to make a loop that allows the two Alus to bind to each other. This messes up the editing, because the cell then snips out the introns and the loop, throwing away exon 6. Uh-oh. That means that instead of producing the full length TBXT, we make a shortened version lacking exon 6, called TBXT-Δexon6.

This observation was tested with a couple of nifty experiments. First question: is it really the Alus that are causing this error in splicing? Yes. Doing a little gene editing and knocking out either Alu in human embryonic stem cells causes them to generate full length TBXT transcripts. These are just single cells in a dish, and while you might be curious to know if deleting those specific Alus in a human embryo would lead to it developing a tail, that would be unethical. In a sense, you’d be generating a neural tube defect, never a desired outcome, and we don’t know what other compensatory or cooperative genes to our, for us, normal TBXT-Δexon6 exist.

But hey, good news, we don’t have the same ethical restrictions when working with mouse embryos! Let’s dive into the mouse genome and insert Alus, just like ours, into the introns of the mouse TBXT gene! And so it was done, producing mice that made TBXT-Δexon6, and lo, they had little stumpy tails, or no tails at all.

There are a few complications. Mice that were homozygous for TBXT-Δexon6 died embryonically with substantial neural tube defects. Heterozygotes for TBXT-Δexon6 survived, and exhibited the tailless phenotype with variable penetrance, that is some mice were lacking the whole shebang, missing sacral vertebrae (sv) and all caudal vertebrae (cv), and others lost variable numbers of caudal vertebrae.

It’s lovely work, but I still have to disagree a little bit with their interpretation. Their model of hominoid evolution puts the tail-loss mutation right at the base of the progression.

That’s too simple. The lethality of the homozygous mutant in mice, while we homozygous mutants are fine, tells me that there are a lot of other genes that work together with TBXT to make a viable embryo — that we have a suite of supporting genes that can compensate for the lethal effects of TBXT-Δexon6. This model assumes that all those supporting roles evolved after the TBXT-Δexon6 mutation occurred. There is no reason to think that. Why not consider that our ancestral hominoid had a few exaptations that made it slightly more fault-tolerant in axis formation? Put those additional mutations ahead of the AluY insertion. Then have additional mutations afterwards. Our ancestors were not mice, so there’s no reason to think they’d have had the same response (that is, the lethality) to TBXT-Δexon6 as do modern mice.

Also, now I’m really interested in those additional mutations. TBXT isn’t the whole story.

Xia, b, Zhang W, Wudzinska A, Huang E, Brosh R, Pour M, Miller A, Dasen JS, Maurano MT, Kim SY, Boeke JD, Yanai I (2021) The genetic basis of tail-loss evolution in humans and apes. https://www.biorxiv.org/content/10.1101/2021.09.14.460388v1

We’re in this business for the unanswered questions

What I like about this episode of Crash Course Zoology is that it shows that it shows how scientists aren’t at all afraid of evolutionary mysteries, or of being wrong about something. Take that, creationists! That seems to be their primary line of attack, and all they’ll get out of me when they point out how our knowledge is incomplete is bafflement. Yeah, we know. That’s why we’re scientists.

Also, it’s got spiders in it.

The next episode is going to be about the species concept. Gosh, it’ll be nice when that one is finally explained!

Bring back the weird

The paleontological literature is a showcase for tragedy — it’s a graveyard of long-dead species, all snuffed out millions and millions of years before any human was around to appreciate them, and all we can do is look in awe at their fossilized corpses. In particular, fans of the Cambrian fauna can only pine for magnificently weird creatures that have been extinct for hundreds of millions of years, and represent entire exotic lineages that have left no descendants today. Two of the strangest are Anomalocaris and Opabinia.

Two of the most peculiar Burgess Shale animals, Anomalocaris and Opabinia, illustrate the complicated history of research of many Cambrian soft-bodied taxa – a result of their unfamiliar morphologies compared to the occupants of modern oceans. Both Anomalocaris and Opabinia possess compound eyes, lateral swimming flaps, filamentous setal structures, and a tail fan. Recent work has revealed that Anomalocaris and its relatives, the radiodonts, are united by the presence of paired sclerotized protocerebral frontal appendages and mouthparts composed of plates of multiple sizes, forming a diverse group containing over 20 taxa. Radiodonts range in age from the early Cambrian to at least the Devonian, and have been recovered from numerous palaeocontinents. Meanwhile, the most celebrated animal from the Burgess Shale, Opabinia regalis, with its head bearing five stalked eyes and a proboscis, remains the only opabiniid species confidently identified and is only known from a single quarry in the Burgess Shale. Myoscolex ateles from the Emu Bay Shale was proposed as a possible close relative, though this interpretation was hotly contested, and other authors have proposed a polychaete affinity.

The radiodonts (arthropods with mouths containing plates arranged in a wheel, that irised open and closed) are diverse and notorious. For a time, they were the largest predators on the planet, with their paired long spiky Great Appendages extending from the front of their head. Like the quote says, the opabiniiids are known from one location and one species, but they are weird. A similar array of swimming flaps like Anomalocaris, but then having 5 eyes on stalks and a long snout with a mouth on the end of it…it’s heartbreaking that they no longer exist. Spiders are cool and all, but I’d love to have schools of anomalocariids or opabiniids swarming in our local lakes.

At least one new opabiniid species has been identified, though. This cutie:

For perspective, here’s where they fall on the phylogenetic tree.

Tardigrades and velvet worms and mantis shrimp are certainly wonderful and interesting animals, but I have to yearn to see more of that glorious radiation of interesting forms in between. All gone, though. If gods were real, they’d never have let them die off.

I am inclined to like this hypothesis

I’m still going to criticize it, though.

For years, anthropologists and evolutionary biologists have struggled to explain the existence of menopause, a life stage that humans do not share with our primate relatives. Why would it be beneficial for females to stop being able to have children with decades still left to live?

According to a study published today in the journal Proceedings of the Royal Society B, the answer is grandmothers. “Grandmothering was the initial step toward making us who we are,” says senior author Kristen Hawkes, an anthropologist at the University of Utah. In 1997 Hawkes proposed the “grandmother hypothesis,” a theory that explains menopause by citing the under-appreciated evolutionary value of grandmothering. Hawkes says that grandmothering helped us to develop “a whole array of social capacities that are then the foundation for the evolution of other distinctly human traits, including pair bonding, bigger brains, learning new skills and our tendency for cooperation.”

I guess I’m personally inclined to appreciate the importance of grandmothers, having had a pair of good ones myself, and seeing how much time my wife invests in our granddaughter, but I’m less impressed with the study, which is based entirely on a computer simulation. I don’t trust simulations of complex phenomenon that necessarily have to simplify all the parameters. What about aunts and sisters? What about uncles?

What about the grandfathers?

None of those individuals are of interest, because this version of the hypothesis is structured around explaining menopause as the product of selection. Nope, I don’t buy it.

But why would females evolve to only ovulate for 40 or so years into these longer lives? Hawkes and other advocates of the hypothesis note that, without menopause, older women would simply continue to mother children, instead of acting as grandmothers. All children would still be entirely dependent on their mothers for survival, so once older mothers died, many young offspring would likely die too. From an evolutionary perspective, it makes more sense for older females to increase the group’s overall offspring survival rate instead of spending more energy on producing their own.

I’m willing to accept the benefit of an extended family and social cooperation, but the effort to justify menopause seems misplaced. There are many grandmothers who are not menopausal, and there would have been even more in ancient populations, where pregnancy shortly after the onset of menstruation would have been common. It also doesn’t explain the contributions of sisters and aunts to childrearing, or that brothers and sisters, who are also “distractions” from the business of raising a single delicate child. Why couldn’t it benefit a woman to raise her own child born late and also contribute to the well-being of grandchildren born to previous offspring? I suspect the simulation has assumptions built into the code about how much grandparental investment can be offered if they also have a child.

But, yeah, what about the grandfathers?

We help, too. So why isn’t there a male menopause where our testicles shrivel up and make us more willing to contribute to child-rearing? A man has a certain number of progeny, then boom, the reproductive urge goes away and he has to sit down and focus on taking care of the kids he’s got. Or his grandchildren. Or his nieces and nephews. That would be the logical endpoint of this arch-selectionist model, after all, and what’s good for the goose is good for the gander.

Yet somehow people feel compelled to come up with adaptationist explanations for accidents of evolutionary history.

Did native Americans have more equality 9000 years ago than we do now?

A pretty picture of a Peruvian hunter from 9000 years ago, bringing down vicuna with her atlatl and spear:

The image is based on the remains of the dead hunter, and an analysis of grave goods.

At Wilamaya Patjxa, an archaeological site in southern Peru, archaeologists unearthed the skeleton of a young woman whose people buried her with a hunters’ toolkit, including projectile points. The find prompted University of California Davis archaeologist Randall Haas and his colleagues to take a closer look at other Pleistocene and early Holocene hunters from around the Americas.

Their results may suggest that female hunters weren’t as rare as we thought. And that, in turn, reminds us that gender roles haven’t always been the same in every culture.

“The objects that accompany [people] in death tend to be those that accompanied them in life,” Haas and his colleagues wrote. And when one young woman died 9,000 years ago in what is now southern Peru, her people buried her with at least six stone spear tips of a type used in hunting large prey like deer and vicuña (a relative of the alpaca). The points seem to have been bundled along with a stone knife, sharp stone flakes, scraping tools, and ocher for tanning hides.

I also learned a new genetics fact! The bones were fragmentary, and the bits that you use for a morphological assessment of sex had crumbled to dust. But you can sex a skeleton by looking at the proteins that make up tooth enamel.

Tooth enamel contains proteins called amelogenins, which play a role in forming the enamel in the first place. The genes that produce these proteins are located on the X and Y chromosomes, and each version is slightly different. As a result, people who are genetically female have slightly different amelogenins than people who are genetically male. The proteins in the ancient hunter’s tooth enamel had a distinctly female signature, with no trace of the Y chromosome version.

The hunter from Wilamaya Patjxa is a young woman with the tools of an activity usually associated with men. If the objects people are buried with are the objects they used in life, then that raises some questions.

Maybe she was some weird outlier, I hear you ask. So they surveyed what was found at other grave sites, and it looks like a significant fraction of ancient hunters in the Western hemisphere happened to be women.

The hunter from Wilamaya Patjxa raises a similar question: was she the exception that proved the rule, or does her burial suggest that (in at least some ancient cultures) women were sometimes hunters? To help answer that question, Haas and his colleagues looked for other ancient people who had been buried with hunting tools. In published papers from archaeological sites across the Americas, they found 27 people at 18 different sites: 16 men and 11 women.

…the fact that so many apparent women turned up on that list is surprising. “Female participation in early big-game hunting was likely nontrivial,” wrote Haas and his colleagues. They suggest that as many as a third to half of women across the ancient Americas may have been actively involved in hunting.

The final line in this article is perfect.

Based on animal bones at Wilamaya Patjxa, large game like vicuña and taruca (a relative of deer) were extremely important to the community’s survival. In that case, hunting may have been an all-hands-on-deck activity. Haas and his colleagues also suggest that letting other members of a community keep an eye on the kids while the parents hunted might have freed more women up to bring home the bacon—or venison, in this case.

In other words, whether women hunted or fought probably depended on social factors, not biological ones.

I thought I ought to let David Futrelle know about this, since it makes the title of his blog even more ironic, but he beat me to it and has already posted about how She Hunted the Mammoth.