Rooting for Australian arthropods in amber

I think the title is a double entendre in Australian, but it’s not a language I am fluent in. Anyway, a paper in Nature describes an assortment of organisms found in amber from Australia and New Zealand, ranging in age from 230 million years to 40 million years. It’s lovely stuff.

Significant bioinclusions of plants and animals in Southern Gondwana late middle Eocene amber of Anglesea, Victoria. (A to B) Liverworts of the genus Radula (Marchantiophyta: Radulaceae). (C) Two stems with perfectly preserved phyllids or leaf-like structures of mosses of the genus Racopilum (Bryophyta: Racopilaceae). (D) Juvenile individuals of spiders. (E to F) Springtail of the living genus Coecobrya (Entomobryomorpha: Entomobryidae) in two views. (G) A Symphypleona springtail. (H) Light photograph of large piece of yellow amber with two dipterans, Dolichopodidae at left and Ceratopogonidae at right, and at top of image a mite of the living genus Leptus (Arachnida: Acari: Trombidiformes: Erythraeidae). (I) Dipterans of the family Dolichopodidae (long-legged flies) in copula. (J) Worker ant of the living genus Monomorium or a “Monomorium-like” lineage (Hymenoptera: Formicoidea: Formicidae).

I don’t know about you, but I was most interested in D, the two juvenile spiders.

Wait, I do know about you — you’re most interested in I, the two flies caught in the act. So here’s a closeup.

Count yourself lucky. Now if you want to take a pornographic selfie, you just whip out your phone, capture the moment, and go on with your life. Forty million years ago, you had to say “Freeze! Look sexy!” and wait for a drop of sap to ooze over you, and then you had to hold the pose for tens of millions of years.

There are laws about this kind of congregatin’

The snow is back. Not much of it, but it was mixed with freezing rain and now everything is covered with a thin glaze of extraordinarily slippery ice, so I guess Nature is enforcing the stay-at-home order.

These scofflaw birds don’t care at all, though. My yard was covered with sparrows for a while, and the birdfeeder in my front yard has become the most popular meeting spot in the area. KEEP YOUR DISTANCE. STAY INDOORS. Stupid birds.

Michael Egnor agrees with me, I’m having a panic attack

Uh-oh. Michael Egnor is writing about me over on the Discovery Institute site. He’s commenting on that summary of the origin of SARS-CoV-2 virus I wrote the other day, which is fine. What isn’t fine is that he agrees with it.

I threw up in my mouth a little bit.

Reading further, though, he agrees with it for all the wrong reasons, so I feel a little better.

Myers, like the Nature Medicine scientists, uses the scientific inference to intelligent design to search for (and discount) human intelligent agency. Design science is at the forefront of research on the emergence of coronavirus. Based on the available evidence and using the inference to design as a scientific hypothesis, intelligent design of the COVID-19 virus seems unlikely.

That is incorrect. “Design science” is not at the forefront of the research. The authors of that paper came to their conclusion by extensive comparisons of the viral sequence with viruses in other organisms, and by a functional analysis of the structure of the receptor binding domain. Conspiracy theorists and creationists have been poisoning the global conversation with nonsense about the virus being “designed”, so they addressed and dismissed that idea. The primary interest was in the original source, and what properties of the virus make it dangerous to us.

They also pointed out two major adaptations of the virus spike protein: changes to the receptor binding to allow it to bind effectively (but not optimally) to the human ACE2 protein, and an insertion that adds a polybasic cleavage site which also allows the linkage of glycans to the protein that assist in immunoevasion. Two mutations at once! Doesn’t his pal Michael Behe have something to say about the improbability of multiple mutations?

But there is another lesson about design and evolution to be learned from scientific research on this virus. Natural selection, if understood as undirected variation and differential reproductive success, is a destructive process. Natural selection destroys biological functional complexity — it produces diseases, cancer, and pandemics. It weakens and kills. Natural selection does to living organisms what rust does to a machine. Natural selection corrodes and destroys life, and plays no role in creating it.

Not for the virus, it wasn’t a destructive process. What was undergoing natural selection here was the virus, not us, and it has acquired attributes that make it wildly successful — it is now colonizing vast fields of billions of human beings, producing uncountable numbers of progeny, infecting more people at an accelerating rate. The virus is stronger and thriving thanks to those features, and doing very well thank you very much.

Humans are now possibly undergoing a round of natural selection in response. I don’t know if there’s a pool of heritable resistance to the virus in the population, so it’s possible we’re experiencing a field of bullets scenario, where nothing heritable is being selected for, but if there is a genotype that has an advantage here, natural selection would increase their frequency over time. Natural selection could make us more resistant as a species to SARS-CoV-2, and definitely wouldn’t be a destructive process.

Also, one of the features of the virus is the addition of short sequences, so SARS-CoV-2 may have had a slight increase in complexity over its predecessors.

Egnor is basically wrong about everything. Balance is restored to the universe.

Another perk for my Patreon patrons

For patrons only, I’m going to post the YouTube videos I’m doing for my courses during this period of isolation. Note that these are rough, I’m not doing any fancy editing at all, and abbreviated. I’m aiming too keep them under 15 minutes, and then they are supplemented by discussion sessions on Zoom…and by the textbook, of course.

I have to whip out a couple of these every week so when I say rough, I mean rough — they’re just recordings of Keynote presentations. Normally I’d hope to be interacting with students and handling questions and throwing out problems to solve, and these 10-15 minute summaries would expand out to an hour, but we gotta do what we gotta do during this pandemic.

Lawyers and self-importance go together like a slime & maggot sandwich

This New Yorker interview with “legal scholar Richard Epstein” is one of the most amazing exhibitions of arrogance I’ve read lately…and I’m living in the age of Donald Trump. Epstein earlier wrote an essay for his home base, the right-wing think tank the Hoover Institution, in which he predicted that the coronavirus pandemic was over-exaggerated, that it would peak with about 500 deaths and then fade away. His work was widely cited by conservatives, claiming that it showed that the cure was worse than the disease. His estimate was passed within a week, and the death toll is still rising. He’s wrong, definitively, and his prediction was quickly falsified. But he’s still defending it!

Most galling, his defense is that his prediction is supported by evolutionary theory. I know a little bit about evolution, so that was a startling claim. He’s a lawyer, not a biologist. He tries to explain his justification in this interview, and it turns out to be built on wishful thinking and faulty beliefs in how evolution works.

Here’s why he thinks the pandemic wouldn’t be as bad as the experts say.

But then adaptation starts to set in. And, in my view, adaptation is a co-evolutionary process in which things change, not only in human behavior but also change in genetic viral behavior.

OK, sure, humans are evolving, the virus is evolving, but how does that support the notion that the virus will kill 500 and not 100,000 people? There’s a leap there that emerges murkily.

…as the virus becomes more apparent, adaptive responses long before government gets involved become clear.

Wait, so his argument is that the virus will adapt to become relatively harmless before any public health work can take effect? I seem to recall that this viral adaptation to become weaker didn’t happen with, say, polio. He’s making assumptions about the rate of change.

Well, what happens is it’s an evolutionary tendency.

Also assumptions about a “tendency”. How does this work? He explains that. It’s jaw-droppingly stupid.

So the mechanism is you start with people, some of whom have a very strong version of the virus, and some of whom have a very weak version of the virus. If the strong-version-of-the-virus people are in contact with other people before they die, it will pass on. But, if it turns out that you slow the time of interaction down, either in an individual case or in the aggregate, these people are more likely to die before they could transfer the virus off to everybody else.

So his idea of why slow-the-spread works is not that it gives health services time to treat severe cases, it’s that he imagines there is this substantial variation in lethality of the virus, and that isolation allows people carrying strong strains to die, eliminating those variants, giving weak strains a selective edge. This ruthless Darwinian winnowing of viral strains will occur over the course of a few weeks.

He’s postulating a hyper-evolutionary acceleration; it’s very similar to the arguments of creationists who think all the vast amount of variation in species emerged from a few kinds preserved from the Flood 4000 years ago. Good evolutionary biology does not treat selection as a god-like force that instantly generates an optimal solution — we’re entirely aware of the limitations and how fast it can potentially work. We can use math. Epstein’s mechanism might work…over a few hundred thousand generations, which I suspect is even slower than our dilatory president’s response to the crisis.

And you’re not an epidemiologist, correct?

No, I’m trained in all of these things. I’ve done a lot of work in these particular areas. And one of the things that is most annoying about this debate is you see all sorts of people putting up expertise on these subjects, but they won’t let anybody question their particular judgment.

No, he’s not trained in those particular areas. He’s a lawyer. They work contrary to how scientists work. Lawyers start with the conclusion that they want to reach, and then select evidence that fits that conclusion.

That comment is particularly ironic because it applies spectacularly well to him. He’s claiming expertise he doesn’t have. You know, as I said, I actually do have some training in evolutionary biology, but I understand the limitations of what I know. I understand general principles and basic rules, but I also know that there are domains of specialization, like epidemiology, that I know very little about. I wouldn’t try to trump an epidemiologist’s detailed understanding of pandemics with my general knowledge of evolution of fish and spiders and cephalopods. Yet here’s Epstein, asserting that his legal training qualifies him to know better than epidemiologists.

I also wouldn’t declare that my knowledge of biology means I know better than Epstein how the law works.

What I’m doing here is nothing exotic. I’m taking standard Darwinian economics—standard economic-evolutionary theory out of Darwin—and applying it to this particular case.

There is actually a field of Darwinian economics. It’s mostly a bunch of economists who are smart enough to know that biologists have built up a lot of theory about how evolutionary biology works, and they’re trying to apply biological principles to economics. That’s not what Epstein is doing. He’s trying to jigger his fantasy Libertarian notions of economics to fit biology, and throwing a snit because biology is not obliging.

Oh yes, a snit. The following exchange is a stunning demonstration of how thin-skinned Richard Epstein is.

I was just asking about—

I’m saying what I think to be the truth. I mean, I just find it incredible—

I know, but these are scientific issues here.

You know nothing about the subject but are so confident that you’re going to say that I’m a crackpot.

No. Richard—

That’s what you’re saying, isn’t it? That’s what you’re saying?

I’m not saying anything of the sort.

Admit to it. You’re saying I’m a crackpot.

I’m not saying anything of the—

Well, what am I then? I’m an amateur? You’re the great scholar on this?

No, no. I’m not a great scholar on this.

Tell me what you think about the quality of the work!

O.K. I’m going to tell you. I think the fact that I am not a great scholar on this and I’m able to find these flaws or these holes in what you wrote is a sign that maybe you should’ve thought harder before writing it.

What it shows is that you are a complete intellectual amateur. Period.

O.K. Can I ask you one more question?

You just don’t know anything about anything. You’re a journalist. Would you like to compare your résumé to mine?

Wow. Like, wow. I’m speechless. A bit touchy, isn’t he?

Richard Epstein, you are an amateur and a crackpot, and also arrogant and ignorant. I hope this interview follows you for the rest of your days and demolishes your credibility in all scholarly things.

I may have made a small mistake

In my struggle to get my classes back on track as quickly as possible after spring break, I wanted to get everyone thinking and focused again, so…

  • In my intro class, I assigned a set of homework problems, due on 30 March.
  • In my intro class, I gave a take-home exam on Friday, due on 30 March.
  • In my genetics class, I assigned a set of homework problems, due on 30 March.
  • In my genetics class, I gave a take-home exam on Friday, due on 30 March.

They were supposed to send them to me by email.

Today, you may notice, is 30 March.

I opened my inbox this morning, and recoiled in horror. So many of my students were industrious and on the ball and possibly bored out of their minds, so they got everything done early. There are others who are still working on them, so I expect even more to trickle in during the course of the day.

The next exams are staggered a bit, at least, but I should have done that this time. The shock of the sudden isolation event just put everything in sync.

Where did SARS-CoV-2 come from?

I’ve been seeing some wild speculation that this pandemic is the product of genetic engineering — that it’s a biowarfare weapon that escaped from a lab somewhere. This is nonsense. I’ll refer you to an article in Nature Medicine, The proximal origin of SARS-CoV-2, which discusses a systematic analysis of the structure of SARS-CoV-2 in comparison to other coronaviruses.

It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted. Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone. Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer. We also discuss whether selection during passage could have given rise to SARS-CoV-2.

A little translation: the virus has a spike protein that binds to an enzyme on the surfaces of cells, called angiotensin converting enzyme, or ACE. This enzyme is important in regulating blood pressure, and is expressed by cells in lung capillaries (fun fact: your lungs play an endocrine role in sending out signals that maintain blood pressure). This is one reason the virus has such a dangerous respiratory effect — the lungs are the primary targets, where it can use the spike protein to bind to cells that express ACE and drill into them.

The RBD is the Receptor Binding Domain of the viral spike, and is the most variable part of the virus. This makes sense: the RBD is the key the virus uses to get access to your cells, and it varies because it confers target specificity. So there are all these different varieties of coronavirus, most of which don’t bother humans because they lack the human key — they are adapted to invade other animals’ cells. SARS-CoV-2 has acquired a spike with a human unlock code. Could some cunning super-villain have modified the spike?

Not likely, for several reasons. The virus has other similarities to coronaviruses in other animals; it’s not a de novo construct, but is a member of a large family of viruses. The modification to the spike protein is unusual. It works, but it’s not one that scientific experts would have used — they would have used something that would have been previously modeled. Then also bioengineers have lots of clever tools that could be used to stuff a desired sequence into a virus, but they all leave tool marks, little scraps of the molecule used to do the replacement. Those marks aren’t there. The best explanation is that we’re just seeing natural selection amplifying random variations in the spike.

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

Yeah, see, if I were a nefarious super-villain, we already have an even better RBD we could yank out of other viruses, and I would have used that to build a deadly virus. But instead, the SARS-CoV-2 RBD is some clunky variation that came out of nowhere, by accident, without any other signs of intentional manipulation.

They also consider the possibility that this was an accidental variation acquired in a lab — if you pass a virus through a lot of host cells in a cell culture system, it will continue to evolve, and you might imagine the RBD might acquire a random variation that allows it to thrive in those cells, and then it accidentally escapes the lab. This is also unlikely, because it shares a lot of similarities with the pangolin coronaviruses. It’s more likely to have arisen from an existing pool of related viruses in the wild, then either acquired its novel binding site there, or after infecting humans and experiencing selection for better binding to human cells.

The best strategy is to look for intermediates in animals, or in the sequences of humans who were infected early in the pandemic.

The identification of a potential intermediate host of SARS-CoV-2, as well as sequencing of the virus from very early cases, would similarly be highly informative. Irrespective of the exact mechanisms by which SARS-CoV-2 originated via natural selection, the ongoing surveillance of pneumonia in humans and other animals is clearly of utmost importance.

Sorry, conspiracy theorists. The best explanation is evolution and natural selection, not Evil Intelligent Design.

The viral spike protein. The RBD is in green.

Friday Cephalopod: Blinking lights! Wings! It’s an alien spacecraft!

I still dream about cephalopods, even if the arachnids are snaring most of my attention.