Assessing Ronald Fisher: should we take his name off everything because he espoused eugenics?

January 18, 2021 • 11:00 am

Many consider Ronald Fisher (1890-1962) one of the greatest biologists—and probably the greatest geneticist—of the 20th century, for he was a polymath who made hugely important contributions in many areas. He’s considered the father of modern statistics, developing methods like analysis of variance and chi-square tests still used widely in science and social science. His pathbreaking work on theoretical population genetics, embodied in the influential book The Genetical Theory of Natural Selection, included establishing that Mendelian genetics could explain the patterns of correlation among relatives for various traits, and helped bring about the reconciliation of genetics and natural history that constituted the “modern synthesis” of evolution. His theoretical work presaged the famous “neutral theory” of molecular evolution and established the efficacy of natural selection—the one part of Darwin’s theory that wasn’t widely accepted in the early 20th century.

Fisher also made advances important to medicine, like working out the genetics of Rh incompatibility, once an important cause of infant death. His statistical analyses are regularly used in modern medical studies, especially partitioning out the contributors to maladies and in analyzing control versus experimental groups (they were surely used in testing the efficacy of Covid vaccines).  As the authors of a new paper on Fisher say, “The widespread applications of Fisher’s statistical developments have undoubtedly contributed to the saving of many millions of lives and to improvements in the quality of life. Anyone who has done even a most elementary course in statistics will have come across many of the concepts and tests that Fisher pioneered.”

That is indeed the case, for statistical methods don’t go out of fashion very easily, especially when they’re correct!

Unfortunately, Fisher was also an exponent of eugenics, and for this he’s recently starting to get canceled. Various organizations, like the Society for the Study of Evolution and the American Statistical Association, have taken his name off awards, and Fisher’s old University of Cambridge college, Gonville and  Caius, removed their “Fisher window” (a stained glass window honoring Fisher’s statistical achievements) from their Hall last year.  Further disapprobation is in store as well.

This article in Heredity by a panoply of accomplished British statisticians and geneticists (Bodmer was one of Fisher’s last Ph.D. students) attempts an overall evaluation of Fisher’s work, balancing the positive benefits against his work and views on eugenics. If you are a biologist, or know something about Fisher, you’ll want to read it (click on the screenshot below, get the pdf here, and see the reference at the bottom.)

The authors make no attempt to gloss over Fisher’s distasteful and odious eugenics views, but do clarify what he favored. These included a form of positive eugenics, promoting the intermarriage of accomplished (high IQ) people, as well as negative eugenics: sterilization of the “feeble minded.” The latter was, however, always seen by Fisher as a voluntary measure, never forced. While one may ask how someone who is mentally deficient can give informed consent, Fisher favored “consent” of a parent or guardian (and concurrence of two physicians) before sterilization—if the patients themselves weren’t competent. But is that really “consent”? Negative eugenics on the population kind (not the selective abortion of fetuses carrying fatal disease, which people do every day) is something that’s seen today as immoral.

Further, Fisher’s views were based on his calculations that the lower classes outbred the higher ones, which, he thought, would lead to an inevitable evolutionary degeneration of society. But he was wrong: oddly, he didn’t do his sums right, as was pointed out much later by Carl Bajema. When you do them right, there’s no difference between the reproductive output of “higher” and “lower” classes.

Contrary to the statements of those who have canceled Fisher, though, he wasn’t a racist eugenist, although he did think that there were behavioral and intelligence differences between human groups, which is likely to be true on average but is a taboo topic—and irrelevant for reforming society. Fisher’s eugenics was largely based on intelligence and class, not race. Fisher was also clueless about the Nazis, though there is no evidence that he or his work contributed to the Nazi eugenics program.

In fact, none of Fisher’s recommendations or views were ever adopted by his own government, which repeatedly rejected his recommendations for positive and negative eugenics. Nor were they taken up in America, where they did practice negative eugenics, sterilizing people without their consent. But American eugenics was largely promoted by American scientists.

My go-to procedure for assessing whether someone should be “canceled”—having their statues removed or buildings renamed and so on—involves two criteria. First, was the honorific meant to honor admirable aspects of the person—the good he or she did? Statues of Confederate soldiers don’t pass even this first test. Second, did the good that a person accomplish outweigh the bad? If the answer to both questions is “yes”, then I don’t see the usefulness of trying to erase someone’s contributions.

On both counts, then, I don’t think it’s fair for scientific societies or Cambridge University to demote Fisher, cancel prizes named after him, and so on. He held views that were common in his time (and were adhered to by liberal geneticists like A. H. Sturtevant and H. J. Muller), and his views, now seen properly as bigoted and odious, were never translated into action.

Of course the spread of wokeness means that balanced assessments like this one are rare; usually just the idea that someone espoused eugenics is enough to get them canceled and their honors removed.  It saddens me, having already known about Fisher and his views, that what I considered my “own” professional society—the Society for the Study of Evolution—and a society of which I was President, is now marinated in wokeness, cancelling Fisher, hiring “diversity” experts to police the annual meeting at great cost, and making the ludicrous assertion—especially ludicrous for an evolution society—that sex in humans is not binary (read my post on this at the link). The SSE’s motivations are good; their execution is embarrassing. I am ashamed of my own intellectual home, and of the imminent name change for the Fisher Prize, for which the Society even apologized. Much of the following “explanation” is cant, especially the part about students being put off applying for the prize:

This award was originally named to highlight Fisher’s foundational contributions to evolutionary biology. However, we realize that we cannot, in recognizing and honoring these contributions, isolate them from his racist views and promotion of eugenics–which were relentless, harmful, and unsupported by scientific evidence. We further recognize and deeply regret that graduate students, who could have been recipients of this award, may have hesitated to apply given the connotations. For this, we are truly sorry.

His promotion of genetics was not relentless, wasn’t harmful (at least in being translated into eugenics, as opposed to being simply “offensive”), and of course scientific evidence shows that you could change almost every characteristic of humans by selective breeding (eugenics). But we don’t think that’s a moral thing to do. And yes, you can separate the good someone does from their reprehensible ideas. Martin Luther King was a serial adulterer and philanderer. Yet today we are celebrating his good legacy, which far outweighs his missteps.

But I digress. I’ll leave you with the assessment of a bunch of liberals who nevertheless use Fisher’s work every day: the authors of the new paper.

The Fisher Memorial Trust, of which the authors are trustees, exists because of Fisher’s foundational contributions to genetical and statistical research. It honours these and the man who made them. Recent criticism of R. A. Fisher concentrates, as we have extensively discussed, on very limited aspects of his work and focusses attention on some of his views, both in terms of science and advocacy. This is entirely appropriate, but in re-assessing his many contributions to society, it is important to consider all aspects, and to respond in a responsible way—we should not forget any negative aspects, but equally not allow the negatives to completely overshadow the substantial benefits to modern scientific research. To deny honour to an individual because they were not perfect, and more importantly were not perfect as assessed from the perspective of hindsight, must be problematic. As Bryan Stevenson (Stevenson 2014) said “Each of us is more than the worst thing we’ve ever done.”

In one of Fisher’s last papers celebrating the centenary of Darwin’s “The Origin of Species” and commenting on the early Mendelian geneticists’ refusal to accept the evidence for evolution by natural selection he said, “More attention to the History of Science is needed, as much by scientists as by historians, and especially by biologists, and this should mean a deliberate attempt to understand the thoughts of the great masters of the past, to see in what circumstances or intellectual milieu their ideas were formed, where they took the wrong turning track or stopped short of the right” (Fisher 1959). Here, then, there is a lesson for us. Rather than dishonouring Fisher for his eugenic ideas, which we believe do not outweigh his enormous contributions to science and through that to humanity, however much we might not now agree with them, it is surely more important to learn from the history of the development of ideas on race and eugenics, including Fisher’s own scientific work in this area, how we might be more effective in attacking the still widely prevalent racial biases in our society.

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Below: Ronald Alymer Fisher, in India in 1937 (as the authors note, Fisher was feted by a colleague for his “incalculable contribution to the research of literally hundreds of individuals, in the ideas, guidance, ans assistance he so generously gave, irrespective of nationality, colour, class, or creed.” Unless that’s an arrant lie, that should also go toward assessing what the man actually did rather than what he thought.

Fisher in the company of Professor Prasanta Chandra Mahalanobis and Mrs. Nirmalkumari Mahalanobis in India in 1940. Courtesy of the P.C. Mahalanobis Memorial Museum and Archives, Indian Statistical Institute, Kolkata, and Rare Books and Manuscripts, University of Adelaide Library.

h/t: Matthew Cobb for making me aware of the paper.

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Bodmer, W., R. A. Bailey, B. Charlesworth, A. Eyre-Walker, V. Farewell, A. Mead, and S. Senn. 2021. The outstanding scientist, R.A. Fisher: his views on eugenics and race. Heredity. https://doi.org/10.1038/s41437-020-00394-6

 

Shabby science reporting in the New York Times

January 10, 2021 • 11:00 am

I’ve noticed lately that the quality of science writing in newspapers has declined, even in The New York Times, which used to have some really good writing, especially by Carl Zimmer, who doesn’t seem to appear in its pages so often.

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CORRECTION:  Zimmer is still writing prolifically in the NYT, but covering a beat—vaccination—that I’d missed, (mis)leading me to believe that he was engaged in activities other than writing for the NYT. He’s asked me to correct this in a comment below, so I’ll just add his comment here:

If you had bothered to look at my author page at the Times, you’d see that I have been busier than ever there as I help cover the science of the pandemic. Over the past 10 months, I’ve written 93 stories about Covid-19, which comes to about two articles a week. Please correct your post. You are misleading your readers about my work. https://www.nytimes.com/by/carl-zimmer

I guess he was peeved. The misstatement was my fault, of course, and I’ve fixed it, but I have to say that this is a rather splenetic reply from someone whose work I’ve always praised.

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Rather, in place of long-form biology and physics, a variety of people now write for the Times‘s biological “Trilobite” column, and seem to take a more gee-whiz approach to science, producing short columns that are also short on information.

Part of the problem may be that many of these columns are written by freelancers who haven’t spent most of their writing career dealing with biology. My general impression is that the NYT is starting to reduce its coverage of science. That would be a damn shame since it was the only major paper to have a full science section (I don’t get the paper issues any longer, so I don’t know if they still have the Tuesday science section I’d read first).

The sloppy writing seems to be the case with this week’s column, a column reporting a new genome-sequencing study in Nature of monotremes: the platypus and the echidna (“spiny anteater”). I have only scanned the paper briefly, and will read it thoroughly, but on reading the NYT’s short summary I spotted two errors—not outright misstatements of fact, but statements that are incomplete descriptions of the truth, and where an extra word or two would have made the column not only more accurate, but more interesting.

Here’s the article (click on the screenshot):

 

Maybe I’m being petulant, but here are two quasi-misstatements in the piece. First, this one (emphases are mine):

When the British zoologist George Shaw first encountered a platypus specimen in 1799, he was so befuddled that he checked for stitches, thinking someone might be trying to trick him with a Frankencreature. It’s hard to blame him: What other animal has a rubbery bill, ankle spikes full of venom, luxurious fur that glows under black light and a tendency to lay eggs?

The facts: Only the males have ankle spurs, and of course only the males have venom. (This probably shows that the trait is used not for defense against predators, but for male-male competition during mating.) Females have no venom and have rudimentary spur nubs that drop off before maturing. Of course, females have the genes for producing ankle spurs and venom, as those genes don’t know which sex they’ll wind up in—just like human males have genes for vaginas and breasts and human females carry genes for penises. But the sex-development pathway prevents the expression of venom and spurs in females, just as it prevented me from developing a vagina.

The sex-limitation of the spurs isn’t mentioned in the Nature piece, but every biologist who knows their platypuses also knows that only the males have venom spurs. And, by the way, the echidna has some genes that used to produce venom, but they’re non-expressed “pseudogenes” that have become inactivated. That shows that the ancestral monotreme was almost certainly venomous (this isn’t mentioned in the NYT piece, either).

About those egg-yolk genes:

For instance, many birds and insects have multiple copies of a gene called vitellogenin, which is involved in the production of egg yolks.

Most mammals don’t have the vitellogenin gene, said Dr. Zhang. But the new genomes reveal that platypuses and echidnas have one copy of it, helping to explain their anomalous egg-laying — and suggesting that this gene (and perhaps the reproductive strategy itself) may have been something the rest of us lost, rather than an innovation of the monotremes. 

Well, yes, mammals do have the vitellogenin gene. In fact, our own species has three of them, but, as in other mammals they’re pseudogenes—genes that are there in the genome but are broken and not expressed. Humans and other placental mammals don’t require egg yolk because we’re nourished through the placenta, not yolks in shells. The platypus has two vitellogenin genes (described in the Nature paper as “genes”, so the statement that platypuses and echnidas have “one copy” is misleading)—they’re just not “functional” genes.

Now you may say this is quibbling, but it’s not. First of all, the statement that playtpuses have one copy of the egg yolk gene is wrong. They have two, but one doesn’t function. More important, the statement that there are nonfunctional yolk genes in all mammals says something powerful about evolution, something that I discuss in my book Why Evolution is True.  Those “vestigial” and nonfunctional genes are evolutionary remnants of our ancestors who did produce egg yolk. Why else would they be there in our genome, doing nothing? Chickens, who of course evolved from reptiles, as we did, have all three vitellogenin genes in working order.

Another error, then, is the statement “suggesting that this genes. . . may have been something the rest of us lost.” No, we didn’t lose it; it’s still there in our genomes. And there’s no “suggestion” about it: it’s sitting there in our DNA, has been sequenced, and has been shown to be nonfunctional. Finally, we KNOW that this gene is NOT an innovation of the monotremes, and have known that for a long time (e.g., see here). It was inherited from their reptilian ancestors.

This isn’t flat out erroneous science reporting, but it’s incomplete science reporting—the summary of a paper phoned in to the NYT. (I also find the Time’s summary curiously devoid of what’s really new in the paper; at least half of it reprises what we already knew.) More important, the reporter missed a good chance to give some powerful evidence for evolution, both in ourselves and in monotremes, whose genomes harbor some dead egg-yolk genes that are active in our avian and reptilian relatives. And yes, those echidnas have dead genes for venom.

h/t: Gregory

The mRNA coronavirus vaccine: a testament to human ingenuity and the power of science

December 27, 2020 • 9:45 am

The Pfizer and Moderna vaccines are a triumph of both technology and of drug testing and distribution. But to me, the most amazing thing about them is how they were designed. Unlike most vaccines, which are based on either weakened or killed viruses or bacteria, these use the naked genetic material itself—specifically, messenger RNA (mRNA). Viral mRNA serves normally to make more viruses using the host’s own protein-making machinery, and the virus’s genome codes for the most dangerous (and vulnerable) part of the virus: its spike protein. This is the protein that, sticking out all over the virus, recognizes and binds to the host cell—our cells. That allows the virus to inject its entire genome into our cells, commandeering our metabolic processes to make more viruses, which then burst out of the cell and start the cycle all over again.

The spike protein is the dangerous bit of the virus; without it, the virus is harmless. If we could somehow get our immune system to recognize the spike protein, it could then glom onto and destroy the viruses before they start reproducing in our cells. And that’s what the Pfizer and Moderna vaccines do.

The vaccine is in fact composed not of spike protein itself, but of artificially synthesized instructions for making the spike protein. Those instructions, coded in mRNA, are packed in lipid nanoparticles and injected into our arms.  The mRNA, engineered to evade our body’s many defenses against foreign genetic material, goes into our cells and instructs our own protein-synthesizing material to make many copies of the spike protein itself.  Since these copies aren’t attached to a virus, they aren’t dangerous, but they prime the immune system to destroy any later-attacking viruses by zeroing in on the spike proteins on the viral surface.

Thus the vaccine uses our own bodies in several ways: to make copies of just the spike protein, and then to provoke our immune system to recognize them, which the body “remembers” by storing the instructions to fabricate antibodies against real viral spike proteins.  The part of this story that amazes me is the years of molecular-genetic studies that went into our ability to design an injectable mRNA, studies that weren’t done to help make vaccines, but simply to understand how the genetic material makes proteins. In other words, pure research undergirded this whole enterprise.

You can read a longish but fascinating account of how the mRNA vaccine was made at the link below at science maven and engineer Bert Hubert’s website (click on the screenshot). Hubert doesn’t go into the details about packaging the engineered mRNA into lipid nanoparticles, which is a tale in itself, so there’s a lot more to learn. At the end, I’ll link to a story about how quickly this vaccine was made—less than a week to both sequence the virus’s RNA, including the spike protein, and then use that sequence to design a vaccine based on the spike protein.  What I’ll do here is try to condense Hubert’s narrative even more. 

Before China even admitted that the viral infection was dangerous and spreading, Yong-Zhen Zhang, a professor in Shanghai, had already sequenced its RNA (the genetic material of this virus is RNA, not DNA), and then deposited the sequence on a public website (a dangerous thing to do in China). The entire viral genome is about 29,000 bases long (four “bases”, G, A, C, and U, are the components of RNA), and makes 6-10 proteins, including the spike protein.

Within only two days after that sequence was published, researchers already knew which bit coded for the spike protein (this was known from previous work on coronaviruses) and then, tweaking that sequence, designed mRNA that could serve as the basis of a vaccine. Once you’ve designed a sequence, it’s child’s play these days to turn it into actual RNA.

The final mRNA used in the Pfizer vaccine is 4282 bases long (if you remember your biology, each three bases code for a single amino acid, and a string of amino acids is known as a protein). But the vaccine mRNA does a lot more than just code for a protein. Here are the first 500 bases of the Pfizer mRNA as given by Bert Hubert, and below you’ll see a diagram of the whole mRNA used in the vaccine:


If you remember your genetics, this sequence looks odd, for mRNA sequences usually contain the bases A, G, C, and U (uracil). Where are the Us? In this vaccine, the Us have been changed into a slightly different base denoted by Ψ (psi), which stands for 1-methyl-3′-pseudouridylyl. I’ll give the reason they did this in a second.

But what you see above is less than one-eighth of the whole mRNA used in the vaccine. I won’t give the whole sequence, as it’s not important here, but the structure of the mRNA is. Remember, this was engineered by people using previous knowledge and their brains, and then entering the sequence into a “DNA printer” that can fabricate DNA that itself can be turned into virus-like RNA. Isn’t that cool? Here’s a picture of the Codex DNA BioXp3200 DNA printer used to make the DNA corresponding to the vaccine’s RNA (photo from Hubert’s site):

And here’s the heart of this post: the structure of the 4282-nucleotide string of RNA that is the nuts and bolts of the vaccine (also from Hubert):

You can see that it’s complicated. The heart of this is the “S protein__mut”, which is the engineered code for the spike protein. But all that other stuff is needed to get that bit into the cell without it being destroyed by the body, get it to start making lots of spike protein to act as a stimulus (antigen) to our immune system, and to get the spike protein made quickly and copiously. The more innocuous spike protein we can get into our body, the greater the subsequent immune response when the virus attacks. Each bit of the mRNA shown in the diagram above has been engineered to optimize the vaccine. I’ll take it bit by bit:

Cap: Underlined in the diagram above, this is a two nucleotide sequence (GA) that tells the cell that the mRNA comes from the nucleus, where it’s normally made as a transcript from our DNA. These bases protect the engineered RNA from being attacked and destroyed by our body, as it makes it look like “normal” RNA.

Five prime (5′) untranslated region (“5′-UTR”) in the diagram.  This 51-base bit isn’t made into spike protein, but is essential in helping the mRNA attach to the small bodies called ribosomes where it is turned into proteins—three-base “codon” by three-base “codon”—with the help of smaller RNA molecules called “transfer RNAs” (tRNAs). Without the 5′-UTR, the protein won’t get made. Besides helping get the engineered mRNA to the ribosomes, this region has been further engineered. First, the Us have been engineered into Ψs, which keeps the immune system from attacking the mRNA without impairing its ability to attach to the ribosomes and make protein. And the sequence has been further tweaked to give it information for making a LOT of protein. To do this, the designers used sequence from our alpha-globin gene’s UTR, for that region makes a lot of protein. (Alpha globin is one half of our hemoglobin molecules, one of the most copious and quickly made proteins in the body.)

S glycoprotein signal peptide (“sig”) in the diagram. This 48-base bit, which does become part of the protein, is crucial in telling the cell where to send the protein after it’s made. In this case, it tells it to leave the cell via the “endoplasmic reticulum”, a network of small tubules that pervades the cell. Even this short bit was engineered by the vaccine designers, who changed 13 of the 48 bases. Why did they do this? Well, they changed the bases that don’t make a difference in the sequence of the protein (these are usually bases in the third position, whose nature isn’t important in protein sequence). But these bases do affect the speed at which a protein is made. Hubert doesn’t explain why this happens, but I suspect that the engineered changes were designed to fit with more common transfer-RNA molecules (tRNAs), which are the small bits of RNA that attach to amino acids in the cytoplasm and then carry them to the mRNA to be assembled into proteins. While there are 64 three-base sequences (4³), there are only 20 amino acids that normally go into proteins. That means that some tRNAs code for the same amino acids. Since these “redundant” tRNAs are not present in equal quantities in the cell, you can make proteins faster if you design an mRNA sequence that matches with the most common tRNAs. I’m guessing that this is what these 13 changes were about.

Spike protein (“S protein__mut”) in the diagram. This is the heart of the mRNA, containing 3777 bases that code for the spike protein. In this code, too, they’ve “optimized” it by changing the “redundant” bases to allow protein to be made faster. The Ψs are now gone, as they’re not needed to evade the body’s defenses.  But there’s one bit that puzzled me until I read Hubert’s explanation. The spike protein made by the body after vaccination differs from the viral spike protein in just two of the 1259 amino acids. The engineered sequence substitutes two amino acids—both prolines—for amino acids in the viral spikes. Why? Because it was known from previous work that these prolines stabilize the spike protein, keeping it from folding up. It thus retains the same shape it has in the native virus. A folded-up spike protein may induce antibodies, but they won’t readily go after the virus’s own spike proteins because their shape is different.  This is just one of the many bits of prior knowledge that came to bear on the vaccine’s design.

The 3′ untranslated region (“3′-UTR”) in the diagram: mRNA’s have these, but we’re not quite sure what they do, except, as Hubert says, the region is “very successful at promoting protein expression.” How this happens is as yet unclear. This bit, too, was engineered by the vaccine designers to make the mRNA more stable and boost protein expression.

The poly-A tail (“poly[A]” in the diagram). This is the 140-base end of the message. All mRNAs made into proteins contain a repeat of the adenine base at the butt (3′) end, so we get an AAAAAAAAAAAAA. . . sequence. It turns out that these A’s are used up when an mRNA molecule makes protein over and over again (they’re like telomeres that get shorter as we age!). When all the As are gone, the mRNA is useless and falls off the ribosomes. Again, previous knowledge told the designers how many As to put at the end of the sequence.  It was known that around 120 As gave the best result in terms of protein production; the designers used 100 As split up with a 10-base “linker” sequence. Hubert doesn’t explain the linker, and I don’t know why it’s there.

Nevertheless, you can see the complexity of this vaccine, whose design rests on an exact knowledge of the spike protein’s sequence (recent mutations in the sequence don’t seem to affect the efficacy of the vaccine, as they probably don’t affect the spike’s shape), as well as on previous research about stuff like the Ψ bases helping evade mRNA destruction, the optimum sequences for high production of protein, the number of As at the end that are most efficacious, and then those two proline substitutions in the vaccine’s spike protein. It’s all marvelous, a combination of new and old, and a testament to the value of pure research, which sometimes comes in mighty handy.

This prior knowledge, combined with fast sequencing of RNA and the development of machines to turn code into RNA, help explain why the vaccine was designed so quickly. Of course it had to be tested and distributed as well, and this Guardian article tells you ten additional reasons why it took only ten months to go from the onset of the pandemic to a usable vaccine.

Finally, a bit of history of science is recounted by “zeynep” at Substack, showing additional reasons why the vaccine came out so quickly (click on screenshot). It’s largely about Yong-Zhen Zhang, the Chinese scientist who published the genetic code of the Covid-19 virus. Zeynep sees him as a hero who took risks with that publication. What’s clear is that without that code (and of course sequencing of DNA and RNA has been done for a long time—another benefit of pure research), we wouldn’t be near as far along as we are in battling the pandemic.

When you think about all this, and realize that only one species has both the brains and the means to make a designer vaccine to battle a devastating virus, and then think about the many scientists whose work contributed over many years to the knowledge involved in designing these vaccines, it should make you proud of humanity—and of the human enterprise of science. Yeah, we screw up all the time, and are xenophobic and selfish, but this time we overcame all that and used the best in us to help all of us.

Thanks to Bert Hubert for helping me understand the complexity of these vaccines.

Why we shouldn’t be worried (yet) about the new strain of Covid-19

December 23, 2020 • 10:30 am

Reader Jim Batterson sent me this 25-minute video with the comment:

I know you prefer to read rather than watch a video, but I wanted to make you aware of a 24-minute YouTube video from Vince Racaniello, a virologist at Columbia University who leads a cast of virology geezers and one younger immunologist in a weekly zoomcast production of “This Week in Virology”.  He did this standalone presentation to rant a bit on the way that this latest variant in the UK is being hyped to the world. I think he does a pretty good job for any viewer who has had a biology course in the past five or so years.
The point is that viruses are mutating constantly, and yet none the coronavirus mutations have yielded a new “strain”—that is, a mutant type that has new biological properties. The property touted for the new virus is its purportedly increased “spreadability”, but, as Racaniello notes repeatedly, that simply hasn’t been demonstrated. As he shows, you can get some variants spreading more widely than others simply by accident: the variant may not have any effect on spreadability itself but can increase in frequency as a byproduct of “superspreader events”—the main way the virus spreads—because only a small subset of all viruses get passed to other humans.

Racaniello then shows the changes in the new mutant “strain”, noting that only one of the several mutants in the spike protein is even a candidate for a change in spreadability, but there is not an iota of evidence that any of those mutations actually make the strain more spreadable.  Nevertheless, all of us are inundated with media scare stories about this “superspreader virus”.

Racaniello’s point is that though there are epidemiological data showing a correlation between the presence of the mutant in some areas and a greater spread of the virus, that’s just  a correlation without evidence of causation. And there could be several causes, including accidents. To show this mutant is a “super virus”, you simply have to do lab experiments; epidemiological correlations show nothing.

Racaniello doesn’t rule out that this mutant spreads faster than its ancestors, but he’s not convinced it is, and doesn’t think that we yet have a reason to be concerned. In fact, he suggests that the changes in the new strain may make it less spreadable. Let me add that Racaniello knows what he’s talking about, as he’s co-author on a well known textbook of virology.

Like all good scientists, Racaniello isn’t declaring that this virus is “neutral” compared to its competitors—he’s simply saying that we don’t have any data suggesting it’s more nefarious. In fact, the same story happened earlier with a different mutant that spread widely, but nothing ever came of that.  We need experimental cell-culture data from the lab on viral shedding, and that doesn’t exist.

His final comment:

“We should move on from the scary headlines, and get ahead with vaccination programs, which are underway—and that is going to be the way we get away from this pandemic.”

Anyway, this is a good and clear mini-lecture, and listening to it should calm you down a bit if the media have gotten you worried.

Fruit Fly Central: the Bloomington Drosophila Stock Center

December 16, 2020 • 11:15 am

Imagine my surprise when several readers sent me a longish article from the New York Times about the Bloomington Drosophila Stock Center at Indiana University (click on the screenshot below). For, when I worked with flies for over four decades, I used their services—and their fly stocks—constantly. Much of my work would have been impossible without the strains they provided, which involve various kinds of mutations, chromosomal aberrations, genetically engineered strains, and so on. Moreover, as the article notes, Drosophila is the best animal model we have for genetics. It’s been useful not just in pure research, but in applied work. As the NYT notes:

Studying these slight mutants can reveal how those genes function — including in humans, because we share over half of our genes with Drosophila. For instance, researchers discovered what is now called the hippo gene — which helps regulate organ size in both fruit flies and vertebrates — after flies with a defect in it grew up to be unusually large and wrinkly. Further work with the gene has indicated that such defects may contribute to the unchecked cell growth that leads to cancer in people.

Other work with the flies has shed light on diseases from Alzheimer’s to Zika, taught scientists about decision-making and circadian rhythms and helped researchers using them to win six Nobel Prizes. Over a century of tweaking fruit flies and cataloging the results has made Drosophila the most well-characterized animal model we have.

And so I’m glad the Center finally got some recognition, which is well deserved. These people have labored diligently—not just accumulating strains of flies, which now number 77,000 (!), but sending them out to workers throughout the world and—the most labor—making the food that fills the fly vials to keep the strains alive, and changing each stock (kept in replicates to preserve them) every couple of weeks. You can’t freeze Drosophila to preserve them alive like you can bacteria, and so keeping the cultures going requires constant attention. I had hundreds of strains in my own lab, and spent many hours a week just changing exhausted vials into fresh vials. (The article calls this “flipping flies”; we called it “changing flies.)

So my kudos to the center, which kept going—as it had to, if Drosophila genetics were to survive—during the pandemic. The Center’s work during the pandemic is a large part of the NYT story.

Now though there are several thousand of Drosophila species in the wild, only one—Drosophila melanogaster—is kept in Bloomington, for that’s the species that fortuitously was developed by Thomas Hunt Morgan, my academic great grandfather, when he began Drosophila work at the beginning of the 20th century. And that’s the species used as the animal model today. Here are all the various kinds of stocks you can order:

That’s a lot bigger list than existed when I got into the game: we had no genome editing stocks, fluorescent proteins, or binary expression systems. We had mostly chromosomal aberrations, deficiencies and duplications of genes or chromosome segments, and, of course, the classical single-gene mutations. Here are some single-gene mutants (from Wikipedia). “Normal” or “wild-type” flies, as you catch them in the wild, look like the one in the middle at the top, but with brick-red eyes (see second photo below).

D. melanogaster multiple mutants (clockwise from top): brown eyes and black cuticle (2 mutations), cinnabar eyes and wildtype cuticle (1 mutation), sepia eyes and ebony cuticle, vermilion eyes and yellow cuticle, white eyes and yellow cuticle, wildtype eyes and yellow cuticle.

A “wild type” fly from the NYT article (photo by Bob Gibbons):

I’ve used all of these mutations at different times, often to see if they were identical to similar-appearing mutations that I found in close relatives that could cross with D. melanogaster and produce offspring. (For example, if I found a “sepia”-like eye color in the sister species D. simulans, I’d cross it to known D. melanogaster sepia; if the offspring all had brown eyes, it was the same mutation. This is known as a “complementation test.”)

Here are a few more photos from the article (captions from the NYT). Some of the 77,000 stocks, kept immaculately:

Thousands of fruit fly stocks at the stock center.Credit…Kaiti Sullivan for The New York Times

Changing flies! Every experimental drosophilist spends much of their life doing this:

Stockkeeper Micaela Silvestre-Razo flipped flies in a spare room of the stock center. Credit: Kaiti Sullivan for The New York Times

Here’s a historic stock: white-one, a white-eye mutant discovered by Thomas Hunt Morgan in 1910. Morgan found that when you crossed white-eyed females to “wild type” males, all the male offspring were white and all the female offspring had normal red eyes. In contrast, if you crossed white-eyed males to wild-type females, you found that all the offspring were red-eyed, but the female offspring from that cross produced half white-eyed males and half-red-eyed males. This weird pattern comes because white is a recessive gene on the X chromosome: it’s “sex-linked”—like red-green color blindness or hemophilia in humans.

You can read about Morgan’s study of white here, and see his 1910 paper here. (He won the Nobel Prize in 1933 for his work on classical genetics, but split the money with his “boys”—his extremely talented group of researchers who occupied the “fly room” at Columbia University.)

The white-one stock below has just been put into fresh vials of medium, which is made with water, soy meal, cornmeal, yeast, and a usually a preservative. Within 10-12 days at 25°C, you will get a new generation of adults, as the eggs are laid on the food, the larvae (“maggots”) hatch and burrow into the food (also eating it), and then crawl onto the sides of the vials to spend 4-5 days as pupae (the fly equivalent of a cocoon) before hatching (“eclosing”) into new adults. After about two generations the food is used up and you have to “flip” the vial.

The vial on the right doesn’t seem to have been cleaned very well, as there are old, empty pupal cases still adhering to the walls, which would be washed off during a proper cleaning.

Here are old, grotty, spent vials (the header of the NYT article).

Here’s the original “fly room” at Columbia where the Nobel-Prize-winning work was done. Six or seven researchers crammed into this space, and food (at that time made with bananas) was also prepared here. Only Morgan himself, as the boss, was allowed to eat one of the bananas. You can see a microscope for examining flies in the foreground, and the milk bottles full of fly food on the table:

Here’s Calvin Bridges in the Columbia Fly Room. Bridges, a wickedly handsome man with a colorful and rogue-ish life, was a fantastic researcher and made many contributions to modern genetics:

This book will give you more information about the early history of Drosophila genetics and how it influenced today’s “Drosophila culture”:

Now a lot of my fly work was done with species other than D. melanogaster, though they were close relatives. That’s because I worked on speciation, and to do the genetics of speciation (i.e., finding out which genes and how many of them change during the split of an ancestor into two or more descendant species), you need several species, ideally ones that can be crossed. Since the Bloomington Center contained only D. melanogaster, I got my other species by collecting them myself, getting them from colleagues who collected them, or ordering them from the National Drosophila Species Stock Center, then at Bowling Green State University in Ohio but now at Cornell University.

I see that the NDSSC still keeps some of the mutant cultures I found in the relatives of D. melanogaster, but, sadly, most of them have been lost, since they used to concentrate only on wild-type flies of different species and didn’t want to take the mutations I had laboriously found and identified. But, like the Bloomington Center, they were a huge help to me when I worked on speciation, and I want to thank them as well.

I could go on and on and on about the Centers and their value and their stocks, but I’d best stop here because it’s lunchtime. I’ll just add that I once combined a mutant called groucho (which had extra bristles over its eyes) with proboscipedia (a fly whose mouthparts transform into leglike structures) to get a Groucho Marx fly with bushy eyebrows that looked as if it were smoking a cigar.

One-off: a melanistic emperor penguin! (+ leucistic lagniappe)

November 23, 2020 • 1:30 pm

Well, I’ll be! IFL Science highlighted the presence in Antarctica of the only melanistic penguin I’ve ever heard of. We’ve all seen or heard of melanistic squirrels and jaguars or leopards (both called “black panthers”); it’s a genetic trait and can be either dominant (one gene copy and you’re black) or recessive (two copies required). But penguins?

For a panoply of melanistic species, go here, and click on the screenshot to read the article:

The one-minute BBC video is below, and though I worried this penguin may be subject to predation or lack of potential mates, the IFL Science article (and the video) says it’s doing fine:

Adult emperors have black heads and wings, gray backs, and white bellies, with their distinctive yellow-orange markings around the neck. This particular penguin spotted when the Dynasties team were filming the Emperor episode in Antarctica, is almost entirely black, but does have the odd patch of white on its chest and wing tips, and a splash of yellow around its neck.

Sometimes, sadly, it’s not good to stand out in a crowd, though. The mutation can make animals with melanism more easy to spot by predators. In this penguin’s case, not just because it may be more visible on the ice, but because penguins’ white bellies make them look invisible to predators swimming below by helping them blend in with the light from the surface.

Though, as the BBC points out, this one isn’t doing too badly, having survived into adulthood.

In fact, according to the BBC the penguin is doing just fine. Filmed amongst hundreds of its besuited brethren and looking healthy, it appeared to show signs of looking for a mate while huddling for warmth with the other penguins.

It looks lonely to me, but maybe I’m just anthropomorphizing.

UPDATE: Reader Bill Turner sent this photo, taken by his wife Yvette, and added the caption,

“Your post today on a melanistic Emperor penguin prompted me to send the attached photos of a leucistic gentoo, taken at the Chilean Captain Arturo Prat Base on Greenwich Island on 24 December 2018. The bird was, apparently, quite a familiar sight around the island.”

I hope this white bird found a mate, too.

h/t: Nicole

Matthew talks about Rosalind Franklin tomorrow

October 15, 2020 • 8:30 am

Mark your calendar for tomorrow: Matthew Cobb, sponsored by the groups indicated below, will be talking about the scientific contributions of Rosalind Franklin, and will, I’m sure, dispel many misconceptions that have accreted around her life. He’s kicking off a series of talks on women in science.

This talk will be virtual, but you have to register in advance to see it (it’s free), and then test your connection, as there are two ways to connect. (The site walks you through it.) Registration is here, or you can click on the screenshot below. And. . . you can even ask questions.

Note that it’s at 11 a.m. Eastern time or 5 p.m. Central European Time.

Here’s Matthew’s own summary:
It’s a 40 minute talk (already recorded), followed by live Q&A that might go on for some time. It’s about Franklin’s life, not simply the DNA years. It puts particular emphasis on her post-DNA work on viruses, and casts a rather different light on people’s impressions of what the double helix meant at the time. It doesn’t go into her love life nor do I call her ‘Rosalind’. She is ‘Franklin’ throughout. It was fascinating working on this and helped clarify my views of her – which are even more positive than they were before I began. Includes lots of photos, extracts from her letters to Watson, etc etc.
And here’s the official blurb for the talk:
If you’ve registered, you can go here and click on the “Already registered? Click here” button, or click on the screenshot below. Note on the webinar page there’s a button for asking questions. Put Matthew in the hot seat!

Gynandromorph Rose-breasted Grosbeak

October 9, 2020 • 9:00 am

Just for the record, and from WESA Pittsburgh, we have a gynandromorph Rose-breasted Grosbeak  (Pheucticus ludovicianus): a bird that’s part male and part female. In this case the bird appears to be largely, but not completely, divided down the middle, similar to the gynandromorph Northern cardinal I wrote about in 2012.

A rare bird has been found at Powdermill Nature Reserve in Westmoreland County.

The newly banded Rose-breasted Grosbeak is a gynandromorph, meaning that it is part male and part female. This particular Grosbeak is male on the right side and female on the left, making it a bilateral gynandromorph.

Researchers at the Carnegie Museum of Natural History said less than 10 bilateral gynandromorph birds have been documented in the reserve’s 64-year bird banding history. The reserve’s only other documented Rose-breasted Grosbeak bilateral gynandromorph was banded in 2005.

Annie Lindsay, Powdermill’s bird banding program manager, said finding the gynandromorph is a “once-in-a-lifetime experience.”

“One [of the banding team members] described it as ‘seeing a unicorn’ and another described the adrenaline rush of seeing something so remarkable. They all are incredibly grateful to be part of such a noteworthy and interesting banding record,” said Lindsay in a press release.

The fact the bird is a gynandromorph is discernible [sic] to the naked eye as it has physical traits of both male and female Grosbeaks. On the right, male side of its body, it has ruby wing pits and a ruby breast spot, along with black wing feathers. On the left it has yellow wing pits and a brownish, speckled wing.

At first, the color appears split down the middle insofar as the “wingpits” and breast color are concerned (see photos below of normal male and female), but the head of the bird shows no black on the male side, which it should if this was a truly “split” gynandromorph like the cardinal. Even young males have darker heads, but this bird has a full female head. Ergo, it appears to be a “more-than-half female” grosbeak.  Researchers are waiting to see if it acts like a female or male; that is, can it produce eggs? Will it sing a male song? My prediction is that if the head is female, the chances are higher that the brain is female, and it will act like a female—if it can find a mate.

This Rose-breasted Grosbeak gynandromorph bird possesses both male and female physical traits, including different colored wing pits. Male Grosbeak have reddish pits, while females have yellow. ANNIE LINDSAY / CARNEGIE MUSEUM OF NATURAL HISTORY

Normal male:

Normal female:

How do these part-male/part-female birds form? I discuss possibilities on the gynandromorph cardinal post, and, in the comments, readers suggest some other possibilities, but we don’t know for sure.  It could involve chromosome loss, a non-genetic developmental accident, fertilization by “unreduced” sperm, and so on. Looking at the chromosomes on the male versus female parts of the bird might give a hint.

h/t: Bruce Lyon

Doudna and Charpentier win Chemistry Nobel for CRISPR/Cas9 method of gene editing

October 7, 2020 • 6:15 am

This year’s Nobel Prize in Chemistry was long anticipated, for the CRISPR/Cas9 system of gene editing was a tremendous accomplishment in biology and chemistry. It promises a lot, including curing human genetic disease (see the first five posts here). Remember, Nobel Prizes in science are designed to reward those who made discoveries potentially helping humanity, not those who just made general scientific advances.

A prize for developing the editing system was, then, almost inevitable. The only question was “who would get it?”, since several people contributed to the work that led to CRISPR/Cas9.  It turns out that the Prize—in Chemistry—went to the two frontrunners, Jennifer Doudna of UC Berkeley and Emmanuelle Charpentier at the Max Planck Institute for Infection Biology in Berlin.  Other serious contenders were George Church of Harvard, Virginijus Šikšnys at the Vilnius University of Biotechnology, Francisco Mojica of the University of Alicante, and Feng Zhang of the Broad Institute (the dispute was largely over whether those who developed ways to use the method in human cells also deserved the Prize). There will be a lot of kvetching today, but if I had had to pick two to get the prize, given that only three can get it au maximum, it would be Doudna and Charpentier. (They could have awarded up to six prizes if they’d split the CRISPR award between Physiology or Medicine and Chemistry.)

The press release from the Nobel Foundation says this:

Genetic scissors: a tool for rewriting the code of life

Emmanuelle Charpentier and Jennifer A. Doudna have discovered one of gene technology’s sharpest tools: the CRISPR/Cas9 genetic scissors. Using these, researchers can change the DNA of animals, plants and microorganisms with extremely high precision. This technology has had a revolutionary impact on the life sciences, is contributing to new cancer therapies and may make the dream of curing inherited diseases come true.

Researchers need to modify genes in cells if they are to find out about life’s inner workings. This used to be time-consuming, difficult and sometimes impossible work. Using the CRISPR/Cas9 genetic scissors, it is now possible to change the code of life over the course of a few weeks.

“There is enormous power in this genetic tool, which affects us all. It has not only revolutionised basic science, but also resulted in innovative crops and will lead to ground-breaking new medical treatments,” says Claes Gustafsson, chair of the Nobel Committee for Chemistry.

As so often in science, the discovery of these genetic scissors was unexpected. During Emmanuelle Charpentier’s studies of Streptococcus pyogenes, one of the bacteria that cause the most harm to humanity, she discovered a previously unknown molecule, tracrRNA. Her work showed that tracrRNA is part of bacteria’s ancient immune system, CRISPR/Cas, that disarms viruses by cleaving their DNA.

Charpentier published her discovery in 2011. The same year, she initiated a collaboration with Jennifer Doudna, an experienced biochemist with vast knowledge of RNA. Together, they succeeded in recreating the bacteria’s genetic scissors in a test tube and simplifying the scissors’ molecular components so they were easier to use.

In an epoch-making experiment, they then reprogrammed the genetic scissors. In their natural form, the scissors recognise DNA from viruses, but Charpentier and Doudna proved that they could be controlled so that they can cut any DNA molecule at a predetermined site. Where the DNA is cut it is then easy to rewrite the code of life.

Since Charpentier and Doudna discovered the CRISPR/Cas9 genetic scissors in 2012 their use has exploded. This tool has contributed to many important discoveries in basic research, and plant researchers have been able to develop crops that withstand mould, pests and drought. In medicine, clinical trials of new cancer therapies are underway, and the dream of being able to cure inherited diseases is about to come true. These genetic scissors have taken the life sciences into a new epoch and, in many ways, are bringing the greatest benefit to humankind.

I haven’t looked it up, but I think this is the first time that two women have been the sole recipients of any Nobel prize.(Correction: I should have said “Prize for Science”, for, as a reader pointed out below, two women shared the 1976 Nobel Peace Prize: Betty Williams and Mairead Corrigan. Their achievement was organizing to suppress sectarian violence during the Troubles in Northern Ireland.

Here are Doudna and Charpentier from the Washington Post (the paper’s caption):

FILED – 14 March 2016, Hessen, Frankfurt/Main: The American biochemist Jennifer A. Doudna (l) and the French microbiologist Emmanuelle Charpentier, then winners of the Paul Ehrlich and Ludwig Darmstaedter Prize 2016, are together in the casino of Goethe University. The two scientists were awarded the Nobel Prize for Chemistry 2020. Photo: picture alliance / dpa (Photo by Alexander Heinl/picture alliance via Getty Images)

Here’s the live stream of the announcement from Stockholm. The action begins at 11:45 with the announcement in English and Swedish, and the scientific explanation starts at 19:10.

Once again, although seven people, including Matthew, guessed the winners in our Nobel Prize contest (here and here), nobody got the Chemistry or Physics prizes. Given your miserable failures, I may have to have contest for the literature prize alone.

Matthew was also prescient in his book, Life’s Greatest Secret (2015), which includes this sentence:

“Whatever happens next, I bet that Doudna and Charpentier—and maybe Zhang and Church—will get that phone call from Stockholm.”

In 2017, I reviewed (favorably) Jennifer Doudna’s new book on CRISPRA Crack in Creation, for the Washington Post. (Samuel Sternberg was the book’s co-author). The book is well worth reading, but I did have one beef connected not with the narrative, but with where the dosh goes for this discovery. Here’s what I wrote then:

. . . this brings us to an issue conspicuously missing from the book. Much of the research on CRISPR, including Doudna’s and Zhang’s, was funded by the federal government — by American taxpayers. Yet both scientists have started biotechnology companies that have the potential to make them and their universities fabulously wealthy from licensing CRISPR for use in medicine and beyond. So if we value ethics, transparency and the democratization of CRISPR technology, as do Doudna and Sternberg, let us also consider the ethics of scientists enriching themselves on the taxpayer’s dime. The fight over patents and credit impedes the free exchange among scientists that promotes progress, and companies created from taxpayer-funded research make us pay twice to use their products.

. . . . Finally, let us remember that it was not so long ago that university scientists refused to enrich themselves in this way, freely giving discoveries such as X-rays, the polio vaccine and the Internet to the public. The satisfaction of scientific curiosity should be its primary reward.

I’m not sure how the legal battle between the participants (via Berkeley and MIT) has shaken out, and can’t be arsed to look it up, but surely a reader or two will know

The intellectual vacuity of New Scientist’s evolution issue: 4. The supposed importance of genetic drift in evolution

September 29, 2020 • 10:45 am

Genetic drift is the random change in frequencies of alleles (forms of a gene, like the A, B, and O alleles of the Landsteiner blood-group gene) due to random assortment of genes during meiosis and the fact that populations are limited in size. It is one of only a handful of evolutionary “forces” that can cause evolution—if you conceive of “evolution,” as many of us do, as “changes in allele frequencies over time” (“allele frequencies” are sometimes called “gene frequencies”). Other forces that can cause evolutionary change are natural selection and meiotic drive.

Genetic drift certainly operates in populations, for it must given that populations are finite and alleles assort randomly when sperm (or pollen) and eggs are formed. The question that evolutionists have been most concerned with is this: “How important is genetic drift in evolution?”  We know that, if populations are sufficiently small, for instance, drift can actually counteract natural selection, leading to high frequencies of maladaptive genes. This is what has happened in small human isolates, such as religious communities like the Amish and Dunkers.  It’s not clear, though, that this has happened with any appreciable frequency in other species.

Drift was once implicated by Sewall Wright, a famous evolutionist, in his well-known “shifting balance theory of evolution“, which maintained that drift was essential in producing many adaptations in nature. That theory was once influential, but has now fallen out of favor, and I take credit for some of that (see my collaborative critiques here and here).

Related to this are various theories that see genetic drift and its maladaptive effects as crucial in forming new species (e.g., the “founder-flush” theory of speciation). In my book with Allen Orr, Speciation, we analyze these ideas in chapter 11 and conclude that drift has been of minimal importance in speciation compared to natural selection.

Finally, genetic drift was an important part of Steve Gould’s theory of punctuated equilibrium, for it was the force that allowed isolated populations to undergo random phenotypic change, tumbling them from one face of “Galton’s polyhedron” to another. This was one of the explanations for why change in the fossil record was jerky. Well, the fossil record may well be punctuated, but Gould’s theoretical explanation was pretty soundly dismantled by population geneticists, including several of my Chicago colleagues (see this important critique).

While one can cite examples of genetic drift operating in nature, like the expected loss of genetic variation in very small populations, in my view it hasn’t been of much importance in speciation, morphological and physiological evolution, or in facilitating adaptive evolution by pushing populations through “adaptive valleys.” Even the view that it has made species vulnerable to extinction by reducing the pool of genetic variation needed to adapt to environmental change has been exaggerated. I know of no extinctions caused by genetic drift, though I haven’t checked on the cheetah example lately (they were said to be highly inbred because of small populations, but I’m not sure that this is what makes them vulnerable to extinction). In fact, for conservation purposes, I believe the importance of loss of genetic variation through drift has been much less than the importance of reduced population size itself that makes populations vulnerable to extinction because individuals can’t find mates or overgraze their environment, or simply because if you’re a small population, random fluctuations in numbers are more likely to make you go extinct. This is demographic rather than genetically based extinction.

But drift has been important in molecular evolution, causing a turnover of gene variants over long periods of time. If those variants are “neutral”—that is, they are equivalent in their response to natural selection—then they will turn over at a roughly linear rate with time, and the changes can be used as a sort of “molecular clock” to estimate divergence times between species. This kind of molecular divergence has been used to construct family trees of species as well as to estimate the times when species diverged. This is a fairly new usage, for such molecular tools and estimates have been available only since the 1960s.

On to the New Scientist bit about drift in its latest issue, a special on evolution.

The 13-point section about how new findings will expand our understanding of evolution includes section 9 about drift, called “Survival of the luckiest.” It first recounts, accurately, how drift operates, but then exaggerates its importance by mentioning two studies of urban populations of animals, populations that in principle should show more drift than wild populations because populations living in cities are small and fragmented. The section says nothing about any of the things I just told you, which is what evolutionists have really been concerned about with respect to genetic drift.

Here’s the entirety of how New Scientist says drift is revising our view of evolution (the author of this section is Colin Barass):

Biologists have known about genetic drift for a century, but in recent years they realised that it could be especially common in urban settings where roads and buildings tend to isolate organisms into small populations. A 2016 study of the white-footed mouse, Peromyscus leucopus, in New York supported the idea. Jason Munshi-South at Fordham University, New York, and his colleagues discovered that urban populations have lost as much as half of their genetic diversity compared with rural populations.

Last year, Lindsay Miles at the University of Toronto Mississauga, Canada, and her colleagues published a review of evidence from about 160 studies of evolution in urban environments, in organisms ranging from mammals and birds to insects and plants. Almost two-thirds of the studies reported reduced genetic diversity compared with rural counterparts, leading the researchers to conclude that genetic drift must have played a role. “Genetic drift can definitely be a significant driver of evolution,” says Miles.

These findings have big implications, because populations lose their ability to adapt and thrive if they lack genetic diversity for natural selection to work on. Of course, genetic drift isn’t confined to urban settings, but given how much urbanisation is expected to grow, the extra threat it poses to wildlife is concerning. It highlights the need to create green corridors so that animals and plants don’t become isolated into ever-smaller populations.

I don’t think those findings do have “big implications”, because the important of reduced genetic variation in urban environments is unclear, particularly when the genes assayed have no clear connection with natural selection. And the import of losing half of your genetic diversity is also questionable: after all, a single fertilize female contains half of the “heritability” of an entire population. Everything rests on whether evolution by natural selection depends on very low-frequency genetic variants, present only in big populations, and we don’t really know if this is the case.  And the above study is in white-footed mice, only one species among millions, and only for populations in urban environments. That’s not to denigrate it, just to point out that its relevance to nonurban nature is unclear and its relevance to evolution is equally unclear.

You can read the Miles et al. study at the link (here), and having read it, I wasn’t impressed, since the authors themselves don’t come to nearly as strong a conclusion as does New Scientist. Here’s from the paper’s conclusions:

Although our review of the literature with quantitative analyses of published urban population genetic data sets demonstrates trends towards increased genetic drift and reduced gene flow, these patterns were not significant and were not universally seen across taxa. In fact, over a third of published studies show no negative effects of urbanization on genetic diversity and differentiation, including studies supporting urban facilitation models at a much higher proportion than previously realized. How populations and species respond to urbanization clearly depends on the natural history of the taxa investigated, the number and location of cities being sampled, and the molecular techniques used to characterize population genetic structure.

In other words, although two-thirds of the studies showed reduced variation or increased inter-population differentiation, these patterns were not significantly different from non-urban populations.  And if those differences were not significant, you needn’t start speculating about genetic drift. The authors conclude simply that different species show different genetic patterns when living in urban environments.

Miles’s statement that “genetic drift can definitely be a significant driver of evolution” is ambiguous, because she doesn’t say what she means by “significant” or by “evolution” (is she talking just about patterns of molecular evolution, like genetic diversity, or other types of evolution?)

New Scientist, in other words, fails to make the case that genetic drift has changed our view of how evolution operates, much less that it’s modified the modern synthetic theory of evolution. We already knew that small populations lose genetic variation because of genetic drift, and that’s been standard lore for decades. The real novel claims about drift—that it facilitates adaptive evolution, that it’s an important driver of speciation, and that it explains punctuated patterns in the fossil record—have disappeared because of the absence of both data and theory supporting those claims.

I am weary of going after New Scientist, and this may be my last critique of that issue. But be aware that virtually every one of the other nine points is exaggerated as well. Move along folks—nothing to see here.