Human genetics accused of furthering white supremacy and racism—today

May 6, 2021 • 11:00 am

All geneticists know, and knew decades ago, that we had a shameful period in our history, particularly human genetics. (This was not predominant, but a blind alley.) Some geneticists, like Galton and Davenport, were explicit “negative eugenicists”, urging sterilization or discouraged breeding of the “inferior”, including not only those who were deemed mentally deficient or of lower class but also those of other races. This history has been reemphasized recently with the rise of anti-racism, and it’s good that we’re constantly cognizant of our past history and its racist (and classist) underpinnings. In fact, this history is already widely taught, but there’s no harm in learning about it—as we should learn the entire history of our field.

What bothers me, though, is the complete neglect of the movement against eugenics that was widespread in America, a history exemplified by articles like these (I’ll try to find links online later). This, too, is part of our history:

and this

and this, the Presidential Address at the American Society of Human Genetics in 1961

You never see this pushback mentioned in the histrionic accusations, like the one below by Lea Davis in the increasingly woke Scientific American, that human genetics in America and the UK not only has a racist past (partly true) but also a racist, white-supremacist present (not true). Lea K. Davis is an Assistant Professor of Medicine at Vanderbilt Medical Center.

Now it’s true that in a few places prisoners have been offered completely voluntary sterilization in return for lighter sentences, but this rarely happens. And it’s execrable. But the accusation that human genetics is ridden with racism and complicit with white supremacy is simply false. These are performative accusations, like those John McWhorter mentioned yesterday.

Davis makes a number of overheated statements and at least one contradictory one. The latter involves the existence of “races”. As I’ve written ad infinitum, there are no discrete and easily distinguishable populations that can be classified as “races”, but we do have populations, distinguished by genetic ancestry, that can, if you use many genes, be almost absolutely identified as to self-identified ethnicity as well as geographical location.

Davis argues that “race” is a social construct, a misleading statement that needs considerable explanation, which she neglects to provide.

Together, could we dispel the myth of biological race? Again, we cannot do this alone, as most of us are ill-equipped to confront the rhetorical science misinformation bombarding society on a daily basis. Engaging experts in strategic science communication, along-side of social scientists and geneticists, is mission critical to meaningfully de-biologizing race.

Let’s ditch the loaded term “race” and just use “ancestry” or “ethnicity”, recognizing that there is substantial genetic information in one’s genome that not only tells you what your self-identified race is with substantial accuracy, but also gives you a good idea of your ancestry and geographic origins. “Race” may be a social construct, but “genetic differentiation of populations” is not.  And Davis makes the mistake of saying that “race” (let’s use “ethnicity”) is something completely different from ancestry:

Others routinely, if naïvely, perpetuate the scientifically inappropriate conflation of race and ancestry. The trouble is that most human geneticists know very little about race. Scholars in sociology, anthropology, critical race theory, gender studies, etc. who have a far more sophisticated understanding of the origins of race and racism, have so much to teach us.

She’s dead wrong here. I’d rather talk about “race” (“ethnicity”) with people like John Novembre or Graham Coop, well known human geneticists, than with critical race theorists or gender studies people, who have no training in genetics, an ideological commitment, and, I’d aver, lack a “far more sophisticated understanding of the origins of race.” Ancestry has everything to do with “race” (read “ethnicity”: it’s differential ancestry that results in geographic populations being genetically different!

But the contradiction is when Davis claims that clinical studies of genes that map near disease genes have largely been conducted on white populations—a form of racism. I don’t think it’s really racism, because white populations are what’s largely available to clinicians (at least locally, as they draw participant from their local universities in Europe and the US), but I’ll grant her that we need to do such studies in people of different ethnicities. But if race is a social construct, on what basis can we do “ethnicity-based” genetic analysis of disease propensity? If ethnicity or race are social constructs that have nothing to do with biology, working on one group is as good as another. That’s not the case, of course: groups differ in their genes and their propensity to get different diseases (cultural differences surely also play a role). You need to IDENTIFY ethnicity to do such work!

Note how she throws in the accusation of explicit and systemic racism for this concentration on focal populations:

Lack of diversity in available genetic data is not an accident; it is an inevitable consequence of systemic racism in biomedical research. The difficulty in recruiting non-European populations into genetic research today is a direct result of our history of white centering, gatekeeping by white academics and decades of human rights abuses suffered at the hands of white researchers. White centering is still so embedded in human genetics that even though we recognize these problems, millions of dollars are being invested in programs to capitalize on Eurocentric genetic scores and tests that are primarily effective for people of European descent, potentially leaving communities of color behind in precision medicine advancements.

If we are to do these tests, we must label people by their ethnicities, for we’ll otherwise have no data. In fact, this is being done right now, so Davis is exaggerating.  She simply must recognize a finite number of ethnicities to do this work, for otherwise it’s of no value. (Furthermore, to have full representation, studies should be done in Africa, but white doctors attempting to collect African data are at risk of being accused of racism and colonialism.

Beyond that, we have the multiple Kendi-an accusatons that all human geneticists are complicit in racism and white supremacy. A few samples:

How do we teach and talk about this incredibly problematic history? Despite the many scholarly texts available, there is rarely an open and frank acknowledgement that the very foundations of our field were rooted in the false and dangerous beliefs of biological race and human racial hierarchies. Today, there is an effort to distance modern genetics from the harms of eugenics. This shameful aspect of our shared history is often separated from the primary curriculum for human genetics trainees, relegated to classes in “ELSI” (ethical, legal and social issues), which are usually electives—or, worse, just one day of training. In large part, we are failing to disclose this startling racist legacy to young scientists entering the field; a sad irony for a discipline devoted to human inheritance. Our failure to acknowledge the racist origins of modern genetics also has repercussions in our (in)ability to attract and retain members of underrepresented communities in genetics and other STEM training programs. Thus, as time marches on, the knowledge of our harmful racist history is fading while the culture of whiteness continues to dominate.

No, there is an effort to teach people about the history of our field. But that should not include the accusation that STEM is racist, for every school I know of is trying to “diversify” STEM as hard as we can. The issue is a “pipeline problem”: few minority candidates have reached the Ph.D. stage. That itself reflects older racism, but not racism imbuing human genetics, for scientists are pretty much anti-racists.

Further, the “very foundations of our field were not rooted in racism”. Yes, some famous geneticists believed that, but by no means all. Was the monk Gregor Mendel a racist? Were the re-discoverers of Mendelism, Hugo DeVries, Carl Correns and Erich von Tschermak, determined to imbue the field with racism? Not that I know of. How about the popularizers of modern genetics: people like T. H. Morgan, Theodosius Dobzhansky, Alfred Sturtevant, Calvin Bridges, Sewall Wright, and J. B. S. Haldane? Nope. You can mention Ronald Fisher in support of racism, but his eugenics was based on poverty, not race, and at any rate never got purchase. No, our field is not founded on racism.

And here’s how we’re still racist:

When we identify white supremacy as the paramount problem in our field’s history, it becomes clear that it is still our problem today. Lack of diversity in available genetic data is not an accident; it is an inevitable consequence of systemic racism in biomedical research.

and this; note the reference to structural violence and our complete complicity (my emphasis). The last sentence might has well come from the pen of Ibram Kendi:

Human genetics is a science that I love, a science to which I have devoted my life, and a science that I believe could be a powerful force against racist ideas in medicine and society. But this potential can only be reached if we are willing to reckon with our role, collectively and individually, past and present, in upholding white supremacy and structural violence in science and academia. As educator and author Catrice M. Jackson has observed, “If you don’t have an antiracism plan, you plan to be racist.”

It is ludicrous to claim that if we don’t have an antiracism plan, we plan be racist. Colleges are already doing their best to get women and minorities into STEM by various programs. That is our antiracism plan, and Davis cannot ask more. Society needs a plan that widens the pipeline, allowing equal opportunity for all to pursue their interests, but this has nothing to do with the supposed ongoing racism in human genetics.

An antiracism plan will require challenging everything from the speed to the priorities of human genetics research, but if we are serious about reducing health disparities through precision medicine we must push back on the culture of whiteness in medicine and research. We can begin by explaining that equitable translation of genetic medicine will be a slow process because of the inequity that our field has already created. Efforts to increase diversity among scientists are desperately needed, and unless we are committed to dismantling inherently racist structures and ideas in science, we will never achieve real equity.

We can empower ourselves and each other to acknowledge our own complicity and call on our funding institutions, our professional societies and our departments to make antiracist action a priority in our daily research practices. The long-overdue awakening emerging in American consciousness is incongruent with business as usual in our field, and it is past time to call in the revolution. Human genetics needs an antiracism plan now, otherwise, we must admit we plan to be racist.

I reject her claim that I’m complicit in racism, even though I’m a fly geneticist. Is Davis unaware of what is being done now? I find it hard to believe her claims, for she raising as a new challenge what is largely a problem already being rectified. As for the “calling in the revolution”, that’s like “sending in the clowns”: “Don’t bother, they’re here.”

As for human genetics being inhabited by figures in pointy hats and white robes, Davis is dead wrong. Genetics was not founded on white supremacy, and although we had racists and bigoted episodes that had some serious consequences, they are largely gone, nor do I see them returning. We are not engaged now in propping up white supremacy.

A retrospective look at a paper: Coyne and Orr (1989)

April 4, 2021 • 12:00 pm

The two best-cited pieces of scientific work bearing my name were both done in collaboration with my graduate student, Allen Orr, who was recommended to me by Bruce Grant, my undergrad genetics teacher at The College of William and Mary. Allen had gotten a B.A. in philosophy there, and went on to do a master’s degree with Bruce in Drosophila genetics. Bruce recommended him to me as a good prospect, but wasn’t sure how he’d work out as a Ph.D. student.

At the time I was at the University of Maryland, took Allen on, and the rest was history. I had no idea how to mentor graduate students—Allen was my first—but it turned out he needed no mentoring: he was a self-starter. Over his few years in my lab, he published about ten papers and won the Society for the Study of Evolution’s Dobzhansky Prize in 1993, given to the person the SSE’s committee considers the best young evolutionary biologist.

The two most cited works include a pair of related papers (Coyne and Orr 1989, 1997), and our coauthored book Speciation (2004).

I summarized the main findings of the two papers, and gave a bit of their history, in a post from October of last year, which includes an interview I did about it in 2017 for Reflections of Paper Past.  At that time I didn’t know that two people, including my last student, Daniel Matute, were writing a retrospective of the 1989 and 1997 papers.

At any rate, in honor of the 75th anniversary of the journal Evolution, it’s been publishing retrospectives of notable papers that have appeared there. One chosen for this treatment was the Coyne and Orr duo. The retrospective paper, by Daniel Matute (UNC Chapel Hill) and Brandon S. Cooper, now at the University of Montana, can be accessed by clicking on the screenshot below, or you can get the pdf here. The reference to the retrospective is at the bottom. It will probably be of interest only to evolutionary geneticists, but it’s here for the record.

I have to say that Daniel and Brandon did a terrific job. It’s far more than a “retrospective” of our papers, but a new meta-analysis of existing data on how reproductive barriers between incipient species grow with time. (That was the subject of our original papers, and you can read the summary at the link above.) The new paper highlights where we were right, where we were wrong, what gaps there are in our knowledge about reproductive isolation, and what directions future research on the time course of speciation should take. In other words, it’s a review paper on a growing area of research rather than a discussion of just two small papers.

I’ll end by giving their abstract, which shows what the paper is about. But if you work on speciation, you’ll want to read their whole paper:


Understanding the processes of population divergence and speciation remains a core question in evolutionary biology. For nearly a hundred years evolutionary geneticists have characterized reproductive isolation (RI) mechanisms and specific barriers to gene flow required for species formation. The seminal work of Coyne and Orr provided the first comprehensive comparative analysis of speciation. By combining phylogenetic hypotheses and species range data with estimates of genetic divergence and multiple mechanisms of RI across Drosophila, Coyne and Orr’s influential meta‐analyses answered fundamental questions and motivated new analyses that continue to push the field forward today. Now 30 years later, we revisit the five questions addressed by Coyne and Orr, identifying results that remain well supported and others that seem less robust with new data. We then consider the future of speciation research, with emphasis on areas where novel methods and data motivate potential progress. While the literature remains biased towards Drosophila and other model systems, we are enthusiastic about the future of the field.


Matute, D.R. and Cooper, B.S. (2021), Comparative studies on speciation: 30 years since Coyne and Orr. Evolution.

Evolution society renames Fisher Prize; some of us wrote a letter in response

April 2, 2021 • 12:00 pm

I’m putting this up for the record, for it’s likely that not many outside of evolutionary biology will be interested in this kerfuffle, though the wokeness of the Society for the Study of Evolution (SSE) may be a harbinger of a general wokeness in science as a whole.

Not long ago the Society for the Study of Evolution, the premier society promoting the study of evolutionary biology, put up the following statement announcing a renaming of the Fisher Prize given for an outstanding Ph.D. dissertation paper published in Evolution, the Society’s Journal. Ronald Fisher (1890-1962) was one of the founders of evolutionary genetics as well as the modern science of statistics. We still use many of the tests and methods he devised.

But he also promoted eugenics, though not of the racist variety but the “classist” variety, urging the “lower classes” to have fewer children and the “upper classes” to have more. As far as we know, none of his recommendations was ever made into policy. Nevertheless, his views on eugenics were sufficient for the SSE to erase his name from the prize.

Here’s the SSE’s statement.

SSE statement on the Fisher Prize

SSE statement on the Fisher Prize This award, formerly called the R. A. Fisher Prize, was renamed the SSE Presidents’ Award for Outstanding Dissertation Paper in Evolution in June 2020. This prize, first established in 2006, is awarded annually for an exceptional PhD dissertation paper published in the journal Evolution. The award comes with a $1000 honorarium. Nominations are due in January of each year. Learn more about the award here.

The original name of the prize was chosen to acknowledge Fisher’s extensive, foundational contributions to the study of evolution, particularly through his development of population genetic and quantitative genetic theory. Alongside his work integrating principles of Mendelian inheritance with processes of evolutionary change in populations and applying these advances in agriculture, Fisher established key aspects of theory and practice of statistics.

Fisher, along with other geneticists of the time, extended these ideas to human populations and strongly promoted eugenic policies—selectively favoring reproduction of people of accomplishment and societal stature, with the objective of genetically “improving” human societies. Fisher and other geneticists, ignoring logical flaws certain to undermine the efficacy of this program, were highly influential in promoting eugenic policies. Fisher in particular maintained his support for these ideas even after others had abandoned them. The eugenics movement was founded in racist ideologies, and although eugenics has been repudiated by the evolution community, the field of population genetics continues to carry the mark of its historical connections to eugenics (read more here), causing harm to Black, Indigenous, Latinx and other communities of color. We sincerely regret that authors of color may have chosen not to submit their work for consideration for this award because of its name.

For these reasons, the SSE Council voted in 2020 to change the name of the award, shifting its focus to the scholarly achievements of the awardee. The name also acknowledges that the winning paper is chosen by the three current society presidents. Going forward, SSE recognizes the need to continue to invest significant effort toward making our Society and our field more inclusive and more equitable. The Diversity Committee, established in 2017, has galvanized SSE’s major strides towards this goal, and welcomes input and involvement from the membership in prioritizing and carrying out its initiatives (read more here).

In September 2020, SSE Council approved a suite of actions proposed by the Diversity Committee to increase inclusion of and support for members of historically excluded groups in the field of evolutionary biology and through all of the activities of SSE. Updates on the progress of these actions can be found on the SSE website.

Ten past Presidents and Vice Presidents of the SSE, including me, objected to this renaming on several grounds (we do not favor renaming existing prizes), and sent the following letter to the officers of the SSE (I’ve omitted the names of the signers, though one was clearly me).

March 23, 2021

To the SSE Council:

While we applaud the efforts of the Society to enhance diversity in science, and to oppose racism and other forms of prejudice, we wish to express our concerns about the statement on the SSE website concerning the reasons for renaming the R.A. Fisher Prize ( There are two issues that we feel should be considered.

First, the statement contains significant inaccuracies, which are injurious to the reputation of one of the greatest of all evolutionary biologists. These inaccuracies are listed below; for further details, see Bodmer et al. 2021 Heredity ( A scientific society surely has the duty to avoid factually incorrect statements.

Second, it is unclear why the Council and Diversity Committee considered only the renaming of the Fisher Prize. The awards named after the following three people should also have been examined in this context. Theodosius Dobzhansky signed the Geneticists’ Manifesto of 1939, which expressed support for eugenic measures (Crew et al. 1939 Nature 144: 521-22). In his book Mankind Evolving, he remarked that “Equality means that all humans are entitled to equal opportunity to develop their capacities to the fullest, not that these capacities are identical” . In his Narrow Roads of Gene Land. Vol. 2. The Evolution of Sex, William Hamilton expressed support for infanticide as a solution to the problem of the accumulation of deleterious mutations in human populations, and a belief that Jews have innately higher mathematical abilities than the English. T.H. Huxley, while opposing slavery, believed that black people were inferior to white people (

There is a general issue that the Society needs to consider carefully: to what extent do views that were held by eminent people in our field, and are today repugnant to most or all of its members, negate their scientific contributions? To focus attention on just one individual is to fail in this task.

Inaccuracies in the SSE statement about the Fisher Prize

First, it contains the misleading statement that “the field of population genetics continues to carry the mark of its historical connections to eugenics (read more here), causing harm to Black, Indigenous, Latinx and other communities of color”. The founder of eugenics, Francis Galton, never accepted Mendelian genetics, and the mis-applications of genetics by white supremacists and the Nazis had nothing to do with population genetics as developed by Fisher, Haldane, Weinberg, Wright and their contemporaries; indeed, population genetics completely undermines the concepts of racial groups as homogeneous entities. This is the opposite of “causing harm” to ethnic groups who have suffered discrimination or persecution.

Second, Fisher was not “highly influential in promoting eugenic policies”. None of his proposed measures (family allowances for the supposedly better endowed intellectually, and voluntary sterilisation of people with learning disabilities) were implemented in the UK, and he never advocated the type of compulsory sterilisations carried out in the USA, Sweden and Germany.

Third, the policies promoted by the Eugenics Society in the UK, with which Fisher was associated until 1941, were not “founded in racist ideologies”. The Society was concerned solely with improving the genetic quality of the UK population, although individual members may have held racist views, as was common at the time. Many people of liberal and left-wing political views were members of the Society. Indeed the “The Geneticists’ Manifesto” of 1939 (Nature 144:521-22) contained statements about improving the human population that went substantially further than Fisher’s proposals. It was signed by Dobzhansky, Haldane, Huxley and Muller, among others. According to the introduction to the Wellcome Trust Archive of documents concerning the Eugenics Society (, the society publicly dissociated itself from Nazi ‘race hygiene’ in 1933.

Fourth, the claim that Fisher “maintained his support for these ideas even after other abandoned them” is not accurate; H.J. Muller continued to advocate eugenic improvement as late as 1959 (Perspectives in Biology and Medicine 3:1-43). Fisher in fact withdrew completely from the Eugenics Society in 1941, and his only later publication mentioning eugenics was in the 1958 Dover edition of The Genetical Theory of Natural Selection; the relevant section was virtually unchanged from the 1930 edition.

Fifth, the statement overlooks the work that Fisher did to encourage the development of statistics in India (see his obituary in Sankhya 24: 207- 208). This work probably achieved more to encourage scientific endeavour by people of color than most scientific societies have done in their entire history. Fisher had relatively few PhD students by modern standards; one was C.R. Rao, the noted Indian statistician, and another was Ebenezer Laing, the Ghanaian geneticist. This was very unusual for academics in the UK at the time. Fisher’s last known letter was a very friendly letter to Laing.

Sixth, the statement claims that there were “logical flaws” in his ideas about improving society; there are no logical flaws in these ideas, but they can of course be questioned on both empirical and ethical grounds.

That’s the letter. The response we got from an official of the SSE, though thoughtful, was basically to reject our objections. I am not at liberty to reproduce the letter, as it was a private response to the ten signers, but I will quote one of its statements:

There emerged a consensus, however, that naming of an award after an individual honors all that person’s dimensions.

This “consensus” is completely misguided, both for the SSE and in general. Who among any famous scientists, particularly before 1940 or so, did not have some views that should not be honored? Most scientists before that time expressed some racist, sexist, or politically “offensive” opinions, and that includes four of the greats, Charles Darwin, Thomas Henry Huxley, Theodosius Dobzhansky, and W. D. Hamilton. The latter three already have SSE Awards named after them. Why shouldn’t the SSE ditch those, too? (Note: as I said, we don’t favor that.)

And if you applied this standard to American history as a whole, virtually all of honored politicians and notables, including Washington, Jefferson, Madison, Lincoln, and so on, have dimensions of their actions or beliefs that aren’t worthy of being honored. My own view is that when we honor someone, we honor them for the good things they did, and I’ll add that such honors should be given when the good they did outweighs the bad. Based on these criteria, Fisher clearly deserves an honorific.

Nobody is perfect, for crying out loud. Who could afford to have all their beliefs and statements put before the public eye?

I still maintain that the purpose of the SSE originally was and should still be to promote the study of evolution, not to promote particular ideological, political, or moral statements. That can be left to the individual members speaking for themselves.

Further thoughts, by Greg Mayer. Putting aside the factual errors noted in the letter from the past presidents and vice presidents, the statement about the Fisher Prize from the SSE seems so suffused with cognitive dissonance as to be redolent of doublethink: Fisher is awful and must be degraded; but Fisher is responsible for extensive and foundational contributions that we use to this day– which is it?

It’s the inability to hold two thoughts at once– epitomized by the claim that an award “honors all that person’s dimensions”– that leads to this muddled thinking. Fisher can be a great scientist worthy of honoring and emulating in his science, without endorsing every part of his life. He had a lousy marriage, eight children, overcame really bad eyesight, held grudges, deeply mourned the death of his eldest son (an RAF pilot in WW II), supported the tobacco industry, was a British patriot, and an anti-totalitarian– some people will want to denigrate him for each of these things. But why would we think  anyone today has an exclusive insight into a final revelation of value? We can only imagine what we will be condemned for in the future; John McWhorter has contemplated a future in which those who have not opposed abortion will be retrospectively condemned.

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.


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.


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.


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.


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.

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.


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!