My trial policy of taking care of grading the instant everything is turned in is biting back today: the first cell bio exam was thrown over the transom last night. I have been locked to my desk this morning. Will continue until it’s done.

The good thing about this practice is that I don’t have work hanging over my head all the time to feed my anxiety. The bad thing is that it demands bursts of focused work.

Empty noise, lazy science

Your disappointingly vapid opinion piece is not going to encourage your book, Benjamin Oldroyd. There’s nothing there. I’m referring to an article titled Epigenetics and evolution: ‘the significant biological puzzle’ of sexual orientation. The author is plugging a new book, Beyond DNA, and is trying to persuade us that maybe he has an answer to why gay people exist by going through a couple of hypotheses.

The first hypothesis is that it is a product of kin selection.

Briefly, the kin selection idea is that a gene that promotes homosexual behaviour can spread in a population if homosexual people contribute significantly to the reproduction of close relatives. Although this idea is plausible, the lack of any genetic marker that is reliably associated with sexual orientation is a strong argument against it.

There is no such thing as a gay gene, though, so you can’t postulate the existence of one and build up an adaptive scenario around it. I agree with Oldroyd. It’s a useless hypothesis.

Another idea is that there are antagonistic alleles.

The “antagonistic alleles” idea is that there are certain genes that are selected in different directions, that is, positively selected in males, but negatively selected in females and vice versa. Hypothetically, because no such gene has been identified, a gene that promotes testosterone production could be at a selective advantage in males if it promoted traits such as muscle development, risk taking, opposite-sex sexual attraction and increased sexual attractiveness to females. But if the same gene were expressed in the same way in females it might be disadvantageous for reciprocal reasons. This means that selection could pull in different directions in males and females, maintaining different gene variants in a population. By that I mean, gene variants that have different selective advantages in males and females can potentially coexist in a population because neither is unambiguously better. If so, sexual orientation may be more fluid than one might expect based on biological sex alone. (Well, “der”, I suspect you are now thinking, but please don’t shoot your even-handed messenger.)

He explains it well, but…”might” and “could be” are not evidence. Again, this hypothesis falls apart because there is an absence of evidence for the existence of such alleles undergoing differential competition in males and females. It’s another adaptive just-so story. It’s a useless hypothesis.

Therefore, if you rule out two hypotheses, the third alternative must be the answer, right? Cue dramatic entrance of Intelligent Design…no wait, not that. Oldroyd knows better than that. But it’s the same rationale: we think we have evidence against the conventional alternatives, therefore that counts as evidence for a different hypothesis.

No, it does not. Now the magical mcguffin we’re all looking for is epigenetics.

The epigenetic hypothesis for the widespread occurrence of human homosexuality is based on the possibility of epigenetic inheritance of adjustments to a foetus’s testosterone sensitivity. Like most other epigenetic marks, sex-specific epigenetic marks are established anew in the early embryo following fertilisation.

Substituting hypothetical “epigenetic marks” for a hypothetical “gay gene” gets us nowhere unless you’ve got something concrete and specific. If you do, that would be very interesting…but epigenetics, by it’s nature, is fuzzy and hard to pin down. That is not to say that epigenetics is non-existent — it’s very real and important — but that you can’t slap a simple causal explanation on many complex phenomena, whether it’s a gene or a epigenetic marker.

My preferred explanation is also a bit fuzzy. We have to get beyond the bogus genetic determinism that appeals so strongly to naive minds, and epigenetic determinism would be just as bad. I think we have to accept that human behavior is sloppy and variable as hell. We are built by a long chain of probabilistic interactions, from molecules bouncing around in a messy cell, to a tangle of cells communicating chaotically with one another, to incompletely specified individuals that are shaped by interactions with a variable, changing environment to end up as people with mostly unpredictable characteristics. Physics and chemistry are biased by biological constraints, but the end result is not rigidly locked in by your genes — there is a messy cascade of genetic, epigenetic, and environmental interactions that is skewed by evolution to produce a generally viable outcome, but is tolerant of variability.

We have to abandon these mechanistic notions of a clockwork biology that spits out adults who were specified at conception by the chemistry of nucleic acids. It just doesn’t work that way. We are all products of stochastic processes.

My personal belief is that evolution has worked to take a population of apes and favor a hierarchy of properties that are all weakly specified, and we’re lucky if the majority of individuals conform to that hierarchy. First in priority is cooperation, building a social environment that promotes mutual aid (we all know how poorly that often works out). The way I look at it is that biology is telling us to love one another…and then it is far less fussy about the details. We don’t need a deterministic explanation for why individuals vary, it’s the nature of how they are built.

Another bad memory

Oh, no. You must understand, in the late 80s and 90s, growth cone navigation was my jam. It’s what I was doing research on, and my head was full of papers from that era. Netrin, robo, slit, various molecules that attracted or repelled growing axons to establish the pattern of connections in the early developing brain…that was what I did. Now I learn that some of those papers, those written by Marc Tessier-Lavigne, were a lie.

Marc Tessier-Lavigne, the former president of Stanford University who resigned following scrutiny of his published papers and an institutional research misconduct investigation, has retracted a third paper, this one from Cell.

Last week, Tessier-Lavigne retracted two articles from Science that had been published in 2001.

The Cell paper, A Ligand-Gated Association between Cytoplasmic Domains of UNC5 and DCC Family Receptors Converts Netrin-Induced Growth Cone Attraction to Repulsion, was published in 1999. It has been cited 577 times, according to Clarivate’s Web of Science.

In my circles, Tessier-Lavigne had a colossal reputation — he was turning out all this work from a prestigious, well-funded lab with an army of students and post-docs. I was teaching developmental biology, talking about netrins, with a textbook that already cited the Tessier-Lavigne work. Such cool stuff, and it can’t be trusted anymore.

Worse, can we trust Cell magazine? They’ve posted the retraction, and it admits that the editors didn’t care about faked data.

In 2015, we, the authors, consulted with Cell editors about issues that had been brought to our attention about this paper, specifically image splicing in Figures 3C, 5A, 5B, and 7B–7D and duplication of blank blots in Figure 7C. Cell declined to publish a Correction at that time because in 1999, when the paper was published, the journal did not have policies prohibiting unmarked image splicing and because, for the duplication, there was insufficient information to determine intent, and the impact of the duplication on the paper’s conclusions was limited. In 2022, when new concerns were raised, Cell posted an Editorial Expression of Concern (Cell 186, 230 [2023], while an institutional investigation was conducted. The investigation is complete and has revealed further issues including manipulation of data-containing portions of Western blot images in Figures 3A–3C, 7A, 7B, and 7D, undermining confidence in the paper’s conclusions ( As a result, we are retracting the paper. We regret the impact of these issues on the scientific community.

Yikes. All it should take is one fudged image to cast doubt on the entire paper. If you’re faking data, we have sufficient information to determine intent — I was brought up with strict instruction that you never never never never ever do that.

What a disgrace. Shame on Tessier-Lavigne, and shame on Cell.


I saw the mommy spider spin the egg sac on 21 August, and this morning, the 6th of September, they finally emerged. These are Parasteatoda tepidariorum — note the leopard pattern on the abdomen. That’ll turn into a more complex mottling as they get older. Also see how the legs are mostly pale, but with distinct bands.

Steatoda triangulosa has a longer incubation time of 30 days, and the spiderlings emerge with pale abdomens and black, hairy legs.

The important thing about this is that we can nail down how long the incubation period for both species is under our specific culturing conditions. Now we wait for the Steatoda borealis egg sac to hatch out so we know its incubation period. Then…comparative embryology!

By the way, the lab was hectic this morning, with 150 tiny baby spiders, each about 3/4 of a millimeter long, emerging all at once and immediately trying to disperse. There was a cloud of barely visible dots all radiating out instantly from the locus of their home vial, while I was frantically trying to gather up individuals and put them in separate containers. Some, I’m sure, escaped.

Hmmm, is it ever a good thing when a scientist says that?

Since I avoid posting spiders here, you’ll have to go to Patreon or Instagram to see the baby picture.

I refuse to mansplain vaginas to you

Instead, I’ll let the Vagina Museum talk about spider vaginas (actually, they’re called epigynes…oh crap, I did it anyway.)

Very few people are interested in spider epigynes, so here, here’s a whole article about vaginas. They’re rather nifty organs, you know, with many different names.

Hah! You probably thought I was going to list a bunch of slang terms, didn’t you?

How about if I show you pictures of vaginas instead?

[Read more…]

The crunch begins

I have resolved that this year, I will get all student assignments graded within 24 hours of their scheduled due date. Guess what? First formal assignment was turned in yesterday for cell bio. I also had to compose a practice exam for Fundamentals of Genetics, Evolution, and Development, which was posted this morning and will be due on Monday.

I can tell already that my discipline is going to be murderous, requiring intense bouts of activity, since I won’t allow myself to drag things out over several days. Periodically intense pain vs. chronic pain? Which is worse? I’ll find out.

Yikes, low enrollments are a problem

I still have to do something about the lack of garish chemicals. They’re mostly clear or gray or cloudy.

Every fall I teach 3 lectures a week in cell biology, and it used to be 3 lab sections. We pared it back to two labs this year, and then…one of them was drastically under-enrolled, so we’re shifting everyone in it to our Wednesday afternoon lab. I’m only teaching one lab this year??!? Feels like cheating.

I’ve still got at least one class every weekday, but suddenly a big block of time opened up for the spiders, which is good. My first year classes are filling up, which probably means I’ll be back to the usual number of lab sections next year. If you want lots of one-on-one attention in biology, though, this is the year to be here.

Open the floodgates

That Washington Post series on arch-racist Ales Hrdlicka has really stung the Smithsonian. The Secretary of the Smithsonian has written an op-ed apologizing for its history.

Anthropologist Ales Hrdlicka served as the head of the Smithsonian’s physical anthropology division from 1903 to 1941, when the majority of the human remains in our collections were obtained. During Hrdlicka’s four decades at the institution, he oversaw the acquisition of hundreds of human brains and thousands of other remains. The overwhelming majority of these remains were taken without the consent of the deceased or their family members, and Hrdlicka took particular interest in the remains of Indigenous people and people of color to undergird his search for scientific evidence of white superiority.

It was abhorrent and dehumanizing work, and it was carried out under the Smithsonian’s name. As secretary of the Smithsonian, I condemn these past actions and apologize for the pain caused by Hrdlicka and others at the institution who acted unethically in the name of science, regardless of the era in which their actions occurred.

I recognize, too, that the Smithsonian is responsible both for the original work of Hrdlicka and others who subscribed to his beliefs, and for the failure to return the remains he collected to descendant communities in the decades since.

OK, that’s a good start, but so far it’s just words. Tell me what you are doing, because that’s where the excuses get weak. The material changes so far are that they have repatriated a few thousand remains, they have formed a task force, and they promise future policy changes.

Our forthcoming policy will finally recognize these remains not as objects to be studied but as human beings to be honored. It is a long-overdue shift, and I regret that human bodies were ever treated with such disrespect at our institution.

If I may suggest an alternative response: reverse the obligations. Assume every single piece of flesh or bone must be traced to their origins as quickly as possible and returned to their peoples; the priority is to get rid of all of it. If anything is to be retained, someone must be named as responsible for the objects, and must have a specific scientific plan for extracting information from them in the near future, and then returned. Right now, everything is backwards, where we just assume if someone has a bunch of bones in a barrel, well, it belongs to them, even if all they can say is a vague assurance that it’s in a “teaching collection.” I always wonder what they plan to teach with them.

If you want to claim something is scientifically valuable, the onus is on you to justify that claim.

Charles Murray is still an ignoramus

I’ve been telling you, Charles Murray is an ignorant hack. I can’t stand listening to this know-nothing pontificating on genetics when he’s so full of shit on the topic, which doesn’t stop him from being arrogantly confident about it.

Anyway, here’s a good critique of The Bell Curve — it’s hard to believe we still have to argue about it.

Understandably, these arguments provoked the ire of progressively minded scientists and commentators. However, the sweeping and reflexive manner in which opponents of the hereditarian arguments advanced their objections to The Bell Curve often led these critics to adopt counterproductive conclusions. Unhelpfully, they conflated two distinct issues. The first is the question of what it means to claim that something is genetic, and the second is the inevitability of certain life outcomes based on the biology of a particular organism.

Properly speaking, genetics concerns some characteristic of an organism varying across individuals in a group in a given context. It is, by definition, not an explanation of the behavior or development of a given individual in a given instance. Conflating the issue of the causes of differences with that of the inevitability of the development of a particular organism is an important part of the hereditarian rhetorical strategy deployed by the likes of Herrnstein and Murray. To the extent that their arguments have managed to gain some traction in the world, it has been because they have managed to convince their critics to commit the error for them.

Whoa there — the heart of my criticisms of Murray has always been that genetics is not as determinative as the naive people who learned about Punnett squares in fourth grade think. But do go on, this is an important definitional issue and bears repeating.

But the confusion in Murray and Herrnstein’s thinking doesn’t just stop at their pessimism about the kind of practical responses to differences purportedly caused by genetics — it goes all the way down to their understanding of what genetics is. Let’s start by clarifying what we mean by “genetic” and outline why that which is genetic is not necessarily inevitable. For one, genetics deals with groups of organisms rather than the life outcomes of individual organisms. All organisms have genes, but it takes groups of organisms to have genetics because genetics is ultimately about how variation is structured within a group.

Take a single tomato plant in isolation. It has a genome that is between one-fourth and one-third the size of that of a human’s in terms of the raw amount of DNA. Inside its genome are a few tens of thousands of genes, which, in this case, are stretches of the genome that form a chemical template for the cellular production of the proteins and other biochemicals that are vital for the structure and function of organisms. However, since we are dealing with a single plant at a single point in time, there is no comparative context that would allow us to identify the differences among organisms that characterize the rich diversity of life.

Exactly! This is also why it’s important that students actually do real crosses with real organisms. The abstractions of theory might tell you that oh, one quarter of the progeny will have a particular phenotype, but when you sit down and have to closely examine a thousand flies, you get to see all the variation you did not predict and you learn that it’s never as simple as the models tell you it is. The variation is also interesting.

But yes, genetics is fundamentally probabilistic. You can’t use it to predict individual destiny. It’s also the case that genetics has significant interplay with the environment.

But even having many organisms to compare is not sufficient for a biological system to display genetics in the proper sense of the term. Genetics in the sense that matters is ultimately about variation that arises from genetic differences. To see this, think again about tomatoes. They can be cloned with ease by taking cuttings from a single plant and growing them in their own allotments of soil. Genetically, the different newly individualized plants will be identical to one another, with the exception of a very few mutations — spontaneous changes to DNA that can occur during cellular replication.

If we were to compare a large number of these cloned tomato plants, we would find many differences among them. The shape and sizes of leaves would differ, as would the coloration of the fruits and the pattern of branching along the stalks. Since, on account of being clones, the plants are all genetically identical, these differences could not be attributable to genetics. While each of the plants has genes and we have a group of plants to form the basis for comparison needed to establish that there is variation, there are no genetic differences among the plants that could account for any of that variation. That is, while our tomato plants have genes, they display no genetic differences among one another despite having physiological differences.

Yes, that’s always been obvious if you actually look at populations. I had tanks of zebrafish that were about as genetically uniform as you can get, highly inbred for over a century — yet I could recognize individuals in a tank and see differences in behavior. I’ve only been inbreeding spiders for a half dozen generations, but I don’t see variation diminishing, at least not yet.

How do people take Murray seriously when his fundamental understanding of biology is so wrong?