Category Archives: biology

Breastfeeding is now Terrorism

So, this is reposted from Vermont Vigilance — a new blogging endeavor [full announcement t/k].

An article from the New York Post describing an incident where a Belgian couple were kicked out of the Metropolis Country Club in White Plains, New York after Roseline Remans began to breastfeed her infant son. In an all-too-common twist these days, their ejection was accompanied by charges of “terrorism”.

Here’s the story. Remans and her husband, Belgian diplomat Tom Neijens (First Secretary of the Belgium Mission to the UN) went to the Metropolis Country Club and asked if they could eat lunch there. They were told yes, they were welcome to eat on the terrace. When Remans started to breastfeed her daughter, a manager came over and told her that she was disturbing the other people at the club, and that she would have to finish in the restroom.

Now, first of all, for the country club to make this request was against New York state law. Section 79-e reads:

Right to breast feed. Notwithstanding any other provision of
  law, a mother may breast feed  her  baby  in  any  location,  public  or
  private, where the mother is otherwise authorized to be, irrespective of
  whether  or  not  the nipple of the mother's breast is covered during or
  incidental to the breast feeding.

In other words, even if you are a private club, once you tell someone that they can eat lunch in your restaurant, you can not then ban them from breastfeeding there. The NYCLU states:


  • To breastfeed your baby in any public or private place where you have a right to be.
  • This includes stores, day care centers, doctors’ offices, restaurants, parks, movie theaters and many other places.
  • No one can tell you to leave any of these places because you are breastfeeding, and no one can tell you to breastfeed in a bathroom, a basement or a private room.

Whether or not Neijens and Remans knew about the law I don’t know, but they argued that they should be able so stay. So, the club called the police, which led to this response, per the Post:

Detective Scott Harding allegedly yelled, “Close the doors!” and two other diners were told to leave the terrace.

“He was walking as if he was acting in a Western movie,” Neijens said. “He had one hand on his gun, one hand on his Taser.”

Neijens said the officer warned the couple they were trespassing and said some people at the club thought they were terrorists because of their black backpack.

When Remans, on the verge of tears, questioned why terrorists would breast-feed at a ritzy club, the cop allegedly replied, “In Sri Lanka, babies are used by terrorists.”

It is not obvious who played the terrorist card here, but there are two main possibilities:

  1. The club told the police that they had possible terrorists on their terrace — an effective way to punish people for not doing what you tell them to do, even if your instructions are illegal.
  2. The police responded to a request to remove some breastfeeding hippies from a swanky club. When they figured out that these were not run-of-the-mill hippies whom they could push around in the interest of catering to the elite, they tried to cover their tracks with, “Um, because, um, terrorism.”

In any event, it seems clear that someone used a disingenuous claim of concerns about terrorism to enforce certain norms of behavior, in violation of the law.

Gene Patents Overturned — and Scalia’s Weird Dissenting Opinion

So, the Supreme Court just ruled that Myriad Genetics does not, in fact, have the right to patent two naturally occurring human genes, BRCA1 and BRCA2. This is good news, because . . . well, because patenting a gene is total bullshit.

If you’re not familiar, these two genes are important because genetic variation in their DNA sequences has been linked to breast cancer. So, the sequence of your DNA in these two genes can reveal if you have a higher-than-average risk of developing breast cancer. It was exactly this sort of test that prompted Angelina Jolie to undergo a preemptive double mastectomy.

The problem is that the tests were really, really expensive, because of Myriad’s patents. So, the immediate consequence of the ruling should be that the prices for these tests should come way, way down.

The opinion (PDF here, if you’re interested) focuses on the difference between “discovering” something — like the sequence or location of a gene — and “creating” something — like a thing that can be patented. So, a gene is a naturally occurring thing that can not be patented. However, if you take the mRNA from a gene and reverse-transcribe it to make cDNA, this new thing might still be patentable. But, the ruling explicitly notes that the cDNA would be a creation because of the removal of introns. So, cDNA from a single-exon gene might not be patentable.

The ruling explicitly states that it offers no opinion on the patentability of genes that have had their DNA sequences deliberately altered — leaving that question for another day.

It also points out limitations of the ruling with respect to plants. The goal here seems to be to ensure that this ruling is not interpreted as invalidating any plant patents covering plant strains that have been developed through selective breeding.

That all seems pretty straightforward. The ruling does seem to leave a number of issues surrounding the patenting of genetic material unresolved, but it is quite clear about which issues it is kicking down the field.

But then there’s this bit of weirdness at the end.

The opinion is pretty much unanimous, which is always nice. Except for a little, tiny bit of dissension from Antonin Scalia. Here is the complete text of his dissenting opinion:

I join the judgment of the Court, and all of its opinion except Part I–A and some portions of the rest of the opinion going into fine details of molecular biology. I am unable to affirm those details on my own knowledge or even my own belief. It suffices for me to affirm, having studied the opinions below and the expert briefs presented here, that the portion of DNA isolated from its natural state sought to be patented is identical to that portion of the DNA in its natural state; and that complementary DNA (cDNA) is a synthetic creation not normally present in nature.

I actually thought Part 1-A of the ruling was a little weird when I first read it. Not because it said anything strange or controversial, but because it read sort of like a Wikipedia entry on basic genetics, and contains a lot of details that don’t seem particularly relevant?.

Here’s the full text of the part of the ruling about which Scalia says, “I am unable to affirm those details on my own knowledge or even my own belief.”

Genes form the basis for hereditary traits in living organisms. See generally Association for Molecular Pathology v. United States Patent andTrademark Office, 702 F. Supp. 2d 181, 192–211 (SDNY 2010). The human genome consists of approximately 22,000 genes packed into 23 pairs of chromosomes. Each gene is encoded as DNA, which takes the shape of the familiar “double helix” that Doctors James Watson and Francis Crick first described in 1953. Each “cross-bar” in the DNA helix consists of two chemically joined nucleotides. The possible nucleotides are adenine (A), thymine (T), cytosine (C), and guanine (G), each of which binds naturally with another nucleotide: A pairs with T; C pairs with G. The nucleotide cross-bars are chemically connected to a sugar-phosphate backbone that forms the outside framework of the DNA helix. Sequences of DNA nucleotides contain the information necessary to create strings of amino acids, which in turn are used in the body to build proteins. Only some DNA nucleotides, however, code for amino acids; these nucleotides are known as “exons.” Nucleotides that do not code for amino acids, in contrast, are known as “introns.” 

Creation of proteins from DNA involves two principal steps, known as transcription and translation. In transcription, the bonds between DNA nucleotides separate, and the DNA helix unwinds into two single strands. A single strand is used as a template to create a complementary ribonucleic acid (RNA) strand. The nucleotides on the DNA strand pair naturally with their counterparts, with the exception that RNA uses the nucleotide base uracil (U) instead of thymine (T). Transcription results in a single strand RNA molecule, known as pre-RNA, whose nucleotides form an inverse image of the DNA strand from which it was created. Pre-RNA still contains nucleotides corresponding to both the exons and introns in the DNA molecule. The pre-RNA is then naturally “spliced” by the physical removal of the introns. The resulting product is a strand of RNA that contains nucleotides corresponding only to the exons from the original DNA strand. The exons-only strand is known as messenger RNA (mRNA), which creates amino acids through translation. In translation, cellular structures known as ribosomes read each set of three nucleotides, known as codons, in the mRNA. Each codon either tells the ribosomes which of the 20 possible amino acids to synthesize or provides a stop signal that ends amino acid production.

DNA’s informational sequences and the processes that create mRNA, amino acids, and proteins occur naturally within cells. Scientists can, however, extract DNA from cells using well known laboratory methods. These methods allow scientists to isolate specific segments of DNA — for instance, a particular gene or part of a gene—which can then be further studied, manipulated, or used. It is also possible to create DNA synthetically through processes similarly well known in the field of genetics. One such method begins with an mRNA molecule and uses the natural bonding properties of nucleotides to create a new, synthetic DNA molecule. The result is the inverse of the mRNA’s inverse image of the original DNA, with one important distinction: Because the natural creation of mRNA involves splicing that removes introns, the synthetic DNA created from mRNA also contains only the exon sequences. This synthetic DNA created in the laboratory from mRNA is known as complementary DNA (cDNA).

Changes in the genetic sequence are called mutations. Mutations can be as small as the alteration of a single nucleotide—a change affecting only one letter in the genetic code. Such small-scale changes can produce an entirely different amino acid or can end protein production altogether. Large changes, involving the deletion, rearrangement, or duplication of hundreds or even millions of nucleotides, can result in the elimination, misplacement, or duplication of entire genes. Some mutations are harmless, but others can cause disease or increase the risk of disease. As a result, the study of genetics can lead to valuable medical breakthroughs.

So, what do you think Scalia is objecting to? Is he just signaling that he thinks that the details of the molecular biology are not important here? Is it the claim that “Genes form the basis for hereditary traits in living organisms”? Is he unable to affirm with his own belief that G pairs with C? That uracil substitutes for thymine in RNA? That humans have 23 pairs of chromosomes?

Please share your most outlandish conspiracy theories in the comments!

How does the FBI know it found “Female DNA”?

So, the latest development in the investigation of the Boston Marathon bombing is a report that the FBI has identified “female DNA” on the remains of at least one of the two bombs used by Dzhokhar and Tamerlan Tsarnaev in the attack. According to the report, published first in the Wall Street Journal, some genetic material has been recovered, and the FBI has gone to collect a DNA sample from Katherine Russell, the widow of Tamerlan Tsarnaev, presumably to see if it matches the DNA recovered from the bomb.

Here’s the thing. How does the FBI know, or think it knows, that it has recovered “Female DNA”? Well, there aren’t a lot of details available yet, but there are a couple of possibilities.

First, let’s start with the basic genetics. Humans normally have 46 chromosomes, which come in 23 pairs, as well as some mitochondrial DNA. From the mitochondrial DNA, and 22 of the 23 other chromosome pairs, there is nothing to tell you whether the DNA came from a male or a female. The genetic difference between males and females resides in that last chromosome pair, the sex chromosomes. At the sex chromosomes, women have two X chromosomes, while men have one X chromosome and one Y chromosome.

So, if you have a discrete source of your DNA sample, like a hair, you could do a couple of things. You could test it for the presence of Y-chromosome genetic material. If the DNA source was female, you should not find any. Of course, that requires basing your conclusion on a negative result (the absence of a Y chromosome), which is not ideal, since it is possible that you could miss the material for technical reasons (e.g., failure of a particular chemical reaction).

The real thing you would look for to indicate that you had DNA from a female is the presence of two different X chromosomes. That means you need to identify the DNA sequence on part of the X chromosome. You can do this by actually sequencing a region of the chromosome, but this is probably unnecessarily expensive. After all, the vast majority of sites on the chromosome are going to be identical, not just in the X chromosomes in your sample, but in every X chromosome in every human being in the world.

What you can do instead is use tools that focus on specific sites that are already known to be variable in the population. Maybe there’s a particular site where it is known that some people have a C in their DNA sequence, while other people have a G. (This is referred to as a “polymorphic” site.) You simply ask whether that site in your particular sample has a C or a G, while simultaneously asking the analogous question about thousands of other sites.

If your DNA sample came from a male, you might find that the answer is C, or G, or whatever, at a particular site. What the answer is is not as important as the fact that there will be a single answer. If your DNA sample comes from a woman, you should find that sometimes you have a mixture of C and G. Of course, at a given site, you could still get a single answer, say, G, if both of the woman’s X chromosomes had a G at this position. However, if you look at a whole bunch of sites, you should find that a decent number of them indicate a mixture of two sequences — revealing the presence of two distinct X chromosomes, and therefore, a female.

But what if you don’t have a discrete genetic sample, like a hair, to work from? There’s not a lot of detail in the original article, so we have to speculate a bit here. (I’ve reached out to the reporters from the original piece, to see if there was some genetics-dork-relevant information that did not make it into the article. I’ll post an update if and when I hear back.) It seems likely that the bombs would also have carried DNA from one or both of the Tsarnaev brothers. Thus it is possible that the DNA collected by the FBI could contain a mixture of cells from multiple different individuals — like, say, they swabbed all around the bomb’s remains to collect their samples. What would they need to do then?

Well, first of all, let’s consider the case where you had a mixture of the two brothers’ DNA. The Y chromosomes from Dzhokhar and Tamerlan would be (virtually) identical, having both been copied from single the Y chromosome of their father. The two would have distinct X chromosomes, each of which would be a patchwork of pieces copied from their mother’s two X chromosomes.

So, the X chromosomes present in this sort of sample would look similar in some ways to the X chromosomes you would get from a female DNA sample: there would be some polymorphic sites where you would find a mixture of DNA sequences in your sample. However, we would not expect to find as many of these mixed sites as in a sample from a female. On average, half of the X chromosome sequence inherited by one brother would be (virtually) identical to the sequence inherited by the other brother. Although, depending on how, exactly, recombination plays out, the identical fraction of their X chromosomes could range anywhere from nearly none to nearly all of it. It is possible, just by chance, that the X chromosomes inherited by Dzhokhar and Tamerlan would be as different from each other as the two X chromosomes present in their mother. Of course, at this point, DNA samples have almost certainly been collected from both brothers, so that investigators would know exactly what sequences to expect.

But what if there was an even messier mixture of DNA, say with samples from both brothers as well as one or more additional people? Well, at some point, the procedure of just looking for mixed sites in the DNA sequence is going to run into trouble. At most of these polymorphic sites, there are just two variants circulating at any frequency in the population. So, simply identifying sites that are polymorphic within your sample will let you distinguish between one X chromosome and more than one, but will not necessarily do a good job of telling you exactly how many different X chromosomes are present.

One approach to deal with this situation would be to look at a different type of polymorphism, one where there are more than two sequence variants present in the population. The polymorphisms most commonly used in this sort of context are short tandem repeats (STRs). These are stretches of DNA where a short sequence, maybe four or so nucleotides long, is repeated over and over again. Due to the nature of the process by which DNA is copied, these sequences are prone to a particular type of mutation, where the number of repeats increases or decreases. So, I might have a stretch of 19 copies of the sequence TCTA at a particular site in my genome, while you might have 23 copies of TCTA at the same location in your genome.

By looking at a whole bunch of these STR sites, the FBI could probably tell if the DNA they collected contained two, three, four, or more distinct X chromosomes. And, these are most likely the sorts of sites they will be using to see if the DNA collected from the bomb matches the DNA collected from Katherine Russell.

Although the focus of this post has been on genetics, and specifically what it means for the FBI to say that they recovered some “female DNA,” I would be remiss if I did not include the caveat (emphasized in the original WSJ article) that there are a lot of different ways that someone’s DNA might have gotten onto one of the bombs without that person having been involved in the bombing — even if that person winds up being Tamerlan Tsarnaev’s widow.

Two more from Fisher and Haldane

So, previously I introduced you to Darwin Eats Cake’s two newest characters, R. A. Fisher’s Pipe and J. B. S. Haldane’s Mustache. Well, the comedy duo have provided two more installations of their series, tentatively entitled, “Stuff Sitting in Jars on a Shelf, Talking.”

I would not necessarily have predicted this, but as it turns out, Fisher’s Pipe has a really juvenile sense of humor.

It’s sort of sad, really.

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Epigenetics and Homosexuality

So, last week featured a lot of news about a paper that came out in the Quarterly Review of Biology titled “Homsexuality as a Consequence of Epigenetically Canalized Sexual Development.” The authors were Bill Rice (UCSB), Urban Friberg (Uppsala U), and Sergey Gavrilets (U Tennessee). The paper got quite a bit of press. Unfortunately, most of that press was of pretty poor quality, badly misrepresenting the actual contents of the paper. (PDF available here.)

I’m going to walk through the paper’s argument, but if you don’t want to read the whole thing, here’s the tl;dr:

This paper presents a model. It is a theory paper. Any journalist who writes that the paper “shows” that homosexuality is caused by epigenetic inheritance from the opposite sex parent either 1) is invoking a very non-standard usage of the word “shows,” or 2) was too lazy to read the actual paper, and based their report on the press release put out by the National Institute for Mathematical and Biological Synthesis.

That’s not to say that this is a bad paper. In fact, it’s a very good paper. The authors integrate a lot of different information to come up with a plausible biological mechanism for epigenetic modifications to exert influence on sexual preference. They demonstrate that such a mechanism could be favored by natural selection under what seem to be biologically realistic conditions. Most importantly, they formulate their model into with clear predictions that can be empirically tested.

But those empirical tests have not been carried out yet. And, in biology, when we say that a paper shows that X causes Y, we generally mean that we have found an empirical correlation between X and Y, and that we have a mechanistic model that is well enough supported that we can infer causation from that correlation. This paper does not even show a correlation. It shows that it would probably be worth someone’s time to look for a particular correlation.

As a friend wrote to me in an e-mail,

I found it a much more interesting read than I thought I would from the press it’s getting, which now rivals the bullshit surrounding the ENCODE project for the most bullshitty bullshit spin of biology for the popular press. A long-winded-but-moderately-well-grounded-in-real-biology mathematical model does not proof make.


Okay, now the long version.

The Problem of Homosexuality

The first thing to remember is that when an evolutionary biologist talks about the “problem of homosexuality,” this does not imply that homosexuality is problematic. All it is saying is that a straightforward, naive application of evolutionary thinking would lead one to predict that homosexuality would not exist, or would be vanishingly rare. The fact that it does exist, and at appreciable frequency, poses a problem for the theory.

In fact, this is a good thing to keep in mind in general. The primary goal of evolutionary biology is to understand how things in the world came to be the way they are. If there is a disconnect between theory and the world, it is ALWAYS the theory that is wrong. (Actually, this is equally true for any science / social science.)

Simply put, heterosexual sex leads to children in a way that homosexual sex does not. So, all else being equal, people who are more attracted to the opposite sex will have more offspring than will people who are less attracted to the opposite sex.

[For rhetorical simplicity, I will refer specifically to “homosexuality” here, although the arguments described in the paper and in this post are intended to apply to the full spectrum of sexual orientation, and assume more of a Kinsey-scale type of continuum.]

The fact that a substantial fraction of people seem not at all to be attracted to the opposite sex suggests that all else is not equal.

Evolutionary explanations for homosexuality are basically efforts to discover what that “all else” is, and why it is not equal.

There are two broad classes of possible explanation.

One possibility is that there is no biological variation in the population for a predisposition towards homosexuality. Then, there would be nothing for selection to act on. Maybe the potential for sexual human brain simply has an inherent and uniform disposition. Variation in sexual preference would then be the result of environmental (including cultural) factors and/or random developmental variation.

This first class of explanation seems unlikely because there is, in fact, a substantial heritability to sexual orientation. For example, considering identical twins who were raised separately, if one twin is gay, there is a 20% chance that the other will be as well.

Evidence suggests that sexual orientation has a substantial heritable component. Image: Comic Blasphemy.

This points us towards the second class of explanation, which assumes that there is some sort of heritable genetic variation that influences sexual orientation. Given the presumably substantial reduction in reproductive output associated with a same-sex preference, these explanations typically aim to identify some direct or indirect benefit somehow associated with homosexuality that compensates for the reduced reproductive output.

One popular variant is the idea that homosexuals somehow increase the reproductive output of their siblings (e.g., by helping to raise their children). Or that homosexuality represents a deleterious side effect of selection for something else that is beneficial, like how getting one copy of the sickle-cell hemoglobin allele protects you from malaria, but getting two copies gives you sickle cell anemia.

It was some variant of this sort of idea that drove much of the research searching for “the gay gene” over the past couple of decades.  The things is, though, those searches have failed to come up with any reproducible candidate genes. This suggests that there must be something more complicated going on.

The Testosterone Epigenetic Canalization Theory

Sex-specific development depends on fetal exposure to androgens, like Testosterone and related compounds. This is simply illustrated by Figure 1A of the paper:

Figure 1A from the paper: a simplified picture of the “classical” view of sex differentiation. T represents testosterone, and E represent Estrogen.

SRY is the critical genetic element on the Y chromosome that triggers the fetus to go down the male developmental pathway, rather than the default female developmental pathway. They note that in the classical model of sex differentiation, androgen levels differ substantially between male and female fetuses.

The problem with the classical view, they rightly argue, is that androgen levels are not sufficient in and of themselves to account for sex differentiation. In fact, there is some overlap between the androgen levels between XX and XY fetuses. Yet, in the vast majority of cases, the XX fetuses with the highest androgen levels develop normal female genitalia, while the XY fetuses with the lowest androgen levels develop normal male genitalia. Thus, there must be at least one more part of the puzzle.

The key, they argue, is that tissues in XX and XY fetuses also show differential response to androgens. So, XX fetuses become female because they have lower androgen levels and they respond only weakly to those androgens. XY fetuses become male because they have higher androgen levels and they respond more strongly to those androgens.

This is illustrated in their Figure 1B:

Sex-specific development is thus canalized by some sort of mechanism that they refer to generically as “epi-marks.” That is, they imagine that there must be some epigenetic differences between XX and XY fetuses that encode differential sensitivity to Testosterone.

All of this seems well reasoned, and is supported by the review of a number of studies. It is worth noting, however, that we don’t, at the moment, know exactly which sex-specific epigenetic modifications these would be. One could come up with a reasonable list of candidate genes, and look for differential marks (such as DNA methylation or various histone modifications) in the vicinity of those genes. However, this forms part of the not-yet-done empirical work required to test this hypothesis, or, in the journalistic vernacular, “show” that this happens.

Leaky Epigenetics and Sex-Discordant Traits

Assuming for the moment that there exist various epigenetic marks that 1) differ between and XX and XY fetuses and 2) modulate androgen sensitivity. These marks would need to be established at some point early on in development, perhaps concurrent with the massive, genome-wide epigenetic reprogramming that occurs shortly after fertilization.

The theory formulated in the paper relies on two additional suppositions, both of which can be tested empirically (but, to reiterate, have not yet been).

The first supposition is that there are many of these canalizing epigenetic marks, and that they vary with respect to which sex-typical traits they canalize. So, some epigenetic marks would canalize gonad development. Other marks would canalize sexual orientation. (Others, they note, might canalize other traits, like gender identity, but this is not a critical part of the argument.)

The model presented in this paper suggests that various traits that are associated with sex differences may be controlled by distinct genetic elements, and that sex-typical expression of those traits may rely on epigenetic modifications of those genes. Image:

The second supposition is that the epigenetic reprogramming of these marks that normally happens every generation is somewhat leaky.

There are two large-scale rounds of epigenetic reprogramming that happen every generation. One occurs during gametogenesis (the production of eggs or sperm). The second happens shortly after fertilization. What we would expect is that any sex-specifc epigenetic marks would be removed during one of these phases (although it could happen at other times).

For example, a gene in a male might have male-typical epigenetic marks. But what happens if that male has a daughter? Well, normally, those marks would be removed during one of the reprogramming phases, and then female-typical epigenetic marks would be established at the site early in his daughter’s development.

The idea here is that sometimes this reprogramming does not happen. So, maybe the daughter inherits an allele with male-typical epigenetic marks. If the gene influences sexual orientation by modulating androgen sensitivity, then maybe the daughter develops the (male-typical) sexual preference for females. Similarly, a mother might pass on female-typical epigenetic marks to her son, and these might lead to his developing a (female-typical) sexual preference for males.

So, basically, in this model, homosexuality is a side effect of the epigenetic canalization of sex differences. Homosexuality itself is assumed to impose a fitness cost, but this cost is outweighed by the benefit of locking in sexual preference in those cases where reprogramming is successful (or unnecessary).

Sociological Concerns

Okay, if you ever took a gender-studies class, or anything like that, this study may be raising a red flag for you. After all, the model here is basically that some men are super manly, and sometimes their manliness leaks over into their daughters. This masculinizes them, which makes them lesbians. Likewise, gay men are gay because they were feminized by their mothers.

That might sound a bit fishy, like it is invoking stereotype-based reasoning, but I don’t think that would be a fair criticism. Nor do I think it raises any substantial concerns about the paper in terms of its methodology or its interpretation. (Of course, I could be wrong. If you have specific concerns, I would love to hear about them in the comments.) The whole idea behind the paper is to treat chromosomal sex, gonadal sex, and sexual orientation as separate traits that are empirically highly (but not perfectly) correlated. The aim is to understand the magnitude and nature of that empirical correlation.

The other issue that this raises is the possibility of determining the sexual orientation of your children, either by selecting gametes based on their epigenetics, or by reprogramming the epigenetic state of gametes or early embryos. This technology does not exist at the moment, but it is not unreasonable to imagine that it might exist within a generation. If this model is correct in its strongest form (in that the proposed mechanism fully accounts for variation in sexual preference), you could effectively choose the sexual orientation of each of your children.

Image: Brainless Tales.

This, of course, is not a criticism of the paper. The biology is what it is. It does raise certain ethical questions that we will have to grapple with at some point. (Programming of sexual orientation will be the subject of the next installment of the Genetical Book Review.)

Plausibility/Testability Check

The question one wants to ask of a paper like this is whether it is 1) biologically plausible, and 2) empirically testable. Basically, my read is yes and yes. The case for the existence of mechanisms of epigenetic canalization of sex differentiation seems quite strong. We know that some epigenetic marks seem to propagate across generations, evading the broad epigenetic reprogramming. We don’t understand this escape very well at the moment, but the assumptions here are certainly consistent with the current state of our knowledge. And, assuming some rate of escape, the model seems to work for plausible-sounding parameter values.

Testing is actually pretty straightforward (conceptually, if not technically). Ideally, empirical studies would look for sex-specific epigenetic modifications, and for variation in these modifications that correlate with variation in sexual preference. The authors note that one test that could be done in the short term would be to do comparative epigenetic profiling of the sperm of men with and without homosexual daughters.

As Opposed to What?

The conclusions reached by models in evolution are most strongly shaped by the set of alternatives that are considered in the model. That is, a model might find that a particular trait will be selectively favored, but this always needs to be interpreted in the context of that set of alternatives. Most importantly, one needs to ask if there are likely to be other evolutionarily accessible traits that have been excluded from the model, but would have changed the conclusions of the model if they had been included.

The big question here is the inherent leakiness of epigenetic reprogramming. A back-of-the-envelope calculation in the paper suggests that for this model to fully explain the occurrence of homosexuality (with a single gene controlling sexual preference), the rate of leakage would have to be quite high.

An apparent implication of the model is that there would then be strong selection to reduce the rate at which these epigenetic marks are passed from one generation to the next. In order for the model to work in its present form, there would need to be something preventing natural selection from finding this solution.

Possibilities for this something include some sort of mechanistic constraint (it’s just hard to build something that reprograms more efficiently than what we have) or some sort of time constraint (evolution has not had enough time to fix this). The authors seem to favor this second possibility, as they argue that the basis of sexual orientation in humans may be quite different from that in our closest relatives.

On the other hand this explanation could form a part of the explanation for homosexuality with much lower leakage rates.

What Happened with the Press?

So, how do we go from what was a really good paper to a slew of really bad articles? Well, I suspect that the culprit was this paragraph from the press release from NIMBios:

The study solves the evolutionary riddle of homosexuality, finding that “sexually antagonistic” epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring. The mathematical modeling demonstrates that genes coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring.

If you know that this is a pure theory paper, this is maybe not misleading. Maybe. But phrases like “solves the evolutionary riddle of homosexuality” and “finding that . . . epi-marks . . . cause homosexuality in opposite-sex offspring,” when interpreted in the standard way that I think an English speaker would interpret them, pretty strongly imply things about the paper that are just not true.

Rice, W., Friberg, U., & Gavrilets, S. (2012). Homosexuality as a Consequence of Epigenetically Canalized Sexual Development The Quarterly Review of Biology, 87 (4), 343-368 DOI: 10.1086/668167

Update: Also see this excellent post on the subject by Jeremy Yoder over at Nothing in Biology Makes Sense.

Two new characters at Darwin Eats Cake

So, if you’re a regular reader of Darwin Eats Cake, you’ll already know that two new characters have been introduced to the strip: R A Fisher’s Pipe and J B S Haldane’s Moustache.

If you’re not a regular reader, you should be, because it will make me happy (and it is, after all, the holiday season), and also because Robert Gonzales once called it “my [meaning Robert’s] new favorite webcomic” over at io9.

For those of you who are not population geneticists, or at least evolutionary biologists, Fisher and Haldane are two of the major figures of the “modern synthesis” in evolution in the first part of the twentieth century. This was basically the integration of the Mendelian idea of the gene with the Darwinian idea of gradual change via natural selection. Fisher, in addition, created a whole lot of modern statistics, which have found applications far outside of evolutionary biology.

R. A. Fisher smoking his pipe. Not a euphemism.
J. B. S. Haldane, um, I guess, having his mustache. Note the lack of “o” in the American spelling of mustache.

Fisher loved himself a good smoke. In fact, late in his life, he publicly challenged research purporting to show a causal link between smoking and lung cancer. Oops.

Haldane once chased my former officemate and his mother down the street in a rainstorm in Calcutta to offer them an umbrella.

These two anecdotes provide all the information you need to accurately reconstruct the political views of each.

Fisher passed away in 1962, and Haldane in 1964. Fortunately, one of the most salient features of each was preserved in a jar for posterity. And now, half a century later, the two have reunited to bring you their genetically inspired comedy stylings.

Here’s what you’ve missed so far:

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The Genetical Book Review: The Mapmaker and the Ghost

So, remember when not all kids books were about teenage wizards and sexy vampires? Well, it turns out that, if you know where to look, you can still find books like that. Enter The Mapmaker and the Ghost, by Sarvenaz Tash.

[Disclaimer: Sarv is a friend of my wife’s. They got to know each other through the fact that both are in the New York area, and both had their debut middle-grade novels come out this year. If you are concerned that this may color the objectivity of this review, may I refer you to the Genetical Book Review’s premise and guidelines.]

The Mapmaker and the Ghost is a story that I would say is of the same general flavor as something like From the Mixed-Up Files of Mrs. Basil E. Frankweiler. The setting is very much our world, and the adventure is on a human scale. In the Mixed-Up Files, a girl and her younger brother run off to the museum, and get caught up in a quest to discover the provenance of a statue. In Mapmaker, a girl (Goldenrod) and her younger brother (Birch) find adventure in the woods at the edge of town, and get caught up in a quest to find a legendary blue rose.

The Mapmaker and the Ghost, by Sarvenaz Tash. Want to buy it already?
Settle down there, sparky! Purchase links will be available at the bottom of the post.

For kids, I think, the human scale makes the story directly relatable to their own lives. At least, that seems to be one of the things that our kid loved about the book. (He was nine at the time he first read it, and has reread it multiple times.) The concerns that the characters have, about curfews and money and permission to go past a certain point in the street, etc., seem to resonate with the experience of childhood in a way that very few authors pull off.

Of course, as in any good adventure, there are exciting things that happen that go well beyond what most children actually experience. But those events have an emotional impact that derives from the realism of the novel. I mean, saving the world from the most evil villain of all time is, of course, exciting, but evading the gaze of a security guard can actually be even more emotionally tense and exhilarating, because it is a situation that a young reader can really embody.

Also, there’s a gang of semi-feral kids with names like “spitbubble” and “snotshot,” a mysterious old lady, a secret lair, and, of course, a ghost.

The book is appropriate for ages 7 through probably about 12. The main character is a girl, but the novel is strongly gendered, and will be engaging for boys and girls. (If you have a son who thinks that they should not read a book like this because it is about a girl, you should definitely buy it, thump him over the head with it, and then watch him enjoy it anyway.)

Now, on with the science!

As I mentioned, the central quest in the novel is the search for a blue rose that blooms in the woods at the edge of town once every fifty years. This is a big deal, because, you know, roses aren’t blue. When you find a rose that is actually blue, it’s blue because it has been dyed blue.

A few years ago, a Japanese company called Suntory made news when they produced the world’s first non-dyed blue rose. They managed this through genetic engineering, taking a gene from a pansy and inserting it into a rose. [Insert juvenile and inappropriate joke here.]

Now, you’re probably looking at this rose and thinking that you have to be pretty colorblind (or have a job in Suntory’s marketing division) to call this “blue.” Fair enough, but, that’s the state of the art at the moment.

Suntory’s “blue” rose, which, while lilac a best, is still pretty cool. As an aside, we could also interpret this as an example of what linguists call “collocational restriction,” where the term “blue” has an idiomatic meaning in the specific context of the phrase “blue rose.” In this case, it might be interpreted as “bluer than a rose normally is,” much as “white coffee” is not actually white, but is at the white end of the distribution of coffee colors. (Image via Wired)

Here is Figure 1 from the publication of Suntory’s work, which shows the biosynthetic pathways responsible for plant color. You don’t find blue roses in nature because roses lack an enzyme in the pathway on the far right, which means that they lack any delphinidin-based anthocyanins.

Anthocyanins are the primary chemicals responsible for 

The gene that the researchers inserted into the rose is the one indicated by F3’5’H in the figure. This enzyme (flavonoid 3′,5′-hydroxylase) is normally absent from roses, which is why they lack the bluish pigments.

Although only one blue rose cultivar has been brought to market (The Suntory “Applause” pictured above), they actually did the transformation with a bunch of different cultivars. Here are a few examples (from the same paper).

In each panel, the flowers on the left are without the F3’5’H gene, and the ones on the right are with it.

If you read Japanese (or trust Google Translate), you can check out more information at Suntory’s dedicated blue-rose webpage, which features topics such as “Legend,” “Brand Concept,” and “Applause Wedding” (new!).

The authors note that there are various things one could imagine doing to make roses even bluer, including tinkering with the pH, getting other pigments in there, etc. How easy these next steps are going to be is less clear, though. It’s hard to tinker without breaking stuff. Perhaps genuinely blue roses will continue to be the symbol of unattainability, and limited to great kids’ books.

Katsumoto, Y., Fukuchi-Mizutani, M., Fukui, Y., Burgliera, F., Holton, T. A., Karan, M., Nakamura, N., Yonekura-Sakakibara, K., Togami, J., Pigeaire, A., Tao, G.-Q., Nehra, N. S., Lu, C.-Y., Dyson, B. K., Tsuda, S., Ashikari, T., Kusumi, T., Mason, J. G., & Tanaka, Y. (2007). Engineering of the Rose Flavonoid Biosynthetic Pathway Successfully Generated Blue-Hued Flowers Accumulating Delphinidin Plant Cell Physiol., 48 (11), 1589-1600 DOI: 10.1093/pcp/pcm131


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Post-copulatory female choice in crickets and Missouri

So, maybe you’ve seen the news today about Representative Todd Akin. He’s the republican nominee for Senate in Missouri, running this year against Claire McCaskill. In an interview he said that he opposed abortion in all circumstances, with no exception for rape, because rape does not lead to pregnancy, see, because, “If it’s a legitimate rape, the female body has ways to try to shut that whole thing down.” (Quotes on Jezebel, video here.)

After realizing that he sounded like a complete shithead, even for a contemporary Republican (and probably after receiving a scolding from national Republicans), he issued a statement in which he claims that he “misspoke,” which is politician speak for, “I accidentally said what I actually thought, and then discovered that it will negatively impact my election chances, so I’m going to lie now. No backsies!”

Although, to be fair to Akin, nowhere in his statement did he back down from the position that abortion should be outlawed without exception, merely that he would advocate for “justice.” Also, jobs!

Setting aside for the moment the woeful state of politics, is it true, or even possible, that the female body could have “ways to try to shut that whole thing down”?

Actually, in a lot of non-human animals, something sort of like that does exist.

In species where polyandry (where females mate with multiple males) is common, there is often competition for reproductive access both before and after copulation, where one male may participate in a larger share of a female’s reproduction. In many cases, this is going to be something like sperm competition, where differential reproductive success depends on traits associated with the sperm, and by extension, with the competing males. This is not really what we’re talking about, though.

In a few cases, you can actually get “post-copulatory female choice,” where it is clearly the female deciding whether or not to allow fertilization. One such set of cases occurs in some spiders and crickets, where the male transfers a spermatophore to the female. This is basically a bag full of sperm that is attached to the female during copulation. She may then modulate the success of the sperm through the amount of time she permits it to remain attached to her.

For example, here‘s a paper on field crickets that shows not only that females modulate spermatophore retention time in response to male song quality, but that this modulation is contingent on the female’s prior experience. This is important because it emphasizes the aspect of female choice.

But what about humans? Well, actually, yes. Human females have the capacity to engage in post-copulatory female choice, such that they do not necessarily have to give birth to their rapist’s child. It’s called safe, legal abortion. It still exists in this country, but if too many more Todd Akins get elected, the American female body will no longer have “ways to try to shut that whole thing down.”

Rebar, D., Zuk, M., & Bailey, N. W. (2011). Mating experience in field crickets modifies pre- and postcopulatory female choice in parallel Behavioral Ecology, 22, 303-309

The selfish herd

So, one of the most interesting questions in evolutionary biology is the origin of collective behaviors. This can be the complex division of labor that we see in social insects and human societies, flocking behavior in migratory birds, or microbial formation of biofilms. It can be predators engaging in collective hunting, or prey engaging in collective being hunted. It’s this last one that we’re going to be talking about today.

As with many questions in evolutionary biology, there are a couple of dimensions that people are interested in untangling: proximal and ultimate causation. Proximal explanations focus on the “how” part of the solution, as in, “what are the molecular, genetic, etc. mechanisms and environmental cues that result in this behavior?” Ultimate explanations focus on “why,” in the evolutionary sense of “what were the selective pressures that led to the evolution of this behavior?”

Herding or flocking behavior is a classic case. For example, why do sheep hang out in a big group, in contrast to say, leopards, which tend to be pretty solitary? There are a number of possible (and not mutually exclusive) ultimate explanations, but the most talked about one is probably defense against predators.

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Back in the mid-twentieth century, it was common for biologists to talk in fairly loose terms about collective behaviors having evolved as a result of their benefits to the group. Then, in 1966, G. C. Williams published Adaptation and Natural Selection, which dropped a lot of truth into the community. In particular, it emphasized the gene-centered view of natural selection that hit the public consciousness with Richard Dawkins’s 1976 book, The Selfish Gene, and which has remained the dominant paradigm in evolutionary biology ever since.

Williams demonstrated that group selection, while possible, will generally be a much weaker force than selection acting on the individual. Therefore, it is good practice to look for evolutionary explanations at this lower level. Given plausible adaptive stories at the individual and group levels, one should favor the individual-level story. While the two stories might not be mutually exclusive, individual-level selective pressures are more likely to have played an important role in  the evolution of any particular trait than group-level selective pressures (all else being equal, of course).

In 1971, W. D. Hamilton published a theoretical analysis that brought this individual-level perspective to herding behavior. Hamilton argued that all you need is for animals to be trying to evade predators as individuals. If there are other individuals of their type around, they just need to try to position themselves between other individuals. Here’s how Hamilton draws it:

This frog wants to position itself between the two frogs on the right. That way, when the sea snake comes up, it will eat one of the frogs at the edge, and the one in the middle will be safe.

All you need is for everyone to follow one simple rule: when a predator comes, position yourself between two other individuals. What you get then is a tight cluster of individuals.

You can actually try this at home. You probably need about eight or ten people. So, most of you might not be able to try this at home, but you could maybe try it at school or work. Have each person pick two other people in the group (but don’t tell who your picks are). Then, everyone tries to get between the two people they picked. What you’ll get is something a lot like a cluster of frogs climbing all over each other to get away from a sea snake.

Frogs maneuvering to get between other frogs results in the formation of a clusterf**k of frogs. I know, right? I was surprised, too, but my herpetologist friends assure me that “clusterf**k” is the official collective noun for a group of frogs. Don’t even ask about sea snakes. You don’t want to know.

Bonus activity: after you’ve disentangled yourselves from the frogpile, try this one. Each person picks two people again, labeling them “A” and “B” (in your head). Again, no one needs to say whom they picked. Now, each person should position themselves so that their “A” person is between them and their “B” person. If it helps, imagine that “A” is Mitt Romney, that “B” is the American People, and you are Mitt’s tax returns. Your job is to position yourself so that Mitt keeps the American People from seeing you. I won’t spoil how it comes out.

So, Hamilton’s model provides a nice, simple model that can produce the observed behavior. The model is attractive because (1) it requires selection only at the level of the individual, and (2) it requires each individual only to follow a very simple behavioral rule. The collective behavior is an emergent property requiring no coordination at the group level.

Now, there’s a new paper out that is attempting to look at this empirically, in sheep. The study involves strapping adorable GPS backpacks on a bunch of sheep (Figure 1c, below) and then letting a sheepdog chase them around.

You can look at the movies here. It’s only a brief communication, and does not really nail anything down, but the authors interpret their results as broadly consistent with the selfish herd model. In particular, they are able to see that individual sheep seem to be trying to get to the center of the flock.

The cool thing is more the potential for this type of experiment. Yes, Hamilton’s model is attractive and parsimonious, but if we want to understand the rules that actually govern the behavior of sheep when they are faced with a predator (or, in this case, an annoyator), we will need to get good quantitative data on individual behaviors in a variety of contexts.

Plus, look at that little GPS backpack!

I’ll leave you with this.

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King AJ, Wilson AM, Wilshin SD, Lowe J, Haddadi H, Hailes S, & Morton AJ (2012). Selfish-herd behaviour of sheep under threat. Current biology : CB, 22 (14) PMID: 22835787

Hamilton, W. D. (1971). Geometry for the Selfish Herd Journal of Theoretical Biology, 31, 295-311 DOI: 10.1016/0022-5193(71)90189-5