Comics and convergent evolution in trees

Here’s a recent xkcd strip called “Magic tree”, which has an evolutionary twist:

magic_tree

When you “mouse over” the strip, you see this:

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In other words, artist Randall Munroe is giving a humorous example of “convergent evolution,” in which those trees that most closely resemble cellphone towers are those that leave their genes. This form of evolution would, over time, produce trees that resemble those towers. This example is bogus, of course, because a tree generation lasts a long time—longer than cellphone towers have been around. But if you want to read about real examples of convergent evolution, try the Wikipedia article or Eric Pianka’s nice essay at the University of Texas zoology website.

In WEIT I briefly discuss convergent evolution, giving the famous example of convergence between species of placental mammals and marsupials in Australia. I also give an example from plants: the strong resemblance between cacti in the New World and euphorbs in the old.

But there are also examples in which non-treelike plants have, similar to the example above, evolved to resemble trees. I’ll leave readers to hunt for those, but put your answers in the comments below.

h/t: Steve, John

Will Provine died

I’m saddened to report that historian of science and population geneticist Will Provine, a professor at Cornell, died on September 1 at 73.  His wife has posted an unbearably sad memoriam on her Facebook page, and Casey Bergman, one of our Chicago Ph.D. students and now a professor at Manchester, reported the news on his website An Assembly of Fragments.

Will was a student of my own Ph.D. advisor, Dick Lewontin—Dick’s first student who was a historian rather than a working scientist. (Dick went on to work with and mentor many other students of the history and philosophy of science.) Will’s Ph.D. thesis became a short book, The Origins of Theoretical Population Genetics (1971), that was (and remains) essential reading for students in population genetics.

Will was a delightful guy, but those who knew him quickly learned that he pulled no punches. He was, as they say, “strident”: strident about creationism and intelligent design, which he detested, strident about religion (he was a diehard atheist, although, as I recall, his father was a preacher), and strident in his later-life opposition to genetic drift, which he viewed—erroneously, I think—as a misguided concept. Religionists often quoted with disdain his remark about the incompatibility of science and religion, “You have to check your brains at the church-house door if you take modern evolutionary biology seriously.”

But opinionated as he was, he was a pleasure to talk to, ever friendly and helpful. As Casey wrote on his site:

I’m moved by his death to recall my experience of having Provine as a lecturer during my undergrad days at Cornell 20 years ago, where his dramatic and entertaining style drew me fully into evolutionary biology, both as a philosophy and as a profession. I can’t say I knew Provine well, but I can say our interactions left a deep impression on me.  He was an incredibly kind and engaging, pulling you onto what he called the “slippery slope” where religious belief must yield to rationalism.

And that is my impression, too.

A long time ago Will developed brain cancer—a glioma, as I recall, which is a deadly form of the disease. He spoke openly about it and gave the impression that he didn’t have long to live. But he beat the odds, and must have survived for at least 15 or 20 years after diagnosis.

I remember that when we held a retirement symposium for Dick Lewontin at Harvard, Will gave the opening talk, and was wearing on each side of his head a metal disk with a target on it—a target for the radiation therapy aimed at his tumor. At that time we thought he would die soon, and that, combined with his deeply moving tribute to Lewontin, brought many of us to tears. It was the only time in my life that I saw Dick in tears as well: he had to put his head in his hands.

But it is a great mercy that Will lived so long after that talk—which was years ago—and remained active to the last. I, and many others, will miss him.

William-Provine

                                           Will Provine (1943-2015)

On the poor reproducibility of psychology studies

I wrote a short post yesterday about a huge attempt to answer the question, “What proportion of results reported in psychology journals can be repeated?” This was a massive study in which dozens of psychology researchers simply went and repeated 100 studies published in three respectable experimental psychology journals: Psychological Science, Journal of Personality and Social Psychology, and Journal of Experimental Psychology: Learning, Memory, and Cognition.  The full paper, along with a one page summary, is published in Science (see reference and free download below); the authors call themselves the “Open Science Collaboration” (OSC). There’s also a summary piece in the New York Times, a sub-article highlighting three famous studies that couldn’t be repeated by OSC (including one on free will, which I wrote about yesterday), and a newer op-ed in the Times arguing that this failure to replicate doesn’t constitute a scientific crisis, but simply shows science behaving as it should: always scrutinizing whether published results are reliable.

Even before this paper was published, I argued that people should do in biology what these folks did in psychology: test experimental results that are impressive but rarely repeated. In psychology, as in evolutionary biology and ecology, significant findings aren’t often repeated, for doing so takes hard-to-come-by money and a concerted effort— an effort that isn’t rewarded. (You don’t get much naches or professional advancement by simply repeating someone else’s work.) Further, in biology (and presumably in experimental psychology), work isn’t often repeated as the normal by-product of building on previous results. For example, if you want to use new gene-replacement methods, you are obliged to indirectly replicate other people’s protocols before you can begin to insert your own favorite gene.

It’s thus been my contention that about half of published studies in my own field (I include ecology along with evolution) would probably not yield the same results if they were replicated. I’m excluding those studies that use genetics, as genetic work is easily repeated, particularly if it involves sequencing DNA.

Failures to repeat a published result don’t mean that the experimenters cheated, or even that the work was faulty. They could mean, for instance, that the results are peculiar to a particular location, time, or experimental setup, or that there’s a publication bias towards impressive results, so only the ones whose results are highly statistically significant get published. Finally, given the conventional probability ceiling of 0.05, 5% of all experiments will yield a significant deviation from chance (thus falsifying the null hypothesis), even when that null hypothesis is true.

On to the experiment. The OSC decided to finally test reproducibility in a quite rigorous way. A whole group of people agreed to test a passel of papers taken from three journals, winding up with 100 replicated experiments. To enforce rigor, they chose papers from only prominent journals (they wound up with exactly 100 replicates), replicated only the last study in each paper (so that they weren’t just replicating preliminary results, which are often reported first), and then did each replication, as far as they could, in an identical way as the initial study—with the exception that sometimes they had higher sample sizes, giving them even greater power to detect effects.

To the credit of the original authors, they provided the OSC team with complete data and details of their experiments, ensuring that the replications were as close as possible in design to the original results. There were many other controls as well, including the use of statisticians to independently replicate the probability values for the replication experiments.

All the original studies had results that were statistically significant, with p values (i.e., the chance of getting the observed effect as a mere statistical outlier when there was no real effect) below 5% (a few were just a tad higher). When the chance of getting a false positive is 0.05 or less, researchers generally consider the result “statistically significant,” which is a key to getting your paper published. That cutoff, of course, is arbitrary, and is lower in areas like physics, which, for experiments like detecting the Higgs boson, drops to 0.00001.

So what happened when those 100 psychology studies were replicated? The upshot was that most of the significant results became nonsignificant, and the effects that were found, even if nonsignificant, dropped to about half the size of effects reported in the original papers. Here are the salient results:

  • Only 35 of the original 100 experiments produced statistically significant results upon replication (62 did not, and three were excluded). In other words, under replication with near-identical conditions and often larger samples, only 35% of the original findings were judged significant.
  • That said, many (but not nearly all) of the results were in the same direction as those seen in the original studies, but weren’t large enough to achieve statistical significance. If the replications had been the original papers, most of them probably wouldn’t have been published.

Here’s a chart showing the correlation between the p values for the original papers and those for the replicates. Each dot plots the size of the effect seen in the replicate (Y axis) against the effect size for the same study in the original paper (X axis).  If a dot is green, the replicate was also statistically significant (as were all effects in the original study). Pink dots mean that the replicate study did not yield statistically significant results. This shows that effect sizes were generally lower than those of the original studies (most points fall below the diagonal line), and most of the replicates (62%, to be precise) did not show significant effects.

F1.large

(From the paper): Original study effect size versus replication effect size (correlation coefficients). Diagonal line represents replication effect size equal to original effect size. Dotted line represents replication effect size of 0. Points below the dotted line were effects in the opposite direction of the original. Density plots are separated by significant (blue) and nonsignificant (red) effects.

The chart also shows that the larger the effects observed in the original study, the more likely they were to replicate, for the pink dots are clustered on the left side of the graph, where the original effect sizes (normalized) are small. This goes along with the investigators’ findings that the lower the p value seen in the original experiment, and thus the more significant the result, the more likely it was to also be significant in the replicate.

  • While most of the results of replications were in the same direction as the original study, there were an appreciable number (I count about 20%) that were close to showing either the opposite direction or no effect at all. And remember, even if there is no real biological effect in the original study, half of the replications will, by chance alone, be in the same direction as in the original study.
  • The OSC team also asked each team doing a replication whether they considered that their results actually replicated that of the orignal paper. This assessment was subjective, but mirrored the results based on p-value significance: only 39% of investigators concluded that their results replicated those of the original study.
  • Finally, it’s possible that many of the p values in replications came close to the magic p = 0.05 cutoff point, which of course is more or less an arbitrary threshold for significance. To see if that was the case, the authors did a density plot of p values in the original paper versus those found in the repicates. Here are the results, with p values from original studies on the left and from the replicates on the right.
Screen Shot 2015-09-02 at 12.18.58 PM

Density plots of original and replication P values and effect sizes. P values.

As you can see, the p values for replications were distributed widely, and so were not hovering somewhere near the magic cutoff value for significance (0.05). Of course, all the p values in the original studies (left) were at or below that level of significance, or they wouldn’t have been published.

What does it all mean?

There are two diametric views about how to take this general failure to replicate. The first is to celebrate this as a victory for science. After all, science is about continually testing its own conclusions, and you can only do that by trying to see if what other people found out is really right. This, in fact, is the conclusion the authors come to. I quote from their paper:

Scientific progress is a cumulative process of uncertainty reduction that can only succeed if science itself remains the greatest skeptic of its explanatory claims.

The present results suggest that there is room to improve reproducibility in psychology. Any temptation to interpret these results as a defeat for psychology, or science more generally, must contend with the fact that this project demonstrates science behaving as it should. Hypotheses abound that the present culture in science may be negatively affecting the reproducibility of findings. An ideological response would discount the arguments, discredit the sources, and proceed merrily along. The scientific process is not ideological. Science does not always provide comfort for what we wish to be; it confronts us with what is. Moreover, as illustrated by the Transparency and Openness Promotion (TOP) Guidelines, the research community is taking action already to improve the quality and credibility of the scientific literature.

We conducted this project because we care deeply about the health of our discipline and believe in its promise for accumulating knowledge about human behavior that can advance the quality of the human condition. Reproducibility is central to that aim. Accumulating evidence is the scientific community’s method of self-correction and is the best available option for achieving that ultimate goal: truth.

There’s a lot of sense in this, of course. A result isn’t widely accepted (in most fields) unless it’s repeated or makes firm predictions that can be tested. Self-correction is a powerful too—one of the most important characteristics of science, and one that makes it different from, say, theology.

The “all is well in science” interpretation is also that pushed by Lisa Feldman Barrett in her new NYT op-ed about the study, “Psychology is not in crisis.” (Barrett is a professor of psychology at Northeastern University.) But her piece is a mess, comparing failure of psychology-study replication to changing the environment in which a gene is expressed. In some environments, she says, a gene producing curly wings makes the wings less curly, a common phenomenon that we geneticists call “variable expressivity”. And that’s indeed the case, but it doesn’t meant that the “Curly” mutation doesn’t cause the wings to become curled—something she implies. Variable expressivity is not a failure to replicate the finding that a particular genic lesion is responsible for curly wings.

Barrett also compares the OSC study’s failure to replicate to other studies in which failure to replicate depends on “context” (e.g., mice given shocks at when they hear a sound develop a Pavlovian response), so that one doesn’t see the same results under different conditions (mice won’t develop the Pavlovian response if they’re strapped down when shocked). But that, like the curly-wing result, is irrelevant to the OSC’s efforts, which tried ensure that the context and experimental conditions were as close as possible to those of the original studies.  In other words, the OSC tried to eliminate context-specific effects.  In Barrett’s eagerness to defend and exculpate her field, and affirm the strength of science, she makes arguments based on false analogies.

One thing that we can all agree on—the middle ground, so to speak—is that there’s a problem with the culture of science, which always favors big and impressive positive results over negative results, and favor publication of novel results while largely ignoring attempts to replicate. (Sometimes a failure to replicate isn’t even accepted by scientific journals!) That’s even more true of the popular press, which is quick to tout findings of stuff like a “gay gene,” but can’t be bothered to publish a caveat when that study—as it was—failed to replicate.  This problem, at least in the scientific culture, can be somewhat repaired. Most important, we need more studies like that of the OSC, but replications applied to other fields, especially biology.

And that brings me to my final point, which gives a less positive view of the results. As I said above, I think many studies in biology—particularly organismal biology—aren’t often replicated, especially if they involve field work. So such studies remain in the literature without ever having been checked, and often become iconic work that finds its way into textbooks.

In this way biology resembles psychology, although molecular and cell biology studies are often replicated as part of the continuing progress of the field.  I think, then, that it’s not as kosher to claim that ecology and evolution experience the same degree of self-checking as, say, physics and chemistry. Yes, all work should in principle be checked, but you find precious few dollars handed out by the National Institutes of Health or the National Science Foundation to replicate work in biology. (That’s because there isn’t that much money to hand out at all!) In my field of organismal biology, then, the self-correcting mechanism of science, while operative at some level, isn’t nearly as strong as it is in other fields like molecular and cell biology.

My main conclusion, then, is that we need an OSC for ecology and evolutionary biology. But it will be a cold day in July (in Arizona) when that happens!
_______

Open Science Collaboration. 2015. Estimating the reproducibility of psychological science. Science, 349 online, DOI: 10.1126/science.aac4716

The marine toad

by Greg Mayer

Jerry had us spot the toad a few posts ago (I earlier posted an easier ‘spot the frog‘), and in the comments some readers mentioned the marine toad, Bufo (Rhinella) marinus, also known as the cane toad (especially in Australia) or the giant toad. This species, native from south Texas to central Brazil, has been widely introduced in the West Indies (including Bermuda), Florida, Australia, and the Pacific islands. They were introduced primarily as a way to control a beetle which attacked sugar cane; the toads were not very good at this, and have had negative effects on more desirable faunal elements in some places.

Adult female Bufo (Rhinella) marinus, in 2012; origianlly collected on Bermuda, 1999.

Adult female Bufo (Rhinella) marinus, in 2012 in my back yard (Racine, Wisconsin); originally collected on Bermuda, 1999.

The above is my pet female, collected for me during a visit to Bermuda in 1999 by Bermuda’s foremost naturalist and conservationist, David Wingate. He has succeeded in eliminating the toads from Nonsuch Island, a preserve where the restoration of Bermuda’s indigenous fauna and flora is being promoted, with considerable success. She is fairly large, being 165 mm snout-vent length; unfortunately, I did not measure her when I first got her, but she was adult-sized at the time. The largest one I have ever found myself was a 178 mm one in Nicaragua. They get up to around 250 mm; the largest ones are said to be from the Guianas. A rather large preserved individual at the Museum of Comparative Zoology is about 230 mm long, and has long resided in a large Agassiz jar on the coffee table in the herpetology department.

In addition to being large, she’s getting old. I had thought she must be a record, but found that ages up to 25 years have been reported. “Toady” must be at least 17, perhaps a bit more, so she’s got a few years to go. Her only sign of aging is a cataract-like opacity in her right eye, which does not seem to have interfered with her ability to spot prey.

Notice the very large parotoid gland behind her ear; these secrete a milky poison when the toad is stressed, and I have been told that d*gs, not being terribly bright, have been sickened and even killed by attempting to ingest the toads. In South America, carnivorous mammals are said to flip the toads over, and eat them from the belly side, where the skin does not contain toxins (or at least not as much). When being defensive, Toady angles her back toward the unwanted stimulus. The best overall guide to the biology of these toads is still “The Marine Toad, Bufo marinus: a natural history resume of native populations” by my friend and mentor, George Zug, and his wife Pat.


Easteal, S. 1981. The history of introductions of Bufo marinus (Amphibia: Anura); a natural experiment in evolution. Biological Journal of the Linnean Society 16:93-113. abstract

Slade, R.W. and C. Moritz. 1988. Phylogeography of Bufo marinus from its natural and introduced ranges. Proceedings of the Royal Society of London B 265:769-777.  pdf

Wingate, D.B. 2011. The successful elimination of Cane toads, Bufo marinus, from an island with breeding habitat off Bermuda. Biological Invasions 13:1487-1492.  abstract

Zug, G.R. and P. B. Zug. 1979. The marine toad, Bufo marinus: a natural history resume of native populations. Smithsonian Contributions to Zoology 284, 58 pp.   pdf

Readers’ wildlife photographs

This is the second dollop of reader/photographer Colin Franks‘s delivery of a batch of lovely bird photos (Colin’s Facebook page is here). I’ll put up the third and final installment in two days or so.

Cinnamon Teal (male), Anas cyanoptera:

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White-crowned Sparrow, Zonotrichia leucophrys:

7D__4054

Savannah Sparrow, Passerculus sandwichensis: 

7D__4101

Great Blue Heron, Ardea herodias:

7D__4360

Canada gooseBranta canadensis:

7D__4465

Pileated Woodpeckers (babies), Hylatomus pileatus:

7D__4516

 

Thursday: Hili dialogue (with Cyrus and Cleo lagniappe)

It’s Thursday, and predicted to be another high of around 90 degrees F in Chicago, with perhaps some thunderstorms late in the day, which might cool things off. Summer is hanging on tenaciously. My hunt for crayfish unwisely leaving their pond has come up empty, so I haven’t had to perform emergency pond re-insertion. Meanwhile in Dobryzyn, Hili is having problems dealing with the world.

Hili: Don’t you think that all this is very complicated?
A: No, I don’t, but it’s not simple.
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In Polish:
Hili: Czy nie myślisz, że to wszystko jest bardziej skomplikowane?
Ja: Nie sądzę, ale proste nie jest.
And lagniappe #1: Cyrus and Andrzej sharing a quiet moment in the evening:
11950251_10206977436021685_4909791062550785180_o
And, as an extra treat, Joyce Carol Oates sends an update on Cleopatra in her new Forever Home:
Cleopatra has commandeered the most comfortable chair in the study.  nap time now.
photo
Look at that spotted belly! Don’t you just want to rub it?

 

Eagle 1, Drone 0

An Australian eagle (who was apparently unhurt) takes down a drone. Click on the icon at lower right if you want sound.

Credit: Melbourne Aerial Video

Did you spot the frog?

It wasn’t all that hard—especially compared to those infernal nightjars. Here’s the frog (or toad), conveniently marked with an arrow by reader Amy, who took the picture:

frog-arrow

 

Spot the frog!

Well, nobody’s interested in science today, I see. I could post on internet drama, but I’m revolted at such a tactic. Instead we’ll have a “spot the beast” contest.

Reader Amy contributed a “spot the frog” photo. I’ll put the answer up in a few hours. Her note:

My d*g was barking at something and it took me a moment to find that it was a frog. (And yes I realize it might be a toad but that’s not alliterative!)
So can you spot the frog/toad?
frog1

A gynandromorph moth comes to the light – and tells a story about science

by Matthew Cobb

This tw**t popped up in my feed the other night, from “wildlife illustrator and invertebrate enthusiast” Richard Lewington [Richard has a website showing his art here]. Richard was running a moth trap in the night when he found this beauty:

If you look carefully, you can just see the male’s feathery antenna on the left; the female side presumably had a straighter antenna (these different shapes relate to the different functions – males have to detect female pheromones from far away; females primarily need to be able to detect food plants on which to lay their eggs). You can see this clearly in another example Richard tw**ted:

Gynandromorphs are mixtures of male and female, often occurring because of a developmental problem – we highlighted the potentially gynandromorph cardinal bird here three years ago. There is a link between birds and moths, in that both groups have an unusual form of sex determination. In mammals, females have identical sex chromosomes (XX) while males have one X and one Y chromosome – they can produce two kinds of gametes (X and Y sperm) and so are called the heterogametic sex. For reasons that are unclear, in birds and lepidoptera (moths and butterflies),  females are the heterogametic sex (to avoid confusion, their sex chromosomes are called Z and W; males in both groups are ZZ).

It seems probable that these moths are gynandromorphs because, at a very early stage of development – probably when a fertilised female ZW egg divided into two cells – one of the daughter cells ‘lost’ the W chromosome because of some glitch. The tissues that were produced by that cell were therefore ‘ZO’ – you need the W chromosome to be female, so the tissues became male. The sharp dividing line down the middle of the moths, and the ‘mirroring’ of sexually dimorphic external structures on either side reinforces this intepretration.

There are many examples of gynandromorph lepidoptera on Google, which is probably a combination of people’s interest in these insects and the striking sexual dimorphism that exists in many species, making it easier to spot:

Image taken from here.

Here’s a photo of a gynandromorph gypsy moth, clearly showing the different shaped antennae (the male side is on the right):

Image taken from Jerry’s colleague Greg Dwyer.

As Jerry pointed out in his original cardinal post, those of us who work on the fly Drosophila (which, like us, has XX females and XY males) would occasionally see gynandromorphs in our stocks, although unless you are doing some funky genetics with sex-linked eye- or body-colour, male and female flies are not as different as the examples of the moths seen above. However, I do recall finding an apparently female fly with a male foreleg (male forelegs have ‘sex combs’ that are involved in sexual behaviour). Jerry’s explanation bears repeating:

In flies the sex is determined by the ratio of X chromosome to autosomes.  Flies, like all diploid species, have two copies of every autosome. If you also have two X chromosomes, you’re a female because the ratio of autosomes to Xs is 1:1. If you have one X chromosome and one Y chromosome, your ratio is 2:1 and you’re male.  The Y doesn’t matter here: if you lose a Y chromosome, and hence are XO, you still look like a male, although you’re sterile (the Y carries genes for making sperm).

So to get gynandromorphs in flies, all that has to happen is that one X chromosome gets lost in one cell when the initial cell in a female (XX) zygotes divides in two.  One half of the fly then becomes XX, the other XO, and the fly is split neatly down the middle, looking like the one below.  But gynandromorphs don’t have to be “half and halfs”.  X chromosomes can get lost at almost any stage at development, so flies can be a quarter male, have irregular patches of maleness, have just a few male cells, or even a male patch as small as a single bristle.

Way back in the day (i.e., 1970s), making mosaic flies in which different patches of tissue are either male or female was the only tool we had for identifying which tissues were involved in controlling various behaviours. This was fastidious work pioneered by one of the greats of post-war science, the physicist-turned-molecular-geneticist-turned-behaviour-geneticist, Seymour Benzer. [JAC: see my mini-post at bottom in which I used these methods for another purpose.]

Along with Yoshiki Hotta, Benzer was able not only to show tissue-level genetic control of behaviour, but also to show where in the embryo those tissues were determined, thereby constructing what he called a fate map of the action of a particular mutation. They adapted this technique from one of the founders of genetics, Arthur Sturtevant, who originally proposed it in 1929.

Here are some figures from Hotta and Benzer’s 1972 paper in Nature: ‘Mapping of behavior in Drosophila mosaics’. The first shows the range of mosaics that they produced – they were much more varied than the naturally occurring gynandromorphs because of the way they manipulated a special kind of X-chromosome in these flies, called a ring-X chromosome (known as X-R). This X-R chromosome could be lost at varying times in development, changing tissues from female (XX-R) to male (XO). The later the chromosome was lost, the more specific the tissues that would be male. By using a body-colour mutation on the X-chromosome, Hotta and Benzer could track from the outside of the fly which tissues were male and female, because they had different colours.

The top left fly in the figure apparently lost its X-R chromosome at the earliest stage of development, hence the straight line. As you can see, the effect doesn’t need to be symmetrical – if the chromosome is lost at a later stage, then a very specific part of the fly could be affected, such as the right wing in the top right fly (the left wing is still female).
240527a01

The second figure shows how they interpreted which parts of the fly embryo were involved in determining the behaviour of a mutation called hyperkinetic in which the fly shakes its legs when anaesthetised (this rather odd behaviour turned out to be of major importance, as it is produced by changes to the activity of ion channels in the fly’s neurons). Unsurprisingly, it appears that the hyperkinetic gene was exerting its influence in three separate regions (one for each of the fly’s pairs of legs), all of which are involved in producing the part of the fly’s nervous system that controls movement.

240527a0The arduous nature of the technique – it was not possible to predict which tissues would lose their X-R chromosome, and often no detectable change occurred – and the problems of identifying which tissues underneath the cuticle had changed sex, meant that it was not not widely adopted. By the late 1980s this method was  overtaken by direct manipulation of genes and the tissues they are expressed in, but for many years it was cutting edge science, available in only a few leading laboratories.

_______

Jerry’s addendum: I used gynandromorphs, and Benzer and Hotta’s ring-X stock, to determine where in the fly the females’s sex pheromone (a waxy substance on her cuticule that incites the males to court her and mate with her) resided.  As Matthew noted, that stock of flies, which still exists, is prone to losing X chromosomes when they’re contributed by a male parent. The male’s XX (female) zygotes often lose the X at different stages of development, producing patches of tissue that are XO and therefore male. You can tell which patches are male because the female’s X carries a recessive gene causing yellow body color, so male bits (XO) are yellow and female bits (XX, with one gene for normal coloration) are normally pigmented.

XX females have very different sex pheromones from XY and XO males, so by correlating which bits of a gynandromorph fly were male vs. female, and then extracting each fly’s sex phreromones with hexane and testing the chemicals’ identities on a gas chromatograph, Ryan Oyama (an undergraduate student) and I were able to determine where in the fly’s body the sex pheromones were produced and/or sequestered. It turned out that this was in the cuticle of the abdomen only: flies with female heads, legs, or thoraxes but male abdomens produced only male pheromones. The amount of female pheromone was proportional to the amount of female tissue in the abdomen, at least as seen in the visible cuticle.

This correlated with behavioral observations, too, for when gynandromorphs were tested with normal males (always horny), those males courted gynandromorphs most vigorously when their abdomens were female.  (This could, of course, have been associated with behavior or morphology of those gynandromorphs rather than pheromones, so we needed to do the pheromone tests as well.) Later workers actually localized the pheromone-producing cells to a layer right below the abdominal cuticle, confirming our results.

We published our results in the Proceedings of the National Academy of Sciences (reference and free download below), and I thought it was a very clever way to use old genetic technology to study behavior and biochemistry. Sadly, the paper didn’t get much notice!

__________________

Coyne, J. A. and R. Oyama. 1995. Localization of pheromonal sexual dimorphism in Drosophila melanogaster and its effect on sexual isolation. Proc Nat. Acad. Sci. USA 92:9505-9509.

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