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wikipedia_peppered_moths.jpgToday a paper came out that should get special attention from evolutionary biologists, evolution educators, and creationism fighters. It is:

Cook, L. M.; Grant, B. S.; Saccheri, I. J.; Mallet, J. (2012). “Selective bird predation on the peppered moth: the last experiment of Michael Majerus.” Biology Letters, Published online before print February 8, 2012. doi: http://dx.doi.org/10.1098/rsbl.2011.1136. Abstract at Journal, Supplementary Online Material.

Abstract

Colour variation in the peppered moth Biston betularia was long accepted to be under strong natural selection. Melanics were believed to be fitter than pale morphs because of lower predation at daytime resting sites on dark, sooty bark. Melanics became common during the industrial revolution, but since 1970 there has been a rapid reversal, assumed to have been caused by predators selecting against melanics resting on today’s less sooty bark. Recently, these classical explanations of melanism were attacked, and there has been general scepticism about birds as selective agents. Experiments and observations were accordingly carried out by Michael Majerus to address perceived weaknesses of earlier work. Unfortunately, he did not live to publish the results, which are analysed and presented here by the authors. Majerus released 4864 moths in his six-year experiment, the largest ever attempted for any similar study. There was strong differential bird predation against melanic peppered moths. Daily selection against melanics (s ≃ 0.1) was sufficient in magnitude and direction to explain the recent rapid decline of melanism in post-industrial Britain. These data provide the most direct evidence yet to implicate camouflage and bird predation as the overriding explanation for the rise and fall of melanism in moths.

As long-time readers of Panda’s Thumb know, I’ve had an axe to grind about the peppered moth case since the beginning of my serious involvement with creationism-fighting. Back in 2002 I wrote a long review of Jonathan Wells’s creationism/ID book Icons of Evolution for Talkorigins.org. Wells’s strategy was very clever; rather than attacking the science of evolution head-on, he attacked high school biology textbooks. He engaged in a delicate dance of selective citation and quote-mining so as to make it appear that the criticisms of standard textbook examples used to introduce various evolutionary concepts were coming from scientists.

Extinctions weirdness

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When a paper gets press, the authors get some weird reactions. With the extinctions paper, one guy emailed us to say that he agreed that species extinctions were a big problem, and that humans were the cause. However, he said, we had the details of the cause was wrong. The real cause was contrails.

That, though, was not nearly as weird as this: “Congrats Nick Matzke for Publishing ID Sympathetic Paper in Nature!” by Sal Cordova.

Can anyone explain the psychology here? I’m normally pretty good at psyching out creationists, but this one leaves me mystified.

Denisovans

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Well this is pretty cool. And apparently they interbred with modern humans, also. I can’t wait to see what Reasons to Believe has to say…

Jerry Coyne reports on a new paper in Science by Manyuan Long and colleagues on the origin and history of new genes in a large group of Drosophila that have recently had their full genomes sequenced.

Having this much phylogenetic and genomic information allows researchers to estimate the phylogenetic position of the origin of a new gene (566 new genes amongst the group of 12 fully sequenced genomes, actually), and the periods of time in which directional selection, stabilizing selection, or drift were the dominant regime that the new genes were evolving under. In many cases, there is a period of high selection after the origin of the gene, which weakens later – which is just what you would expect if the well-known, standard model for the origin of new genes is correct.

Two additional points are worth mentioning: (1) in some cases (about 30%, 59 out of the 195 they targeted for knockout studies), these new genes have become essential to viability for the species in question – even though they are totally absent in other, basically similar, flies that do just fine without them! This is strong support for the notion that one way “irreducible” systems evolve is by evolving parts that are helpful at first, but later become essential as other parts coadapt to become dependent on them. (2) I’m sure Luskin, Ewert, and other DI people would like to dismiss this as just another case of evolutionists “illegitimately” inferring common ancestry from “mere” sequence similarity, and that “common design” could be the explanation. However, in any other context, these creationists, and virtually any creationists including the young-earthers, would easily say that all of these Drosophila are just different varieties of the Drosophila kind, and that whatever variety exists between them (minor, in the grand scheme of biology) is “merely” “microevolution within the kind!” (And in the Edge of Evolution, Behe clearly puts his estimated “edge” well above the genus level.)

What’s that? Standard boring microevolutionary processes can produce new genes with modified sequences and new functions, which is clearly new information on anyone’s definition, even the creationists’ and even (explicitly so) Michael Behe’s definition? Oh my goodness, someone better call the DI news blog to put out this fire and reassure the faithful!

References

Chen, S., E. Zhang, and M. Long. 2010. New genes in Drosophila quickly become essential. Science 330:1682-1685.

A previous bit of ranting on this topic by me (responding to Luskin’s ridiculous critique of another famous paper by Manyuan Long, entered into evidence in the Kitzmiller case as exhibit P-245, actually: Long et al. (2003), Nature Reviews Genetics, “The origin of new genes” (free online in many places).

Synthese issue on “Evolution and its rivals”

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The news is out (see John Pieret) but I’ll repeat it here. Synthese, An International Journal for Epistemology, Methodology and Philosophy of Science, has an entire issue devoted to the topic of the title edited by Glenn Branch. It includes papers by names we know like Robert Pennock, John Wilkins (of TO fame), Wes Elsberry and Jeff Shallit on Dembski’s info theory foibles, Sahotra Sarkar, Barbara Forrest, and others. Best of all, all the articles are free online until December 31. Get ‘em while they’re hot!

Cover of Science, behavioral science issue, May 18After you have been in the habit of creationism-watching for a few years you become extremely familiar with all of the usual creationist arguments, half-baked talking points, unchecked assertions taken as obviously true, etc. If you really get into it you learn the creationist movement’s long and specific history, and you learn that whatever form of creationism you are studying at the moment inevitably traces back basically to American protestant fundamentalism, and before that to something sometimes called “naive Biblicism.”*

But there comes a point when you don’t think you can learn anything much new about the creationists. You might stumble on a new mutation of a creationist urban legend or quote mine, or a new bit of creationist history like Dean Kenyon actually being a young-earther despite this fact being carefully hidden by the ID movement for 15+ years. But basically, you don’t expect to find out much that is new.

Well, if you thought you were at this point, you would be wrong. A review article in this week’s Science magazine (with a special focus on behavioral science) shows that scholars can ring out yet another twist in creationism studies.

The PNAS Early Edition webpage has just posted a series of papers from the December 2006 National Academy of Sciences Sackler Colloquium, “In the Light of Evolution: Adaptation and Complex Design,” organized by Francisco Ayala and John Avise. The series of papers, on topics ranging from color vision to beetle horns, is now available (I will post the list below the fold). Eugenie C. Scott (aka Genie) was invited to speak at this meeting about evolution education and the history of opposition to it, and the speakers wrote papers to be published in PNAS and a forthcoming NAS volume.

Genie brought me on as a coauthor on the paper she was asked to write. This became:

Now that’s a stretch

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The Discovery Institute’s Casey Luskin is all atwitter about a new web article from German creationist Wolf-Ekkehard Lönnig [1] about how the giraffe is some kind of massive problem for evolution. Major planks [2] include the alleged lack of transitional fossils between the different fossil giraffe genera (never mind that creationists elsewhere typically accept that the differences between mammalian genera are small, and put the “created kind” or “basic type” at a higher taxonomic level), some confusion about whether one of the giraffe vertebrae is cervical or thoracic or something in between (note to creationists: read about homeotic shifts), and the allegation that there is no evidence for a feeding advantage for tall giraffes, relying on the fact that male giraffes are taller than female giraffes and a 1996 paper in American Naturalist (Simmons & Scheepers 1996, “Winning by a Neck: Sexual Selection in the Evolution of Giraffe”) that attempted to buck conventional wisdom and suggest that sexual selection was the cause of long necks in giraffes.

Sadly, the last plank is particularly bogus, since it completely ignores and displays no knowledge of a massively relevant and quite brilliant paper, published just back in January 2007 in American Naturalist, that constitutes an experimental demonstration of the relative feeding advantage of giraffe height:

Evolution by Any Other Name

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A little more than a week ago, word went around our circles here at The Thumb regarding a paper published on Public Library of Science on the use of the word evolution in medical journal articles. In essence, the authors compare the use of the word evolution in articles written by and published in journals generally read by evolutionary biologists versus physicians. Unsurprisingly, the evolutionary biologists mentioned evolution more by name, even if both groups appealed to the same concepts. Why physicians don’t use the word evolution to describe implications or the concept of evolution is the issue.

Other authors (PZ Myers, Orac, and Sequiteur, among others) have dealt with the topic, but it hasn’t appeared here on PT yet, so I thought I’d just ditto Orac’s opinion with a few thoughts of my own. Find them below, after the jump.

The control and eventual eradication of the smallpox virus from the wild is one of the most heralded success stories in all of public health. Indeed, smallpox has played a central role in the history of vaccination. Even prior to Edward Jenner’s use of the related cowpox virus to protect against smallpox disease, it was known that inoculation with materials from an infectious smallpox pustule or scab (dubbed “variolation”) could protect an individual from death due to smallpox, generally resulting instead in a mild form of the illness. Jenner’s observation that milkmaids seemed to be protected from the disease–and his use of material from cowpox pustules instead of smallpox–resulted in the development of the science of vaccination. World-wide use of the smallpox vaccine, along with a mass vaccination campaign led by the World Health Orgainzation, resulted in the end of naturally-occurring smallpox on the planet, with the exception of stores of the virus held in the United States and Russia.

This feat is being attempted currently with measles and polio viruses, but it’s been much more difficult, and eradication of these viruses may never be attainable. Below, I discuss some aspects that are critical to a campaign that seeks to eradicate a disease, and a new paper on the evolution of smallpox viruses.

(Continued at Aetiology)

Miller et al. 2006, Public Acceptance of Evolution, Science Magazine

Science magazine has just published the results of international polls assessing public acceptance of evolution around the world: Jon D. Miller, Eugenie C. Scott, and Shinji Okamoto (2006) “.” Science Aug 11 2006: 765-766 (Supporting Online Material)

The results are at left. Only one country beats the U.S. in the race to the bottom: Turkey, probably the only country in the list with more severe fundamentalism vs. modernism issues than the U.S. But the people in the U.K. can take heart – a BBC poll this spring (which was widely cited by creationists to support the idea that U.S. antievolutionism is not weird), said that less than half of Britons went for evolution. That result is strongly contradicted by this survey, where the U.K. ranks near the top in accepting evolution (as well they should, Darwin is on the money there).

I wrote here that pili–long, filamentous surface molecules involved in adhesion and bacterial “sex”–had recently been discovered in gram positive organisms; pecifically, in group A and B streptococci (Streptococcus pyogenes and Streptococcus agalactiae, respectively), using a genomics approach. Though this publication is quite recent, this is a fast-moving area of research, as evidenced by two new papers which extend this earlier research into pili in the group B streptococcus (GBS).

(Continued at Aetiology)

Listeria monocytogenes is a gram-positive, rod-shaped bacterium. It can be found in the environment as a soil inhabitant. However, it also can be a frequent contaminant of our food supply. As the latter, the bacterium is a significant public health concern, as it is capable of causing serious infections. Listeriosis (infection with Listeria) causes ~2500 serious illnesses and 500 deaths each year in the United States, and the hardest-hit are those with poor immune systems due to age (the very young and old), other immunocompromsing conditions (such as chemotherapy, organ transplant, or AIDS), and pregnant women. Once ingested, the bacterium is able to cross the intestine and spread throughout the body via the bloodstream, where it can attack organs and cause serious damage.

The very fact that it’s typically an environmental organism (rather than a solely pathogenic agent) likely accounts for some of its virulence and transmission. It’s able to survive a number of environmental stresses, including low temperature and high salt concentrations. Indeed, its ability to grow at relatively low temperatures is one way it evades our efforts to control it: it can grow in food even at refrigeration temperatures.

Listeria is particularly insidious as a cause of fetal death or other complications during pregnancy. Intrauterine infection can lead to preterm labor, spontaneous abortion, stillbirth, or serious–and potentially deadly–infection of the neonate. However, fairly little is known regarding exactly how this condition develops, or the mechanisms that lead to infection of the fetus. It has been thought that the increased susceptibility to infection with Listeria during pregnancy is largely due to a decrease in cell-mediated immunity that occurs as a result of pregnancy. This is a particularly attractive hypothesis for Listeria, which is an intracellular pathogen. A new paper in PLoS Pathogens examines this phenomenon in greater detail, using a guinea pig model of infection.

(Continued at Aetiology)

Those of you who have followed creationism/intelligent design literature over the years have probably felt as if you’re living in an alternate universe sometimes. In that literature, many times it seems as if “up” means “down” and “highly supported by the evidence” means “a theory in crisis.”

You may not have been following the comments to this post on AIDS denial (and lord, I can’t blame you), but if you have been, you’ve seen a similar phenomenon, where it’s suggested that mutations found in RNA viruses are just due to sloppy lab work, essentially blowing off an entire field of research.

This, of course, has implications far beyond HIV. Phylogenetic analyses based on genetic mutations are used to determine relationships for all kinds of organisms–including humans. In infectious disease epidemiology, they can be used to pinpoint the origin of a virus, or to track and predict its spread, as I’ve written about previously. A new paper in Nature uses similar methodology to examine the introduction of influenza H5N1 into Nigeria.

(Continued at Aetiology).

More prion news

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Last fall, Andrea wrote an excellent piece on prions, and how they “contradict century-old biological assumptions and seem to defy the expectations of Darwinian evolutionary theory.” He gives an overview of prions and discusses their potential role in heredity. My interest in them, of course, comes from the diseases they cause. Over at Aetiology, I have a post up discussing a new Lancet paper on the prion disease, kuru, and its potential to act as a model for other human prion diseases (such as “mad cow”). The authors suggest two things: one, that the incubation period of so-called “mad cow” disease may be longer than previously thought, and two, that there may be “waves” of epidemic, determined partly by host genetics.

Evolution by gene loss

Sometimes it’s amazing just how little we know about the microbes around us. For precious few microbes, we know a good deal about virulence factors–genes and proteins that, when present, increase the severity of disease either in animal models or in humans (or both). However, much of this research has been done investigating acute infectious diseases, where one is infected, becomes ill, and gets better in the course of a few weeks to a month. Much less is known about factors that affect long-term (or chronic) infection. A recent study addressed one gap in this research, tracking the evolution of the bacterium Pseudomonas aeruginosa in chronically infected cystic fibrosis patients.

(Continued at Aetiology)

Won for All

Last night, I had to read this book RPM mentioned. It's not very long—about 100 pages, counting a preface, an epilogue, and an afterward, and it has lots of pictures—but be warned: it's very inside baseball.

The book is Won for All: How the Drosophila Genome Was Sequenced(amzn/b&n/abe/pwll) by Michael Ashburner, and its subject is the rush to sequence the Drosophila genome in 1998-1999. It's a rather strange twist on what I expected, though. While the subtitle says "How the Drosophila Genome Was Sequenced," there is almost no science at all in the body of the book; instead, it's all about the people and the politics, with Ashburner flitting about from place to place, yelling at people and eating sushi. It's phenomenally entertaining.

Continue reading "Won for All" (on Pharyngula)

It can’t be said often enough that “nothing in biology makes sense except in the light of evolution.” Moving from physical characteristics–color, bone shape, the form of bacterial cells–to genetic characteristics in order to classify organisms–and infer phylogenies–was a giant advance. That the molecular characteristics confirmed what was known using physical characteristics was a breakthrough, and allowed for more sophisticated analyses of organisms that don’t have bones or other easily-observable physical features that allow for simple classification into groups: microbes. I’ve previously pointed out the utility of phylogenetic analysis in tracking the spread of pathogens. A new study on the origin and evolution of HIV employs a similar approach in order to elucidate the history of the virus in Africa.

(Continued at Aetiology).

Getting it wrong

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So, archaea are apparently the topic of the week. While I wrote here about the pathogenic potential of some species of these organisms, a new essay in Nature and a new review in Science focus more on their evolution (and the evolution of the other two domains of life) than any health application.

In the essay mentioned, Norman Pace discusses the eukaryote/prokaryote dichotomy. Currently the archaea are classified as prokaryotes since they, like bacteria, lack a true nucleus. However, molecular sequence analysis has shown that the archaea and eukaryotes are actually more closely related to each other than either group is to bacteria (see figure, from Pace’s Nature essay). As such, nomenclature that places the bacteria and archaea together into a group is misleading.

(Continued at Aetiology)

A new study in the journal Pediatrics suggests that a tonsillectomy may improve the condition of kids diagnosed with attention defecit/hyperactivity disorder (ADHD). I think it’s an excellent case of some true “alternative explanations” for the data that the creationist/ID types often crow about.

Creationists often try to validate their position by saying that both they and mainstream scientists start from the same data, but that creationists use their “Bible glasses” to interpret it, while scientists view it through their “evolution glasses.” In other words, they’re not wrong–it’s just a different interpretation of the same data, and where you end up depends on your initial biases and worldview. Though this is bogus when it comes to creationism, there are indeed real debates in the literature, where two hypotheses may be similarly compelling.

(Read more at Aetiology)

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