john hawks weblog

In honor of the season, HowStuffWorks.com has an article on the workings of zombies.

Nota bene:

Mummies can bear a striking resemblance to zombies, even down to the guttural speech and shambling walk. Their deliberate physical preservation, however, sets them apart from ordinary zombies.

Here is some good advice if zombies are chasing you:

Also, avoid common mistakes like:

• Sheltering in a vehicle to which you do not have the keys
• Leaving blades, cudgels or other basic weapons out for zombies to find
• Teaching zombies how to use firearms
• Giving your only weapon to anyone who is hysterical
• Retreating to a basement or cellar without taking supplies with you
• Getting into an elevator in a building infested with zombies
• Letting personal feelings and arguments get in the way of survival

My favorite part? When I viewed the article, there was a list of "popular searches" on the sidebar. The "popular searches": Bounty Hunting, Dreams, Halloween, Tarot Card, Witchcraft, and Creationism!

OK, I'm sure everyone has seen this story already, but can I just say, "Amen"?

A new study finds that the correspondence of Albert Einstein, as well as that of Charles Darwin, followed patterns similar to modern e-mail communication.

Einstein sent more than 14,500 letters. But he received more than 16,200, and responded to only a quarter of them. Darwin mailed more than 7,500 letters. He responded to 32 percent of the roughly 6,530 letters he received.

Of course letter writing takes more time than e-mail, but the mathematical relationship between quick replies and delayed responses was similar, explains Joao Gama Oliveira of the University of Aveiro in Portugal.

Last week I hoovered 400 messages out of my inbox. Thankfully, I can maintain a lower reply rate than Einstein, since only about five or ten e-mails a day require some kind of reply. And short e-mails are much more acceptable than short letters -- they're more in the nature of telegrams really. So if you run the numbers, I send around a quarter of Einstein's lifetime output every year. But almost all of these are very short contacts -- just a way of keeping in touch, keeping projects going, or affirming queries.

In that way, it's not hard to see why e-mail has become more central than letter-writing as a form of correspondence (at least in science): it is much more polite to be able to send short replies than nothing at all -- but most letters don't really require anything more than a short reply, which wouldn't be worth sending in the post. From that standpoint, e-mail is certainly much more personal. On the other hand, the more formal nature of letters means that even in something that is only a short reply, you put in lots of filler -- how are you, I remember fondly that summer at the Cape, how are the kids -- that make letters read a lot more pleasantly (and open more of a channel for personal relationships) than e-mails. So there are pluses and minuses for this change in correspondence, but it is one that is very much in accord with the culture.

This is sort of interesting to me because I have been reading the letter and telegram correspondence of Einstein and Leo Szilard. It's fascinating they way that people exchanged considered arguments by letter, which would often take weeks to get a reply, but would telegraph (literally) their arguments in sentence form to bring attention to an oncoming letter, or to let a sender know that they got something and had something more to say. Sometimes the telegrams were quick probes for interest or snap reaction -- kind of like contact calls in primates. And this during a time that these physicists were trying to coordinate efforts to keep physical descriptions of chain reactions out of journals, since they clearly perceived a war was coming.

Now if Darwin had a blog...that would have been worth reading!

Reuters is reporting on a current study by Joan Silk and colleagues in Nature.

Here's the intro:

Chimpanzees share many traits with humans but altruism, it seems, is not one of them, scientists said on Wednesday.

Although chimps live in social groups and co-operate and hunt together, when it comes to helping non-related group members, they don't put up with any monkey business.

When given the opportunity to help themselves and other chimps they often choose the selfish option.

The experimental setup gave the subject an option between two alternatives:

If the subject (hereafter referred to as the actor) chose option 1, the actor obtained a food reward and another chimpanzee simultaneously received an identical reward (hereafter referred to as the '1/1 option'). If the actor chose option 2, the actor obtained the same size and type of food reward, but no food reward was delivered to the other chimpanzee (the '1/0 option'). As a control, actors were presented with exactly the same reward options when there was no other chimpanzee present (Silk et al. 2005:1357).

So it's not a benefit/cost comparison, but a benefit/benefit. Sort of like if you won a house party from VH1, and you could either decide to invite other people or have the party all to yourself.

The chimpanzees didn't choose the "1/1 option" any more often when another chimpanzee was there (and got the reward) than when there was no other chimpanzee there. Those unfeeling primates!

I'm of two minds about the study. On the one hand, I'm not entirely sure how untutored humans would perform on this one. I think my two-year-old twins would pass -- when we are giving out treats, one will insist on an extra treat to bring to her sister. That situation is pretty analogous to the experiment, I think -- it's not like there's any cost to asking for an extra, since we know they are going to take it to the other twin. Nor is it really analogous to "sharing", which they do inconsistently. But we've had to work pretty hard to teach them to give out treats in that way, and they get direct feedback from us and the grateful sibling.

Considering how complex even this simple case is, I'm not too surprised that the chimpanzees would fail to give out the treats to their groupmates. Nobody has taught them how to do it, and there is relatively little direct feedback (although at one study site, the potential recipients sometimes made begging gestures). And I don't think that untutored humans would do it without explanation and feedback -- it's just that humans have a pretty sophisticated verbal and nonverbal ability to give that kind of feedback. So there is a genuine cognitive difference between humans and chimpanzees that may be involved in the result, although it is not perfectly clear that it is "indifference" in the chimpanzees.

On the other hand, look at the claim at the end of the paper:

These results complement observational and experimental studies that indicate that chimpanzees cooperate mainly with kin and reciprocating partners and show no aversion to inequitable exchanges that benefit themselves (Silk et al. 2005:1358).

This raises a question: would chimpanzees give out the treat to their kin? If not, then we're not seeing a failure to be empathetic toward the "unrelated other", we're seeing a failure to be empathetic at all. But we know that chimpanzees do behave preferentially toward kin in many contexts. So if this test failed to show empathy toward kin, it would be a failure of the test, and not a real indication of chimpanzee behavioral capacities.

So I think there are some missing steps here. Coming up with clear psychological demonstrations of the concept of empathy, or altruism, or welfare of other individuals is tough.

References:

Silk JB et al. 2005. Chimpanzees are indifferent to the welfare of unrelated group members. Nature 437:1357-1359. Full text (subscription)

This article by P. Thomas Schoenemann and colleagues is from earlier this year, but it's worth pointing to as a comparative study of more than just humans and chimpanzees. It includes MRI data from 10 nonhuman primate species, with three to five individuals each! That's a consequential sample in a field where the usual comparison has been with two chimpanzees.

Some history:

Although the human brain is around three times larger than expected for a primate of our body size, it does not seem to be simply a scaled-up version of a primate brain. Because neural tissue is evolutionarily expensive (for metabolic and maturational reasons), changes in relative proportions in different parts of the brain are likely to be behaviorally adaptive. Thus, determining the various ways in which the human brain is different from nonhuman primate brains is of central importance to understanding human evolution. It is clear that at least some areas of the human brain are proportionately smaller than predicted based on primate scaling trends. For example, the human olfactory bulb is only 30% as large and Brodmann's area 17 (primary visual cortex) only 60% as large as predicted for a primate brain our size. Given that the entire human brain is much larger than predicted overall, at least some areas must therefore be significantly larger than predicted.

One area of particular interest for human evolution is the prefrontal cortex, which mediates such important behaviors as planning, working memory and memory for serial order and temporal information, aspects of language (Broca's area and symbolic behavior), attention and social information processing. To the extent that the human prefrontal cortex is disproportionately large, it would suggest that some combination of these behavioral dimensions were particularly important to our evolutionary history (Schoenemann et al. 2005:242, citations elided).

The result is that the total prefrontal cortex volume is relatively larger (i.e., relative to the size of the brain) in humans compared to other primates, and that this increase is mainly attributable to a great increase in the white matter volume. Gray matter in the brain contains a high proportion of cell bodies, while the white matter contains a high density of axons (the fat sheaths around the axons make them white when bundled together).

An increase in white matter probably means that humans have more connections among neurons in the prefrontal cortex has increased in humans relative to other primates. This increase might also mean greater communication between the prefrontal cortex and other parts of the brain.

What does it mean for human evolution? The discussion throws every cognitive change at the problem, from language to social group size to toolmaking. Possibly all are implicated, either separately or together.

In any event, this is one of the clear volumetric differences between the human brain and those of other primates.

References:

Schoenemann PT, Sheehan MJ, Glotzer LD. 2005. Prefrontal white matter volume is disproportionately larger in humans than in other primates. Nature Neurosci 8:242-252. Full text (subscription)

Now that we're in an age where natural selection on functional genes is recognized to have occurred in historic time, stories like last week's paper on the Manchu dynasty Y chromosome patriline have taken on an additional element of complexity.

That's because of the possibility that these newly common variants might carry some selective advantage.

The difference between selection and drift is a question of function: does any gene on the Y chromosome do anything that would have caused an allele to increase markedly in frequency during the past few hundred years?

With most genes, we wouldn't have to ask the question. First, it would be much less plausible for a biparentally inherited allele to increase so rapidly in frequency. With the Y chromosome, there is the chance that a father with a huge number of mates (and offspring) would transmit the opportunity for similar high reproduction to his many sons. Inheritance of cultural power is a cultural mechanism, not a genetic one. Hence, there is the chance of great concentration of reproduction into a single patriline, and the consequent increase in frequency of the patriline's haplotype. An autosomal gene would have only a fraction of the reproductive boost, because the father would have two copies, each would be transferred to only half the offspring, and each son (and daughter) would receive another copy from his (or her) mother. After a few generations, there is even a fair chance that neither of the founder's alleles would be left, replaced by the alleles coming in from the wives, son's wives, and so on. Inbreeding would prop up the frequency of the original founder's alleles within the dynastic lineage, but it would limit the spread of those alleles across the region. Hence, if we observed a huge recent increase in the frequency of an autosomal variant, the most likely hypothesis would be selection.

Second, autosomal genes give us the possibility to localize selection to a single locus. Recombination breaks up chromosomes every generation, so that after a relatively few generations, different parts of chromosomes have different fates. A functional gene under selection will carry a relatively small part of the chromosome with it, a small part that can be identified through linkage disequilibrium. Thus, functional genes under selection can be identified to a relatively small area, often to the gene itself. In contrast, the nonrecombining portion of the Y chromosome is completely linked, so that there is no chance to find out which portion of the Y might have been under recent selection. In principle, one could find whether the successful haplotype had any new functional variants, but in practice genetic studies do not assay the complete sequence but only a small number of markers. Without tying the reproductive excess of a haplotype to a particular functional variant, it is much harder to make the argument for selection.

Personally, I think that the extreme founder effect is the most reasonable alternative, at least for the time being. We know that some rulers in Asia had very high offspring number, and that many of their offspring were made rulers of regions or nations and had similar opportunities. Over a few generations, this extraordinary situation would greatly increase the frequency of the Y chromosome haplotypes carried by such patrilines. Even if geneticists have not yet documented the relationship between the haplotypes and the patrilines, history makes the argument very plausible.

But what's interesting to me is that the original work on these Y chromosome haplotypes does not draw this distinction between founder effect and selection in any clear way. For example:

The historically documented events accompanying the establishment of the Mongol empire would have contributed directly to the spread of this lineage by Genghis Khan and his relatives, but perhaps as important was the establishment of a long-lasting male dynasty. This scenario shows selection acting on a group of related men; group selection has been much discussed (Wilson and Sober 1994) and is distinguished by the property that the increased fitness of the group is not reducible to the increased fitness of the individuals. It is unclear whether this is the case here. Our findings nevertheless demonstrate a novel form of selection in human populations on the basis of social prestige (Zerjal et al. 2003:720).

This is a peculiar use of the word "selection". It is sort of analogous to "kin selection", which is not really natural selection at all, but instead is a structured behavioral pattern that advantages kin compared to nonkin. It's a confusing part of evolutionary biology that "kin selection" has the word "selection" in it, but it is the sort of thing you learn not to confuse. Likewise, it's not "group selection" unless there is some function on the Y chromosome that advantages the group (possibly at a cost to the individual).

Is this a "novel form of selection in human populations on the basis of social prestige"? I don't think so -- I think this is just normal cultural inheritance of power.

But consider what such a hypothesis would actually mean. It would have to imply that there actually has been selection on some Y chromosome variant because of a function leading to social prestige. This hypothesis would be along the lines of the idea that Genghis Khan's Y chromosome caused the Mongol conquests (and the subsequent assignment of strong reproductive advantages to their rulers). It is functionally similar to the idea that reproductive dominance and aggression may be linked to some Y chromosome gene (or genes).

We don't have any reason to think such things are true. The hypothesis would certainly imply a very different genetic history for the Y chromosome than usually assumed.

But here the hypothesis is, stuck in a paper on the "genetic legacy of the Mongols", without any exploration of its meaning. It's one of those things that a careful reader might take as a sign -- a sign that the genetic universe has some strange stuff waiting for us. It's a time to be precise about what we know and don't know.

I wonder how many of these patrilines the Genographic Project will turn up in areas with different histories?

Carl Zimmer has a very nice post describing recent work in bioinformatics, with a view toward explaining what the field is and how it works.

Here's a quote:

The classic method for figuring out what a gene is for is good old benchwork. Scientists use the gene's code to generate a protein and then figure out what sort of chemical tricks the protein can perform. Perhaps it's good at slicing some other particular protein in half, or sticking two other proteins together. It's not easy to tackle this question with brute force, since a mystery protein may interact with any one of the thousands of other proteins in an organism. One way scientists can narrow down their search is by seeing what happens to organisms if they take out the particular gene. The organisms may suddenly become unable to digest their favorite food or withstand heat, or show some other change that can serve as a clue.

Even today, though, these experiments still demand a lot of time....

This dilemma has helped give rise to a new kind of science called bioinformatics. It's an exciting field, despite its woefully dull name. Its mission is to use computers to help make sense of molecular biology--in this case, by traveling through vast oceans of online information in search of clues to how genes work.

A study by Yali Xue and colleagues in the advance section of American Journal of Human Genetics

Here's the abstract:

We have identified a Y-chromosomal lineage that is unusually frequent in northeastern China and Mongolia, in which a haplotype cluster defined by 15 Y short tandem repeats was carried by 3.3% of the males sampled from East Asia. The most recent common ancestor of this lineage lived 590 ± 340 years ago (mean ± SD), and it was detected in Mongolians and six Chinese minority populations. We suggest that the lineage was spread by Qing Dynasty (16441912) nobility, who were a privileged elite sharing patrilineal descent from Giocangga (died 1582), the grandfather of Manchu leader Nurhaci, and whose documented members formed 0.4% of the minority population by the end of the dynasty.

While introducing the problem, the paper presents a couple of stumbling blocks that the study had to overcome. The Y chromosome is relatively less variable than much of the rest of the genome, but viewed at an appropriate level of detail (i.e. with a fairly large number of microsatellite sites), geneticists can reach a level of variation at which most individuals are completely unique. If you look at 15 or so microsatellites, it is fairly unlikely that two people in a moderately large sample should have the same Y chromosome haplotype, unless they happen to be close relatives.

But there are lots of reasons why close relatives might actually end up in a moderately large sample. For one thing, the sample usually comes from a small number of locations, which means that some alleles may have relatively high frequency in the sample because of their predominance at a single location. This happens when distant cousins (perhaps unbeknownst to each other) get in the sample. In small villages and towns, this becomes more likely because of inbreeding.

On the other hand, alleles that are common and occur in many locations are truly unusual. These alleles must not only represent the history of a small village or town, but must represent a more widespread pattern of ancestry across large regions. Alleles ultimately come from people, and Y chromosome haplotypes ultimately come from a single man.

As discussed by Xue et al. (2005), there are at least two such unusually common alleles in East Asian populations. These are instances in which the descendants of one man had unusually great success in passing their Y chromosomes to many descendants, across broad geographic areas. Sons, grandsons, and further descendants spread out and maintained much higher rates of reproduction (at least, of sons) than other men who lacked the peculiar widespread Y haplotype.

One of these haplotypes was described by Zerjal et al. (2003), in their paper "The Genetic Legacy of the Mongols".

In case you missed that paper, here is its abstract, which pretty much says it all:

We have identified a Y-chromosomal lineage with several unusual features. It was found in 16 populations throughout a large region of Asia, stretching from the Pacific to the Caspian Sea, and was present at high frequency: 8% of the men in this region carry it, and it thus makes up 0.5% of the world total. The pattern of variation within the lineage suggested that it originated in Mongolia 1,000 years ago. Such a rapid spread cannot have occurred by chance; it must have been a result of selection. The lineage is carried by likely male-line descendants of Genghis Khan, and we therefore propose that it has spread by a novel form of social selection resulting from their behavior.

The logic leading to this conclusion is indirect, depending on the high frequency and widespread distribution of the haplotype, the general match between the geographic range of the haplotype and the range of Mongol conquests, the historical record of descent of local kings and rulers from Mongol antecedents, and the likelihood that only members of a high-ranking elite would have had the opportunity to maintain high reproduction for many generations across the entire area.

The other widespread recent haplotype is described in detail by Xue and colleagues (2005). Its association to historic events is also indirect, but likewise plausible:

We reasoned that the events leading to the spread of this lineage might have been recorded in the historical record, as well as in the genetic record. The spread must have occurred after the cluster's TMRCA (500 years ago, corresponding to about A.D. 1500) and, most likely, before the Xibe migration in 1764. Notable features are the occurrence of the lineage in seven different populations but its apparent absence from the most populous Chinese ethnic group, the Han. A major historical event took place in this part of the world during this period - namely, the Manchu conquest of China and the establishment of the Qing dynasty, which ruled China from 1644 to 1912. This dynasty was founded by Nurhaci (1559-1626) and was dominated by the Qing imperial nobility, a hereditary class consisting of male-line descendants of Nurhaci's paternal grandfather, Giocangga (died 1582), with >80,000 official members by the end of the dynasty (Elliott 2001). The nobility were highly privileged; for example, a ninth-rank noble annually received 11 kg of silver and 22,000 liters of rice and maintained many concubines. A central part of the Qing social system was the army, the Eight Banners, which was made up of separate Manchu, Mongolian, and Chinese (Han) Eight Banners. The nobility occupied high ranks in the Manchu Eight Banners but not in the Mongolian or Chinese Eight Banners; the Manchu Eight Banners were recruited from the Manchu, Mongolian, Daur, Oroqen, Ewenki, Xibe, and a few other populations. A social mechanism was thus established that would have led to the increase of the specific Y lineage carried by Giocangga and Nurhaci and to its spread into a limited number of populations. We suggest that this lineage was the Manchu lineage (Xue et al. 2005:3-4).

The thing that interests me is the extent to which the hypothesis can be judged only on its historic merits. The date of the founding of the haplotype is very imprecisely known. The paper lists two contrary estimates of around 590 and around 220 years ago, based on different estimates of microsatellite mutation rates, and each having substantial error. If we just take the total range of the standard error of both estimates, which must be less than the confidence intervals, this is a range of anywhere from 1070 AD to 1900 AD for the origin of the haplotype.

So the historical association of the haplotype really depends on historical evidence. It is all plausible, but it serves as a bit of a reality check on genetics. Here we have a good indication from genetics of the scale of the phenomenon -- this one patriline has come to represent a very high proportion of the living people of East Asia. From history alone, we might not have guessed the sheer magnitude of reproductive dominance of the Chinese ruling elite. Here, genetics makes a very important contribution.

But whether this patriline was Manchu or some earlier ruling elite, or whether it was a ruling elite at all instead of some extraordinarily active farmer -- those details depend on a full rendering of the relevant history. Genetics gives only a bare skeleton of the timing and place of the founding of the patriline and its later dispersal. History can focus on one hypothesis because it can rule out alternatives -- perhaps only the Manchu ultimately had the right distribution and access at the right time to explain the pattern of genetic data.

I don't think the matter is decided yet. Again, I think the association is perfectly plausible. But historians need to wake up and address these kinds of genetic inquiries with their evidence. At the moment, we have suspects and circumstantial evidence.

The geneticists would like to add more:

Our hypothesis could be tested by examining the descendants of the Qing nobility (Li 1997). Unfortunately, extensive warfare during the 20th century and the Cultural Revolution (1966-1976) led to enormous social upheaval, during which descent from the nobility was usually hidden and relevant documents were destroyed. As a result, very few well-attested descendants are known, and they were not available for testing. Thus, our hypothetical explanation remains unproven (Xue et al. 2005:4).

Up to now, genetics has remained a consumer of historical evidence. It is on a course to become a major producer as well. I'd like to read the historian who is ready to adapt to this new source of information.

References:

Xue Y, Zerjal T, Bao W, Zhu S, Lim S-K, Shu Q, Xu J, Du R, Fu S, Li P, Yang H, Tyler-Smith C. 2005. Recent spread of a Y-chromosomal lineages in northern China and Mongolia. Am J. Hum Genet 77 (early access). Full text (free)

Zerjal T, Xue Y, Bertorelle G, Wells RS, Bao W, Zhu S, Qamar R, Ayub Q, Mohyuddin A, Fu S, Li P, Yuldasheva N, Ruzibakiev R, Xu J, Shu Q, Du R, Yang H, Hurles ME, Robinson E, Gerelsaikhan T, Dashnyam B, Mehdi SQ, Tyler-Smith C (2003) The genetic legacy of the Mongols. Am J Hum Genet 72:717-721. Full text

A new paper in PLoS Biology examines the recent evolution and dispersal of the Δ32 allele at the CCR5 locus (via Gene Expression). The introduction has a great paragraph summarizing the importance of the allele:

The CCR5 Δ32 mutation is a good example of an advantageous allele with a well-characterized geographic distribution. The Δ32 mutation currently plays an important role in HIV resistance because heterozygous carriers have reduced susceptibility to infection and delayed onset of AIDS, while homozygous carriers are resistant to HIV infection [1]. The mutation is found principally in Europe and western Asia, where average frequencies are approximately 10%, although the frequency varies within this geographic area. HIV only recently emerged as a human pathogen, so researchers were surprised when various sources of evidence showed strong selection in favor of Δ32 throughout its history. The age of the Δ32 allele has been estimated to be between 700 and 3,500 y based on linkage disequilibrium data [2,3], and recent ancient DNA evidence suggests the allele is at least 2,900 y old [4]. If Δ32 were neutral, population genetics theory predicts it would have to be much older given its frequency. The alternative explanation is that the Δ32 mutation occurred recently and then increased rapidly in frequency because of a strong selective advantage [2,5]. Quantitative studies have concluded that heterozygous carriers of Δ32 in the past had a fitness advantage of at least 5% and possibly as high as 35% [2,3]. Bubonic plague was initially proposed as the selective agent [2], but subsequent analysis suggested that a disease like smallpox is a more plausible candidate ([6-8], with reviews in [9-11]) (Novembre et al. 2005:e339).

This allele is one of the best-characterized recently selected variants in humans. Its selective advantage at least at some times in European history was huge, and it has a very recent origin (as assessed by linkage disequilibrium around the variant site).

Here we fit a simple population genetic model to the geographic distribution of Δ32 in order to infer features of the processes of dispersal and selection that shaped the historical spread of the allele. In particular we conclude that given current estimates of the age of the Δ32 allele, the allele must have spread rapidly via long-range dispersal and intense selection to attain its current range. We find the Δ32 allele is likely restricted geographically because of limited time to disperse rather than local selection pressures. In addition, we show that the data are consistent with origins of the mutation outside of northern Europe and modest gradients in selection (ibid.).

It's on its way to being a textbook case. At least in my textbook!

References:

Novembre J, Galvani AP, Slatkin M. 2005. The Geographic Spread of the CCR5 Δ32 HIV-Resistance Allele. PLoS Biol 3(11): e339. Full text (free)

On the heels of last month's paper on walking-stick use in gorillas, the AP reports on nutcracking by a juvenile gorilla at the Dian Fossey sanctuary in Congo.

Alecia Lilly, a primatologist in Rwanda who worked for over a decade with a colony of captive gorillas in South Carolina and has seen Itebero at work, said most learning among gorillas occurs through imitation. But Itebero had no instructor, alone in her sanctuary with her keeper.

"Itebero is remarkably proficient at cracking nuts," Lilly told The Associated Press by phone. "It takes most chimpanzees many years to reach similar levels of proficiency."

There is certainly a lot of emphasis given to the "independent invention" aspect of such tool use instead of just "learning from humans." Most primates can learn to do a lot of things by watching humans that they never do in the wild. If anything, the potential to learn tool use is overdeveloped compared to the opportunity to learn tool use in the wild. That points to the hypothesis that such potential exists for other purposes, such as social learning.

But that leaves unexplained the exceptional individual that develops apparently "advanced" behavior on her own. Is such behavioral variation analogous to variation within humans? Or is there more of a chance aspect? Of course, humans have a chance aspect to exceptional behavior also...

From Jerry Pournelle:

Magic and Science were born twins. One of them worked.