john hawks weblog

From Jerry Pournelle:

"'Trust us, we're the professionals' is almost always snake oil, and if you drink the snake oil you should not be astonished to discover that it wasn't even pure snake oil. There's probably kerosene and strychnine in there too."

AFP is reporting possible progress in the hunt for the missing Zhoukoudian bones (via Palanthsci):

Several interesting clues have come to light in recent months, according to members of a recently established committee charged with looking for the Peking Man's bones and other missing relics, the China Daily reported.

If the clues lead anywhere, it could potentially mark a breakthrough in a search that has lasted since the early 1940s.

Five skull fragments belonging to Peking Man were lost under mysterious circumstances during World War II and have never been recovered.

Just in the last two months, the committee has received 63 tip-offs on the whereabouts of the elusive relics, said Liu Yajun, deputy head of the commission.

People's Daily Online has a more detailed account:

FOUR KEY CLUES AMONG 63 PIECES OF INFORMATION

The committee has received 63 pieces of information from areas like Beijing, Jilin Province, Fujian Province and Taiwan Province in the past two months. Experts with the committee screened the information and found four might be important:

A citizen surnamed Wu in Beijing claimed a professor surnamed Gu in Gansu Province once was invited to write autobiography for Jia Lanpo, one of the finders of the Peking Man skulls and also a guru on Peking Man studies. Gu once "recorded an American major's testimony at the Far East Military Court when researching at a Japanese archive, and the testimony mentioned the skulls."

A citizen surnamed Ren in Beijing claimed he knew one person whose father was a doctor in Peking Union Medical College Hospital, where the skulls were kept, and the doctor "took one skull home and the skull now is buried in a house."

A citizen surnamed Liu said he could help contact a wartime revolutionist who "has a Peking Man scull [sic] at hand."

A citizen surnamed Wu from Jiangxi Province said a 121-year-old man in Jiangxi once served as a high-ranking official under Dr. Sun Yat-sen, the forerunner of China's democratic revolution. The old man claimed that "the skulls are still in China" and he knows the whereabouts.

This quote seems like the significant one behind the committee's motivations:

"Mankind can give up many things, but there is one thing that we can never abandon -- that is our ancestors," said Gao Xing, an expert of ancient vertebrates, with the Chinese Academy of Sciences (CAS).

I think it's pretty safe to say that the bones don't have any hidden power to open a fifth dimension or anything. Not exactly the stuff of a Lara Croft movie.

Then again...CourtTV of all places has a long account of the Zhoukoudian discoveries, including the loss of the fossils. That article, by Rachael Bell covers some of the theories (in the crackpot notions sense, not the well-supported scientific ideas sense).

Anyway, don't hold your breath.

Wired is running a compelling story of tribal citizenship, genetic ancestry, and race (via Dienekes).

The subjects of the story are "Black Indians": people of ultimately African descent who are historically affiliated with Indian tribes. In many cases, their ancestors were slaves held by the Indians, who were later freed and continued to live with the tribes as members, called Freedmen. Many of these people intermarried with the Indians, and their descendants today claim tribe membership.

But not without conflicts:

For the better part of the 20th century, black Indians were permitted to vote in elections, sit on tribal councils, and receive benefits. Tribal leaders now insist that the Freedmen were never actually citizens and that they will never attain the honor of membership because they don't have Native American blood. In 1983, the Cherokee tribe established a rule requiring citizens to carry a Certificate of Degree of Indian Blood. This federal document is available to anyone whose ancestors are listed on the Dawes Roll - a 1906 Indian census that excludes Freedmen. In 2000, the Seminoles expelled all 2,000 black members and denied their families a cut of the reparations money - never mind that their ancestors joined the tribe in the 18th century, endured the march from Florida to Oklahoma in the 1830s, and have considered themselves Indian for generations.

Outraged, numerous Freedmen have turned to the courts for help. In the most celebrated case, a black tribal leader named Sylvia Davis filed suit against the Seminole tribe in 1994 to get her son a $125 clothing stipend from the Seminole reparations money. But US courts have repeatedly refused to meddle in Indian affairs, noting that the sovereign nations determine their own membership criteria. Davis suffered a serious - and perhaps final - setback last year, when the Supreme Court refused to consider her appeal of a lower court's ruling that the Seminoles could not be sued in federal court. (The Bush administration filed a brief on behalf of the tribe.)

Now, just as the Freedmen's struggle appears all but lost, new hope is emerging from an unlikely place - the front lines of genetic science. Last year, several Freedmen leaders were approached by a molecular biology professor named Rick Kittles. As head of African Ancestry, a company he had recently founded to sell DNA testing services to amateur genealogists, Kittles promised to reveal any customer's preslavery roots, whether they stretch to the Tikar of Cameroon or the Mende of Sierra Leone.

Hinging on the struggle are opportunities to collect scholarships, reparation funds, casino profits, and tribal development grants.

Genetic methods ought to be of some use here. The article describes the arbitrary assignment of Freedmen to tribes or not in the original Dawes Roll, often based on eyeballing features like the prominence of the cheekbones. But of course genetic methods are not without their problems (also described in my earlier posts).

And there appears to be little prospect that the genetic tests will be accepted:

Other tribes are just as closed-minded. When I ask Jerry Haney, the Seminole chief who expelled the tribe's black members in 2000, whether he might reconsider his stance based on DNA tests, he huffs. "They can claim all the Indian they want," he says, "but they cannot become a member of the Seminole Nation by blood. They're down there [on the roll] as Freedmen. They're separate."

But all this might not matter if the results worked out. That's the really interesting part, and it starts on page 4.

Weaver and Roseman (2005) review the case for Neandertal extinction based on ancient mtDNA. They present simulations that demonstrate that a Neandertal contribution to the modern human mtDNA pool is very unlikely. These simulations are simpler than those carried out by Currat and Excoffier (2004), but considering the publication schedule of Current Anthropology, they were probably completed earlier. Their conclusion is the same: if mtDNA has not undergone a selective sweep, then Neandertals almost certainly became extinct without issue.

But that's not especially news: indeed, it was strongly suspected even before ancient Neandertal mtDNA sequences were discovered (e.g. Manderscheid and Rogers 1996). The question has been, and remains, is human mtDNA actually neutral? Or is its recent pattern of variation in living humans the result of recent selection within the human lineage? If there was a selective sweep in humans, then the mtDNA of Neandertals shouldn't look like modern human mtDNA for that reason. This wouldn't prove that Neandertals contributed other genes to later people, but it would make their mtDNA variation irrelevant to their ultimate fate.

Unlike most papers on the topic, Weaver and Roseman (2005) review this issue. On the basis of their review, they conclude that mtDNA is almost certainly neutral. Here's how they put it:

For the selective-sweep alternative to be correct there would have to have been virtually simultaneous selective sweeps in hundreds of unlinked genetic regions, which seems unlikely (Weaver and Roseman 2005:682).

That does indeed seem unlikely, so it might seem that they have made a solid case.

But -- unsurprisingly to those who read the weblog often -- I think they have left out many important aspects of the story. There is a strong case for mtDNA selection, but Weaver and Roseman (2005) omit much of the data that point to that conclusion. And some of the data that they include actually indicates quite the opposite of what they claim.

They make a very common assumption -- one that is widespread in the human genetics literature -- but one that is nonetheless wrong: every expansion is the same expansion. A review of the sources that Weaver and Roseman (2005) cite shows quite the opposite: expansions are not all alike, and expansions estimated for nuclear DNA may actually prove that mtDNA was selected.

This is a very long post, and I have hidden most of it beneath the fold. Click on in if you want my take on selection on mtDNA....

Is it reasonable to think that mtDNA was selected?

Before embarking on a review of Weaver and Roseman's argument, it is important to tackle one central question: Is it even reasonable to think that mtDNA was selected?

If this were an unreasonable idea, there would be no point to arguing for it. So what reason might one have to think that a selective sweep of mtDNA might have happened?

Within the past 30,000 to 1 million years, human populations have changed radically in longevity (Caspari and Lee 2004), brain size (Lee and Wolpoff 2003; Ruff et al. 1997), diet, and energetics (Leonard and Robertson 1997; Sorensen and Leonard 2001). Human mtDNA variants have been found to be associated with chronic diseases of aging , brain disorders (Zhu et al. 2004), performance in athletes (Niemi and Majamaa 2005), and longevity itself (Niemi et al. 2005). The present pattern of variation also appears to be correlated with climate (Ruiz-Pesini et al. 2004), and may affect the dietary energetics and insulin metabolism (Lowell and Schulman 2005).

Simply put, variation in mtDNA is a strong target for further research into the effects of aging, metabolism, and disorders of the brain for a reason: it impacts all these areas strongly.

Together, these facts strongly suggest that human mtDNA may have undergone multiple adaptive substitutions within the past million years. They don't prove that such selection happened, but they give abundant reason to suppose that it might have. Indeed, Ruiz-Pesini et al. (2004) suggest that adaptive selection has happened on mtDNA in some regions of the world in recent times. This suggestion is fully consistent with -- and even foreshadows -- the idea that mtDNA underwent many adaptive substitutions during human evolution.

In fact, this is exactly the same logic by which many nuclear genes have been asserted to have been positively selected recently in human evolution. Consider the case of FoxP2. Enard et al. (2002) proposed that this gene had undergone a selective sweep within the past 200,000 years in humans, and Klein (2002) made it the centerpiece of his argument that language had evolved recently at the origin of modern humans. Like mtDNA, FoxP2 is strongly out of mutation-drift equilibrium. But human FoxP2 shows many fewer amino acid substitutions compared to chimpanzees than does human mtDNA (2 for FoxP2, 50-60 for mtDNA), meaning that the possibility of selection on human mtDNA should be greater, not less. And FoxP2 is only one functional gene; mtDNA contains 13 peptide-coding regions (Arnason et al. 1996), selection on any one of which would affect the entire molecule.

So what exactly is the difference that leads the same people to say that FoxP2 is selected and mtDNA is not? There is no statistical test of selection that shows FoxP2 to be selected and mtDNA not. Human mtDNA completely fails standard tests of neutrality such as Tajima's D (Merriwether et al. 1991), the ratio of synonymous to nonsynonymous substitutions (Wise et al. 1998), and comparison of within-species to between-species diversity (Wise et al. 1997).

In fact, the only difference I can find is that there is a literature that assumes mtDNA neutrality and attempts to use its variation to determine what kind of neutral event could explain its variation without selection. The only kind of event that suffices is a massive expansion of the human population -- estimated to be a hundred-fold or greater -- from an initial effective population size of fewer than 10,000 individuals to many millions (Harpending et al. 1998; 1993; Sherry et al. 1994). This event is proposed to have occurred anytime from 40,000 years ago to as much as 150,000 years ago or longer -- although the data indicates that it must have occurred earlier in Africa and later in Europe and East Asia.

There is no history of such an assumption for FoxP2 (although it might equally be suggested to represent such an event), therefore its variation is logically assumed to represent a selective sweep.

Population expansions

Thus, the issue of mtDNA selection cannot be separated from the issue of population expansion. It should be noted that an expansion of the human population does not disprove the hypothesis that a selective sweep occurred, but it does provide an alternative hypothesis that might explain the pattern of variation (although not the involvement of mtDNA in energy metabolism, diseases of aging, brain disorders, etc.).

Happily, we can test this alternative. Other genes, in particular, all neutral regions of the nuclear genome, must reflect the same demographic history as mtDNA. Thus, these genes should also show evidence of a massive population expansion.

What's an order of magnitude between friends?

Here's what Weaver and Roseman (2005:681-682) say about nuclear genomic evidence for population expansions:

We believe that the close correspondence between studies of mtDNA and microsatellites and recent studies of autosomal and X-chromosome SNPs that controlled for ascertainment bias and population subdivision makes it reasonable to assume a model of rapid human population growth from a small size, starting 200,000-40,000 years ago.

The microsatellite study they cite is the review by Zhivotovsky et al. (2003). Here's what Weaver and Roseman (2005:681) say:

Most populations show strong signatures of population growth with estimated start times that are consistent with those for mtDNA.

Here are the actual figures from Zhivotovsky et al. (2003:1179):

Estimate:	Africa (Hunter-gatherers)	Africa (farmers)	Eurasia	East Asia
Estimated expansion time (kya)	4.3	35.3	25.3	17.6
Effective population size before growth	2609	1883	1760	1688

In short, these populations are all estimated to have expanded from an effective size of less than 2000 at a time between 17,000 and 35,000 years ago (except hunter-gatherers, who are estimated to have expanded 4300 years ago).

Weaver and Roseman (2005:681) cite a wide range of estimates for mtDNA expansion times: from 200,000 to 40,000 years ago. This range of estimates is wide mainly because of uncertainty about the mtDNA mutation rate. In their simulations, Weaver and Roseman (2005:679) assume a growth starting at 40,000 years ago; this is at or near the latest possible date of expansion for Europe only from other studies (e.g. Harpending et al. 1993; Sherry et al. 1994). Weaver and Roseman (2005:679) assume a preexpansion female effective size of 1000.

Compared to these mtDNA estimates, the microsatellite estimates are not so bad. They are more recent than the most recent possible for mtDNA by a factor of two, but their preexpansion population size is consistent.

What about the SNPs? The autosomal and X chromosomal SNP study they refer to is Marth et al. (2004). Weaver and Roseman (2005:681) say this:

They concluded that all samples showed signatures of population growth consistent with the results for mtDNA. The East Asian and European-American diversity fit a model of a bottleneck followed by growth while the African-American sample fit a model of growth alone. Marth et al. estimated that post-bottleneck growth began 84,000-60,000 years ago for the East Asian sample and 86,000-54,000 years ago for the European-American sample, which overlaps the 200,000-40,000 years ago range for mtDNA. They estimated that growth in the African-American sample started earlier.

Here are the actual figures from Marth et al. (2004:360), for the best-fit models (bottleneck for European and Asian, expansion for Africa), with generations converted to years (assuming 20-year generations):

The sharp-eyed will notice a couple of things about these tables. First, the initial population size between the microsatellite estimates and the SNP estimates is different by an order of magnitude. Now, that has an immense effect on the coalescence times expected for autosomal genes. The initial effective size of 10,000 in the SNP study recognizes that autosomal genes have coalescence times ranging from as little as 200,000 years (or less) to as ancient as 3 million years (or older). This range of dates is simply inconsistent with a long-term effective size of 1000-2000. This inconsistency alone means that the microsatellite estimates must be wrong.

This is a more severe problem than it might appear, because the signature for population expansion from the microsatellites requires a very, very small initial population size. This is because the estimates are based on the variance of allele size taken among sites -- meaning that different loci must have nearly exactly the same coalescent time to show a sign of population expansion (Kimmel et al. 1998; Zhivotovsky et al. 2000). The methods used to substantiate an expansion on microsatellite data simply lack the power to detect an expansion from a initial size as great as 10,000.

In other words, expansions are not all alike: the "expansions" estimated for the SNPs lie outside the statistical power of microsatellites entirely; the expansions estimated to explain microsatellite data are absolutely inconsistent with the large initial population size estimated for SNP data. Both these kinds of loci are autosomal: their evolution -- if neutral -- must follow precisely the same constraints.

Of course, the dates are also different, by a factor of three or more. But the other key difference is that these SNPs indicate not a simple expansion, but a bottleneck.

Can this bottleneck be consistent with the diversity of mtDNA? On the surface, it might seem that a post-bottleneck expansion and an expansion are the same thing. And Fay and Wu (1999) showed that certain kinds of bottlenecks might be consistent with mtDNA disequilibrium and nuclear DNA equilibrium. But the bottleneck estimated by Marth et al. (2004) is much less severe than the simulations of Fay and Wu (1999): [CORRECTION 9/5/05: these bottlenecks simulated by Fay and Wu (1999) are] three times longer (30,000 years) and involves one-half to one-third the population size during the bottleneck. In contrast, the simulations that are most consistent with the estimates of Marth et al. (2004) show that no large effect is expected upon mtDNA variation.

The same conclusion may be drawn from the simulations presented by Ambrose (1998), who tested whether a bottleneck associated with the Toba volcanic event 71,000 years ago might be consistent with human mtDNA variation. These simulations found that such a bottleneck could not be excluded by mtDNA variation. But they also found that the bottleneck could not by itself explain the pattern of mtDNA variation. Instead, a more ancient reduction in population size must have occurred, if mtDNA is neutral. Such a reduction has not been found for nuclear genomic data.

So, the evidence for population expansion from nuclear DNA is not consistent with mtDNA variation. Nor are estimates taken from microsatellites consistent with those taken from nuclear SNPs. All bottlenecks and expansions are simply not alike. Weaver and Roseman (2005) imply that these different sources of evidence are converging on a single answer. In fact, they are diverging from each other.

Why isn't an expansion just an expansion?

It is important to keep in mind the parameters of the possible models, to understand why evidence for expansions is not all alike. The simplest model of ancient demography is a one-parameter model: a single population size, unchanging over time back to infinity. This is the hypothesis of "no expansion", and it is in fact an assertion: the assertion that a model with more parameters does not explain the data better than the one-parameter model.

The next simplest model of demography is a three-parameter model. The parameters are the population size before a change, the population size after the change (or alternately, the magnitude of the change), and the time that the change happened. (A two-parameter model would include only time and magnitude of change; as long as the actual size of the population is important to us we are stuck with the third parameter.) This kind of model is often called a "two-epoch" model, meaning that the population was one size for some period of time, and another size for a second period of time. The only two-epoch demographic models are simple expansions and crashes.

A population crash causes genetic drift to increase -- and genetic drift tends to eliminate rare alleles from the population. So populations that have undergone a crash are expected to show a deficit of rare (low-frequency) alleles, or a surplus of high-frequency alleles. (This, by the way, is also the prediction of balancing selection.)

In contrast, a population expansion reduces the strength of genetic drift, meaning that rare (new) alleles should be more common than expected if population size had been constant. It takes a while for these new alleles to appear, so the strength of evidence depends on the time of the expansion -- that third parameter.

Now, let's stop to notice a couple of things. First of all, microsatellites are different from SNPs in that SNPs are often unique mutations, whereas microsatellite alleles are length polymorphisms that can be arrived at by lots of different mutations. This means that "rare" microsatellite alleles do not provide the same kind of evidence for expansion that rare SNPs do. In practice, estimates of ancient demography from microsatellite data do not depend on rare alleles at all; instead, they depend on the pattern of allele size variation among different microsatellite loci. That's one reason why the results of the microsatellite and SNP studies look so different: they are using different, apparently incommensurable, observations of variation.

Second, the consideration of the two-epoch model shows two options: a population crash or a population expansion. But one of these -- the crash -- is extraordinarily unlikely to be true for humans.

For one thing, the human population really did expand in size recently. Not only was there an incredible explosion of populations after the advent of agricultural subsistence, but also there is good archaeological evidence for substantial population expansions in the Late Pleistocene (e.g. Stiner et al. 2000).

For another, the human population is subdivided into many populations -- a structure that itself increases the proportion of rare alleles in the global population (Ptak and Przeworski 2002). So a population crash is essentially not an option. If the data significantly refute the one-parameter model (i.e. constant size), then expansion is the only kind of three-parameter model at play.

In other words, human genetic data are biased. They ought to show evidence of strong population expansion. They ought to be inconsistent with constant population size back to infinity.

So why, in so many cases, aren't they?

No expansion? Are you kidding?

As Weaver and Roseman (2005:681) note, Ptak and Przeworski (2002) reviewed more than 400 genomic regions and found no substantial evidence for expansion. And the "expansion" found by Marth et al. (2004; likewise Marth et al. 2003) is not the manyfold population growth that actually happened: it is an expansion from 10,000 people to 18,000 (at a minimum) or 25,000 (at a maximum) (!). As we have seen, only microsatellite data look remotely like the magnitude of human population growth, but they are completely wrong about the initial size and time of expansion.

There is a simple answer: the proportion of rare alleles is affected by things besides population size. As Ptak and Przeworski (2002), population subdivision is one of these. As Polanski and Kimmel (2003) note, ascertainment bias may be another. And natural selection is very likely to be another influence on the proportion of rare alleles -- even at "neutral" sites, considering the effects of linkage to selected sites (Gillespie 2000).

And as discussed by Marth et al. (2004), nuclear SNP data actually do not fit the three-parameter model. For non-African populations, they fit a five-parameter model: a bottleneck. This model reflects a mix of observations at different sites: there is an excess of low-frequency (rare) alleles, at the same time there is an excess of high-frequency alleles (Sherry 1996), as compared to both the three-parameter and one-parameter models. This excess of common alleles does not greatly reduce the appearance of a slight expansion in the three-parameter model, so it cannot account for the mismatch between genomic variation and archaeological data. But it may also result from the effects of selection, as certain SNPs may have been driven to high frequencies by positive or balancing selection.

Eswaran et al. (2005) suggest another explanation for the signature of a bottleneck in nuclear SNPs. They find that such a pattern is the expected result of the assimilation of archaic human lineages into an expanding modern human population. This pattern contrasts strongly with the expected signature of population expansion under a replacement scenario of modern human origins. They conclude that archaic assimilation is more consistent with the pattern of genomic SNP data than replacement.

As we can see, the explanation of nuclear genomic variation requires the consideration of many complexities that may affect the outcome. These complexities, taken together, mean that nuclear DNA variability bears no simple causal relationship with ancient population sizes. In particular, it cannot replicate the pattern of Upper Paleolithic and Holocene expansions that are reconstructed from archaeological data. Instead, estimates based on genetics (under assumptions of neutrality in up to five-parameter models) are generally more than an order of magnitude different.

It is therefore incorrect to say that nuclear genomic evidence is consistent with mtDNA variation. In fact, it currently appears to be inconsistent, although it is fairer to say that we do not know the relevance (if any) of genomic variation to demographic reconstruction. Strikingly, one of the few ways to make these different sources of data consistent with each other may be to require the survival and proliferation of nuclear gene lineages from archaic humans (Eswaran et al. 2005). Populations did grow, and and this growth may have affected the pattern of mtDNA variation. But the inconsistencies are great enough that they cannot currently be explained by demography alone.

Ancient genes and geography: the data Weaver and Roseman omit

Weaver and Roseman (2005) substantiated their assertion that mtDNA is neutral by using four primary references: Marth et al. (2004), Zhivotovsky et al. (2003), Ptak and Przeworski (2002), and Pritchard et al. (1999). As reviewed above, one of these (Ptak and Przeworski 2002) contradicts their argument, as do two others mentioned more briefly (Pereira et al. 2001; Hammer et al. 2003).

But there are other relevant sources of information not included in the paper. Three of them are absolutely critical, since they bear directly on the hypothesis that genetic material from archaic humans survives in present human populations.

The first category of "missing information" are the many studies of gene-geography relationships by Alan Templeton and colleagues (e.g., Templeton 2002). Based on the examination of the geographic variability of a dozen nuclear genes, these studies have concluded that an Out of Africa replacement of archaic humans cannot explain the pattern of human genetic diversity. Instead, the studies find significant evidence for ancient genetic structure including Europeans and East Asians. Templeton has argued (2002) that the pattern of mtDNA (and Y chromosomal) variation may represent one recent migration among many out of Africa; but the data are also consistent with a recent selective sweep. These data conclusively refute the hypothesis that no archaic gene lineages survived into living human populations.

Templeton's studies have been critiqued on the grounds that they may not actually distinguish survival of archaic gene lineages outside Africa from survival of archaic lineages inside Africa. In other words, it has been claimed (Pearson 2003; Eswaran et al. 2005) that ancient population structure within Africa might mimic the survival of gene lineages from outside Africa. Eswaran et al. (2005) show that this scenario is likely not the case, as nuclear genomic data apparently reflect the survival of archaic non-African lineages. But this equivocation bears little importance to the explanation of mtDNA: even the survival of archaic lineages from within Africa challenges the idea that mtDNA variation reflects the expansion of one small African population and the displacement of others. Instead, survival of archaic African lineages suggests that the ancient population size of Africans was effectively much larger (perhaps many orders of magnitude larger) than a neutral mtDNA hypothesis would admit. Together Templeton's work and the analysis of Eswaran et al. (2005) indicate that the majority of genomic loci preserve allelic variation that originally characterized archaic human populations.

The second category of evidence missing from Weaver and Roseman (2005) also bears on this issue of archaic survival. In addition to the genomewide analyses and Templeton's phylogeographic studies, both of which suggest the survival of a large proportion of archaic gene lineages, recent work has uncovered several genes that cannot be accommodated within the framework of a recent mtDNA expansion and replacement of archaic humans. These genes include (but are not limited to) the region around Xp21.1 (Garrigan et al. 2005), the Xp/Yp and 12q telomeric regions (Baird et al. 2000), and an inversion on 17q21.31 (Stefansson et al. 2005). Several other loci were discussed at the 2005 AAPA meetings, and I know of a few more that are in press.

In short, genomic data are not consistent with mtDNA neutrality, and a growing number of detailed studies have documented loci that represent the survival (and proliferation) of archaic human gene lineages. Much of this literature on specific loci has emerged in the last year; it is no surprise that it is missing from Weaver and Roseman (2005).

But Templeton's analyses have been well known for years, and they bear directly on the issue. They are mentioned by Weaver and Roseman (2005:677) only as evidence that anthropological geneticists "favor a predominantly extra-European origin for the earliest modern populations in Europe" (!!!).

The third category of missing information is the fossil and archaeological record. According to Weaver and Roseman (2005:682):

Our results stress the importance of fully integrating archaeological, fossil, and genetic evidence in investigations of modern human origins.

It is therefore striking that the paper includes no acknowledgement of the fossil and archaeological evidence that supports Neandertal-modern reproductive continuity. This evidence includes (but is not limited to):

1. The persistence of Neandertal traits in post-Neandertal populations (Frayer 1993; Duarte et al. 1999; Wolpoff et al. 2001; Trinkaus et al. 2003). Trinkaus (2005:218) concludes that the model of no interbreeding between Neandertals and modern humans is "intellectually dead."
2. The intergradation of Neandertal and contemporary populations, illustrated by their substantial morphological overlap in West Asia (Kramer et al. 2001; McCown and Keith 1939).
3. Shared directionality of morphological evolution in Neandertals and contemporary populations (Hawks and Wolpoff 2001).
4. The cognitive continuity of Neandertals and succeeding populations, evidenced by their substantially shared technical and symbolic ability (d'Errico 2003).

It seems clear that no genetic model that excludes a role for Neandertal genetic persistence can be considered to be "integrated" with these archaeological and fossil observations. Certainly considerable disagreement exists about the level of Neandertal contribution to later Europeans (as well as the level of Upper Paleolithic contribution to the more recent European gene pool). But evidence of intermixture is clear and recognized even by those who suspect that the actual level of such intermixture was low (Bräuer et al. 2004). Together with the full pattern of genomic evidence, it seems clear that such intermixture is a potent explanation for the evolutionary pattern of the early Upper Paleolithic in Europe, as well as other regions during the Late Pleistocene.

The bottom line

The issue here is not whether a population expansion occurred in the Late Pleistocene and Holocene. It certainly did. But does this expansion by itself explain the distinctive pattern of human mtDNA variation? And if so, does the fate of the Neandertals hinge on this demographic hypothesis?

A consideration of a fuller set of genomic data indicates that the answer to both these questions is no.

Human mtDNA has very likely been under positive selection. The evidence for this selection is as strong as for nearly any other selected locus. Although the specific target of the most recent selective sweep has not yet been identified, the same is true of other genes that are believed to have been under selection, such as FoxP2. The pattern of variation cannot be explained by population expansion, because other genomic regions are either inconsistent with mtDNA, inconsistent with each other, or inconsistent with any expansion at all.

Determining whether Neandertals particularly contributed genetic material to the living human population is a challenge. Even if clear evidence of archaic lineages is found, it is difficult to substantiate that these lineages were found in a particular region of Europe over 40,000 years ago.

Yet, substantial evidence of archaic lineages has been found. There is no question that some -- perhaps most -- human genes preserve allelic variation from archaic human populations.

The morphological and archaeological evidence suggest strongly that Neandertal genetic lineages survived into later Upper Paleolithic populations. Ultimately, the genetic test of Neandertal survival may be carried out by finding nuclear DNA sequences from Neandertal fossils themselves. Until that time, we can say only that some Neandertal contribution to the modern human nuclear gene pool is consistent with the known evidence.

References:

Ambrose SH. 1998. Late Pleistocene human population bottlenecks, volcanic winter and differentiation of modern humans. J Hum Evol 34:623-652.

Arnason U, Gullberg A, Janke A, Xu X. 1996. Pattern and timing of evolutionary divergences among hominoids based on analyses of complete mtDNAs. J Mol Evol 43:650-661.

Baird DM, Coleman J, Rosser ZH, Royle NJ. 2000. High levels of sequence polymorphism and linkage disequilibrium at the telomere of 12q: Implications for telomere biology and human evolution. Am J Hum Genet 66:235-250.

Bräuer G, Collard M, Stringer C. 2004. On the reliability of recent tests of the Out of Africa hypothesis for modern human origins. Anat Rec 279A:701-707.

Caspari R, Lee SH. 2004. Older age becomes common late in human evolution. Proc Natl Acad Sci U S A 101:10,895-10,900.

Currat M, Excoffier L. 2004. Modern humans did not admix with Neanderthals during their range expansion into europe. PLoS Biol 2:e421.

d’Errico F. 2003. The invisible frontier: A multiple species model for the origin of behavioral modernity. Evol Anthropol 12:188-202.

Duarte C, Maurício J, Pettitt PB, Souto P, Trinkaus E, van der Plicht H, Zilhao J. 1999. The early Upper Paleolithic human skeleton from the Abrigo do Lagar Velho (Portugal) and modern human emergence in Iberia. Proc Natl Acad Sci U S A 96:7604-7609.

Enard W, Przeworski M, Fisher SE, Lai CS, Wiebe V, Kitano T, Monasco AP, Pääbo S. 2002. Molecular evolution of FOXP2, a gene involved in speech and language. Nature 418:869-872.

Eswaran V, Harpending H, Rogers AR. 2005. Genomics refutes an exclusively African origin of humans. J Hum Evol 49:1-154.

Fay JC, Wu CI. 1999. A human population bottleneck can account for the discordance between patterns of mitochondrial versus nuclear DNA variation. Mol Biol Evol 16:1003-1005.

Frayer DW. 1993. Evolution at the European edge: Neanderthal and Upper Paleolithic relationships. Prehistoire Europeenne 2:9-69.

Garrigan D, Mobasher Z, Severson T, Wilder JA, Hammer MF. 2005. Evidence for archaic Asian ancestry on the human X chromosome. Mol Biol Evol 22:189-192.

Gillespie JH. 2000. Genetic drift in an infinite population: the pseudohitchhiking model. Genetics 155:909-919.

Hammer MF, Blackmer F, Garrigan D, Nachman MW, Wilder J. 2003. Human population structure and its effects on sampling Y chromosome sequence variation. Genetics 164:1495-1509.

Harpending HC, Batzer MA, Gurven M, Jorde LB, Rogers AR, Sherry ST. 1998. Genetic traces of ancient demography. Proc Natl Acad Sci U S A 95:1961-1967.

Harpending HC, Sherry ST, Rogers AR, Stoneking M. 1993. The genetic structure of ancient human populations. Curr Anthropol 34:483-496.

Hawks J, Wolpoff MH. 2001. The accretion model of Neandertal evolution. Evolution 55:1474-1485.

Kimmel M, Chakraborty R, King J, Bamshad M, Watkins W, Jorde LB. 1997. Signatures of population expansion in microsatellite repeat data. Genetics 148:1921-1930.

Klein R, Edgar B. 2002. The dawn of human culture. New York: John Wiley and Sons.

Kramer A, Crummett TL, Wolpoff MH. 2001. Out of Africa and into the Levant: Replacement or admixture in Western Asia. Quaternary International 75:51-63.

Lee SH, Wolpoff MH. 2003. The pattern of evolution in Pleistocene human brain size. Paleobiology 29:186-196.

Leonard WR, Robertson ML. 1996. On diet, energy metabolism and brain size in human evolution. Curr Anthropol 37:125-128.

Leonard WR, Robertson ML. 1997. Rethinking the energetics of bipedality. Curr Anthropol 38:304-309.

Lowell BB, Shulman GI. 2005. Mitochondrial dysfunction and Type 2 diabetes. Science 307:384-397.

Manderscheid EJ, Rogers AR. 1996. Genetic admixture in the Late Pleistocene. Am J Phys Anthropol 100:1-5.

Marth G, Schuler G, Yeh R, Davenport R, Agarwala R, Church D, Wheelan S, Baker J, Ward M, Kholodov M, Phan L, Czabarka E, Murvai J, Cutler D, Wooding S, Rogers A, Chakravarti A, Harpending HC, Kwok PY, Sherry ST. 2003. Sequence variations in the public human genome data reflect a bottlenecked population history. Proc Natl Acad Sci U S A 100:376-381.

Marth GT, Czabarka E, Murvai J, Sherry ST. 2004. The allele frequency spectrum in genome-wide human variation data reveals signals of differential demographic history in three large world populations. Genetics 166:351-372.

McCown TD, Keith A. 1939. The stone age man of Mount Carmel: The fossil human remains from the Levalloiso-Mousterian, volume 2. Oxford: Clarendon Press.

Merriwether DA, Clark AG, Ballinger SW, Schurr TG, Soodyall H, Jenkins T, Sherry ST, Wallace DC. 1991. The structure of human mitochondrial DNA variation. J Mol Evol 33:543-55.

Niemi AK, Majamaa K. 2005. Mitochondrial DNA and ACTN3 genotypes in Finnish elite endurance and sprint athletes. Eur J Hum Genet 13:965-969.

Niemi AK, Moilanen JS, Tanaka M, Hervonen A, Hurme M, Lehtimäki T, Arai Y, Hirose N, Majamaa K. 2005. A combination of three common inherited mitochondrial DNA polymorphisms promotes longevity in Finnish and Japanese subjects 13:166-170.

Pearson O. 2003. Has the combination of genetic and fossil evidence solved the riddle of modern human origins? Evol Anthropol 13:145-159.

Pereira L, Dupanloup I, Rossser ZH, Jobling MA, Barbujani G. 2001. Y-chromosome mismatch distributions in Europe. Mol Biol Evol 18:1259-1271.

Polanski A, Kimmel M. 2003. New explicit expressions for relative frequencies of single-nucleotide polymorphisms with applications to statistical inference on population growth. Genetics 165:427-436.

Pritchard JK, Seielstad MT, Perez-Lezaun A, Feldman MW. 1999. Population growth of human Y chromosomes: A study of Y chromosome microsatellites. Mol Biol Evol 16:1791-1798.

Ptak SE, Przeworski M. 2002. Evidence for population growth in humans is confounded by fine-scale population structure 18:559-563.

Ruff CB, Trinkaus E, Holliday TW. 1997. Body mass and encephalization in Pleistocene Homo. Nature 387:173-176.

Ruiz-Pesini E, Mishmar D, Brandon M, Procaccio V, Wallace DC. 2004. Effects of purifying and adaptive selection on regional variation in human mtDNA. Science 303:223-226.

Sherry S. 1996. Estimating human effective population sizes with genetic models incorporating demographic fluctuation. Ph.D. thesis, Pennsylvania State University.

Sherry ST, Rogers AR, Harpending H, Soodyall H, Jenkins T, Stoneking M. 1994. Mismatch distribution of mtDNA reveal recent human population expansions. Hum Biol 66:761-775.

Sorensen MV, Leonard WR. 2001. Neandertal energetics and foraging efficiency. J Hum Evol 40:483-495.

Stefansson H, Helgason A, Steinthorsdottir GTV, Masson G, Bernard J, Baker A, Jonasdottir A, Ingason A, Gudnadottir VG, Desnica N, Hicks A, Gylfason A, Gudbjartsson DF, Jonsdittir GM, Sainz J, Agnarsson K, Birgisdottir B, Ghosh S, Olafsdottir A, Cazier JB, Kristjansson K, Frigge ML, Thorgeirsson TE, Gulcher JR, Kong A, Stefansson K. 2005. A common inversion under selection in Europeans. Nature Genet 37:129-137.

Stiner MC, Munro ND, Surovell TA. 2000. The tortoise and the hare: Small-game use, the broad-spectrum revolution, and Paleolithic demography. Curr Anthropol 41:39-73.

Templeton AR. 2002. Out of Africa again and again. Nature 416:45-51.

Trinkaus E. 2005. Early modern humans. Annu Rev Anthropol 34:207-230.

Trinkaus E, Ştephan Milota, Rodrigo R, Mircea G, Moldovan O. 2003. Early modern human cranial remains from the Peştera cu Oase, Romania. J Hum Evol 45:245-253.

Weaver AH. 2005. Reciprocal evolution of the cerebellum and neocortex in fossil humans. Proc Natl Acad Sci U S A 102:3576-3580.

Wise CA, Sraml M, Easteal S. 1998. Departure from neutrality at the mitochondrial NADH dehydrogenase subunit 2 gene in humans, but not in chimpanzees. Genetics 148:409-421.

Wise CA, Sraml M, Rubinsztein DC, Easteal S. 1997. Comparative nuclear and mitochondrial genome diversity in humans and chimpanzees. Mol Biol Evol 14:707-716.

Wolpoff MH, Hawks J, Frayer DW, Hunley K. 2001. Modern human ancestry at the peripheries: A test of the replacement theory. Science 291:293-297.

Zhivotovsky LA, Bennett L, Bowcock AM, Feldman MW. 2000. Human population expansion and microsatellite variation. Mol Biol Evol 17:757-767.

Zhivotovsky LA, Rosenberg NA, Feldman MW. 2003. Features of evolution and expansion of modern humans, inferred from genomewide microsatellite markers. Am J Hum Genet 72:1171-1186.

Zhu X, Smith MA, Perry G, Aliev G. 2004. Mitochondrial failures in Alzheimer’s disease. American Journal of Alzheimers Disease and Other Dementias 19:345-352.

As the new semester gets underway, it's a good time to think of ways to improve all those assignments I will soon be reading. Few are as pain-free as listening to some old-school music. As in classical music.

As most people know, listening to Mozart will make you smarter. At least, that was the theme of the book The Mozart Effect, loosely based (very loosely) on work in the early 1990's that found that people did better on a spatial IQ test after listening to Mozart, as compared to listening to a relaxation tape.

Dave Munger at Cognitive Daily has been reviewing how the Mozart Effect has fared in the recent psychology literature (via Keats' Telescope). This post reviews a 2002 study that challenges the idea. That paper, McKelvie and Low (2002), shows no effect at all from listing to Mozart:

So in their task, McKelvie and Low used repetitive dance music by the group Aqua to compare to Mozart.

Students were divided into two groups -- one which listened to Aqua first, and the other which listened to Mozart first. After listening to an 8-minute musical excerpt, students were tested on spatial ability. Then they listened to the other excerpt and took a different version of the same test. The result: no significant difference for any of the music. All the test scores were statistically the same. There wasn't even a trend for Mozart.

This about sums it up:

If contrasting music doesn't result in lower IQ scores, then we're really not talking about Mozart enhancing spatial IQ scores, we're talking about verbal relaxation tapes inhibiting them.

Of course, that may explain Deepak Chopra as well...

But one later paper, reviewed in this later post, tends to support some kind of positive effect of classical music on performance, although pointedly not limited to Mozart.

Ivanov and Geake offer some interesting guesses as to why the music improves performance. They point to Rausher's argument that cognitive processing levels remain essentially the same while listening to Mozart's music. They also suspect that music may help to mask the otherwise distracting background noise that is present in nearly all "silent" classrooms.

Munger also reviews a second paper with equivocal results: it doesn't support a Mozart-specific increase, but it may be consistent with a music-related increase in performance.

As for myself, I wonder if this is related to the "mariachi effect" -- you know, how they play fast music in restaurants to make you eat faster.

References:

McKelvie P, Low J. 2002. Listening to Mozart does not improve children's spatial ability: Final curtains for the Mozart effect. Br J Devel Psych 20: 241-258.

Perhaps after the announcement of the draft chimpanzee genome, you're feeling the need for another DNA rush. How long will you have to wait for a gorilla sequence? How about an orangutan? Will anybody give me a sifaka? Sifaka, anyone?

A Nature article by reporter Carina Dennis gives some details about the future schedule of genome sequencing in primates and beyond. Here's the marching order:

1. Rhesus macaque: public draft already available, revised version "expected by the end of the year"
2. Orangutan: sequencing already underway, draft expected "early next year"
3. Gorilla: sequencing begins in "October this year", draft assembly expected in "a couple of years"

After that, there are more ideas of what to do. They start to run together like an insane bioprospecting auctioneer:

While some researchers are working on the the youngest shoots of the primate family tree, others are delving at the roots, to understand what the earliest primate genomes were like. To this end molecular palaeontologists are keen to sequence representatives from each of the major primate lineages. The sequencing of the marmoset, a New World monkey, has just begun. "I would also like the lemur sequence," says Asao Fujiyama of the National Institute of Informatics in Tokyo, Japan, who was part of the team that sequenced the first chimpanzee chromosome last year.

I have to say, if your goal is to reconstruct phylogeny, these sequences aren't going to help much more than what we already have. On the other hand, if you want to reconstruct the evolution of these other lineages, you're going to need a whole lot more -- not just one lemur but many, not just marmosets, but other New World monkeys as well.

But the thing is, within the next five to ten years, these kinds of projects become more feasible with off-the-shelf technology. Not entirely so -- the commercialization will use shortcuts like gene chips tuned for human-specific sequences. But substantially, so that the completion of a draft genome assembly for a primate may become feasible for a single research lab on NSF-level money.

Personally, I think it's going to generate more data than anybody will have time to analyze. But people interested in evolution in primates -- from sexual dimorphism and mating systems to social hierarchies and affiliation --- are going to have to know a lot more about genomics, or are going to have to enlist population geneticists in a lot of that work.

And then Zoboomafoo can be a genome model just like Craig Venter.

References:

Dennis C. 2005. Chimp genome: branching out. Nature 437:17-19. Full text (subscription required)

In Nature's "Progress" section (9/1/05): a paper by Robert Sean Hill and Christopher A. Walsh titled, "Molecular insights into human brain evolution."

Here's the abstract:

Rapidly advancing knowledge of genome structure and sequence enables new means for the analysis of specific DNA changes associated with the differences between the human brain and that of other mammals. Recent studies implicate evolutionary changes in messenger RNA and protein expression levels, as well as DNA changes that alter amino acid sequences. We can anticipate having a systematic catalogue of DNA changes in the lineage leading to humans, but an ongoing challenge will be relating these changes to the anatomical and functional differences between our brain and that of our ancient and more recent ancestors.

That would be my part, the "ongoing challenge".

The review hits the high points of comparative neuroscience, and is basically a catalog of facts. Here's one I didn't remember:

AHI1, which is essential for axon pathfinding from the cortex to the spinal cord (and hence for normal coordination and gait), is another gene that causes a neurological disease when mutated, but for which subtler changes between primate species suggest positive evolutionary selection in the lineage leading to humans. Patients with AHI1 mutations not only show mental retardation, but can also show symptoms characteristic of autism, such as antisocial behaviour. This raises the intriguing possibility that evolutionary differences in AHI1 may relate not only to human patterns of gait, but potentially species-specific social behaviour.

Overall, a concise review and worth assigning in classes.

References:

Hill RS, Walsh CA. 2005. Molecular insights into human brain evolution. Nature 437:64-67. Full text (subscription required)

Hughes et al. (2005) report on the nature of Y chromosome genomic differences between humans and chimpanzees. The paper is a test of the hypothesis popularized by Bryan Sykes (in his book Adam's Curse: The Science That Reveals Our Genetic Destiny): namely, that in a few million years, the human Y chromosome will disappear entirely because its genes will have become entirely inactive or subsumed on other chromosomes.

The short answer is: not gonna happen.

The long answer has some interesting twists. As it turns out, humans appear to have conserved all of the functional Y chromosome genes that occurred in the human-chimpanzee common ancestor. The paper proposes that this is evidence for a stronger effect of purifying selection in humans than might have been assumed. They were able to confirm this by comparing coding divergence with intron divergence; the coding region sequence divergence between species was significantly low. That leaves an interesting evolutionary question: how strong was purifying selection compared to other chromosomes, and could it have affected standing Y chromosome variation during human evolution? Unknown.

But these genes are ordered very differently on the Y chromosome than the equivalent genes in chimpanzees. In chimps, all the X-degenerate genes are together in one region. In humans, they have been scattered around onto both arms of the Y and intermingled with other sequences.

The study is only of a subset of the Y chromosome: the X-degenerate regions, or the parts that contain genes with X chromosome analogs, but only analogs that are significantly divergent from their X chromosome equivalents. So it does not represent a final answer on many of these questions, but it constitutes what may be the most important source of Y-unique evolution.

Although humans retain all of the functional genes of the common ancestor of the two species, chimpanzees have actually lost several. The authors propose a hypothesis to explain this loss:

Why have X-degenerate genes decayed in the chimpanzee lineage but not in the human lineage? We speculate that X-degenerate gene decay in the chimpanzee lineage may be a by-product of strong positive selection focused elsewhere on the Y chromosome, through a process known as genetic hitchhiking. Because the Y chromosome does not participate in sexual recombination with a chromosome homologue, natural selection acts on the chromosome as a unit. Deleterious mutations in some Y-linked genes can be carried along, even to the point of fixation in a population, by physical linkage to strongly beneficial mutations in other Y-linked genes. In addition to their X-degenerate genes, primate Y chromosomes contain many families of ampliconic genes, which have testes-restricted expression patterns and critical functions in sperm production. Because of this central role in spermatogenesis, the Y chromosome's ampliconic genes may be subject to powerful selective pressures, especially in species such as chimpanzees where females usually mate with multiple males, the sperm of which then compete for a limited number of oocytes. During chimpanzee evolution some X-degenerate genes may have been casualties of selective forces directed at the Y chromosome's ampliconic genes--forces that were not as intense during the evolution of our less promiscuous species (Hughes et al. 2005, references omitted).

Could be true. On the other hand, the fixation of a mutation that deactivates a gene is pretty drastic, even if it is hitchhiking with another favorable variant. It certainly implies that the deactivated genes have little adaptive importance to start with. So this reduction in adaptive importance for the deactivated genes must still be explained. The physical difference between ampliconic and X-degenerate genes may have something to do with it, but it can't be the whole story.

References:

Hughes JF, et al. 2005. Conservation of Y-linked genes during human evolution revealed by comparative sequencing in chimpanzee. Nature 437:100-103. Full text (subscription required)

Gravina et al. (2005) report on the radiocarbon stratigraphy of this cave, which is the original type site of the Chatelperronian industry. I think the paper is a very fine example of most archaeological papers I have read. The thing is, like many other papers, I'm not sure it provides enough information for me to understand the conclusion.

The most relevant finding is this:

Hitherto, direct archaeological evidence for [the temporal overlap of Chatelperronian and Aurignacian industries] has proved controversial, with the suggestion that supposedly direct 'interstratifications' of Chatelperronian and Aurignacian levels at three separate sites in western France and northern Spain (Roc de Combe and Le Piage in southwest France, and El Pendo in northwest Spain) might in fact reflect serious confusions or misinterpretations of the stratigraphy at these sites. The results reported here seem to provide clear evidence for a direct interstratification of distinctively Chatelperronian and Aurignacian occupations at the type-site of Châtelperron itself, closely dated by a sequence of 13 high-resolution radiocarbon accelerator mass spectrometry (AMS) measurements by the Oxford Radiocarbon Laboratory (Gravina et al. 2005:1).

The stratigraphy by itself would seem to be adequate for the conclusion: there are 10 typologically Aurignacian artifacts with provenience from the Chatelperronian levels, two perforated animal teeth consistent with Aurignacian typology, and nineteenth-century excavations recovered three unprovenienced Aurignacian blades and one split-based bone or antler point. The interpretation of "interleaving" comes from the observation that the majority of the provenienced Aurignacian artifacts came from one level (B4) of the Chatelperronian, both above and below other Chatelperronian levels (B1-B5). If these typologically Aurignacian artifacts were made by modern humans, then they demonstrate the temporal overlap of Neandertals and modern humans at the site.

Compared to this--a careful historical review--the dates are a bit of an anticlimax: 40,000 radiocarbon years for the bottom of the sequence, 34,500 to 36,000 for the top, and between 39,000 and 36,000 for level B4 with many of the Aurignacian-type artifacts.

The authors attempt a comparison between these radiocarbon dates and the Cariaco Basin deep sea core, which leads them to an interesting argument:

What is clear from the Cariaco basin data is that the overall time range of the human occupation is likely to be much shorter than the range of the radiocarbon dates, with the occupation of B5 centred on 42,000-43,000 yr BP, B4 on ~41,000-42,000 yr BP and that of B1-B3 on ~40,000-41,000 yr BP (ages estimated from the GISP2 ice core). Interestingly, the occupation in phases B5 and B1-B3 seems to be correlated with brief warmer spells visible in the delta ¹⁸O record. The two samples from B4 are somewhat different in age and correlate with the end of one warmer period and the start of the next, separated by an intervening colder phase. This coincides with the brief episode of Aurignacian occupation in level B4. A displacement of Aurignacian populations from central Europe to France in response to sharply colder conditions at this time (especially perhaps the onset of severe winters) would hardly be surprising in ecological and demographic terms, as winter temperatures in the more oceanic areas of western Europe are likely to have been significantly milder than those further to the east... (ibid., 5).

Interesting to me is the possibility that all this stuff actually unfolded over around 2000-3000 years of real (non-radiocarbon) time. This seems more intuitive than the persistence of distinct, static cultures across 6000 years or more, while intermittently in contact with different groups.

Reading between the lines of my description, you may sense a bit of hesitancy toward the conclusions. I'm not an archaeologist, and many of the concerns of trained archaeologists are lost on me. I wouldn't know an Aurignacian blade from a Chatelperron backed point.

But perhaps unlike many non-archaeologists, I have looked to see if I can tell the difference. I happen to have the edited volume Context of a Late Neandertal: Implications of Multidisciplinary Research for the Transition to Upper Paleolithic Adaptations at Saint-Césaire, Charente-Maritime, France on my shelf. Here are five of the Aurignacian blades from Chatelperron (Gravina et al. 2005:3):

Aurignacian edge-retouched blades from Chatelperron

Here are some of the Chatelperron backed points from Saint-Césaire, approximately to the same scale (Leveque 2003):

Chatelperron backed points from Saint-Césaire (Leveque 1993)

There is of course an obvious difference: the Aurignacian blades are retouched on both sides; the Chatelperron points are "backed", or retouched only on one side. But despite their names, the "points" are not necessarily pointier; the tools would appear to be close functional analogues.

Now here's my question: if you have a sample of 65 Chatelperron points from a site (unlike the upper Chatelperronian level of Saint-Césaire where there are only 8), how likely is it that you might find a few that look like Aurignacian blades?

The answer to that might be "very unlikely". Indeed, the fact that some of the Chatelperron "Aurignacian" artifacts are made on materials brought from far away might give an additional reason to think that they stand apart from the average Chatelperron point. And the split-based point is a likely marker of at least strong Aurignacian influence (although it is unprovenienced).

But I would be more convinced by a statistical answer to that question than a typological one. Out of those 65 backed points, how many of them have some retouch on the backed side? Any extensive? There are 750 artifacts in the Chatelperronian levels. Where did they come from? How many of them come from level H4? From the description here, it appears that the Aurignacian-type artifacts come directly from Chatelperronian layers -- that is to say, they are not "interleaved", they found with Chatelperronian-type artifacts. Is that accurate? If not, why not?

These are questions that I could ultimately answer myself through the magic of interlibrary loan, but that would take weeks. They ought to be in this paper. There is no possibility of understanding the importance of 10 atypical artifacts without some assessment of the range of variation of the "typical" ones. All this paper gives is an assertion that they are in fact Aurignacian. That they may be, but how do we know it?

Other related questions I wouldn't expect the paper to answer, but I would expect somebody else to look at soon. Are there artifacts at other Chatelperronian sites that fit these criteria? What would a finite mixture of two industries look like -- especially in the case where there is a lot of one industry and only a few artifacts of another? After all, the Aurignacian and Chatelperronian differ in a few fossiles directeurs, but for the most part they share a lot of tool types at different frequencies. Would that mix of frequencies be statistically identifiable, or would it be indistinguishable from different facies of the same industry?

Probably I'm thinking too much like a biologist. And to be honest, finite mixture analysis may be a bit much to expect from anybody.

So, the paper may be entirely correct for all I know. I'm just asking naive questions, beyond my expertise. But when two pictures look like the ones above, and they are supposed to be typologically identifiable products of "modern humans" on the one hand, and "Neandertals" on the other -- well, it seems to me there needs to be a bit more than an edge of retouch behind that conclusion.

This week's Nature (9/1/05) has a special feature on the chimpanzee genome (subscription required). The introduction is this perspective by Chris Gunter and Ritu Dhand:

We are therefore extremely pleased to present this special section to commemorate the genome of the common chimpanzee, Pan troglodytes. In doing so, we hope to provide a resource for more than just genomics. We introduce the section with a timeline that charts the history of the chimp. This is followed by four Progress pieces that review recent work on chimp culture and behaviour, psychology and neural processing of number systems, as well as a closer look at brain anatomy and neurogenetics at the single-gene level.

On page 69, the Chimpanzee Sequencing and Analysis Consortium reports analysis of the long-awaited draft genome sequence. This is supported on page 101 by Hughes et al., with the sequence of part of the chimpanzee Y chromosome. Comparing the genetic code of humans and chimps will allow us to comb through each gene or regulatory region to find single changes that might have made a difference in evolution, and the authors list some new candidates for further study. Two more research papers by Cheng et al. (page 88) and Linardopoulou et al. (page 94) detail changes in highly variable regions in the human and chimp genomes; additions or deletions of larger chunks of DNA may be as important as single nucleotide changes in shaping our genomes (links deactivated because they aren't functional).

Finally, we need physical evidence to tell us how chimps and humans may have lived millions of years ago. Surprisingly, to date there has been no fossil record of the chimp; on page 105, McBrearty and Jablonski report the first unequivocal fossil evidence of the genus Pan.

I'll be working through several of the papers and posting my comments on them, as well as links to more information. Keep checking back for updates. Together with some interesting stuff coming next week, this is going to be a busy time here!