I just want to point out, on the "six generations of daughters" story...
The family has an astonishing six generations of daughters still living. The matriarch of the family, Mollie Wood, was born in 1901 and just marked her 111th birthday. The youngest addition to the family, Braylin Marie Higgins, was born in March to Wood’s great, great granddaughter.
...that the baby and the 111 year old share the same fraction of genes as the average European shares with a Neandertal.
Ferris Jabr has begun a series called "Know your neurons", which will be a tour of the types of neurons. The first installment ("Know Your Neurons: The Discovery and Naming of the Neuron") covers the science that established the existence of neurons, in the late nineteenth century, when Santiago Ramón y Cajal used the staining technique developed by Camillo Golgi to visualize and draw detailed pictures of the microscopic cells. At issue was whether all the nerve fibers ultimately merged into a connected network, or reticulum:
Golgi’s “black reaction,” combined with the painstaking work of Karl Deiters and others, clearly distinguished two kinds of projections from cell bodies in nervous tissue: a long slender cable that did not seem to branch much and a cluster of shorter branching fibers. Even though Golgi saw that one cell body’s branching fibers did not fuse with another’s, he did not reject Gerlach’s idea of the reticulum—instead, he decided that the long slender cables probably connected to form one continuous network.
Ramón y Cajal showed that the fibers did not merge into a continuous reticulum, the essential data supporting the neuron theory. I'll look forward to more in the series.
Laura Clarke and colleagues report on the data access and management practices of the 1000 Genomes Project [1].
The larger data volumes and shorter read lengths of high-throughput sequencing technologies created substantial new requirements for bioinformatics, analysis and data-distribution methods. The initial plan for the 1000 Genomes Project was to collect 2× whole genome coverage for 1,000 individuals, representing ~6 giga–base pairs of sequence per individual and ~6 tera–base pairs (Tbp) of sequence in total. Increasing sequencing capacity led to repeated revisions of these plans to the current project scale of collecting low-coverage, ~4× whole-genome and ~20× whole-exome sequence for ~2,500 individuals plus high-coverage, ~40× whole-genome sequence for 500 individuals in total (~25-fold increase in sequence generation over original estimates). In fact, the 1000 Genomes Pilot Project collected 5 Tbp of sequence data, resulting in 38,000 files and over 12 terabytes of data being available to the community. In March 2012 the still-growing project resources include more than 260 terabytes of data in more than 250,000 publicly accessible files.
The paper acknowledges that this large-scale genetic sequencing project nevertheless generates far less data than physics and astronomy projects. The Large Synoptic Survey Telescope, for example, will generate 20 terabytes each night of operation, while the Large Hadron Collider will generate roughly 15 petabytes per year. The 1000 Genomes Project data to date add up to around two weeks of LSST operation. Still, it's not hard to see how high-coverage sequencing will start to catch up in data storage and transfer requirements.
We are now in a golden age of data centralization. But five years from now, we may return to a second era of disposable data, as gene expression and whole-genome resequencing studies will generate far more data than any central repository can store. We will need curation practices to identify and preserve data that have value beyond the project for which they were collected.
The beautiful thing about this is that when data are abundant, they don't all have to work together. There is a real role for a new generation of curators to facilitate the mashups of the future.
A story on NPR examines "social jet lag", an obscure phenomenon in which people stay up late and sleep in late on the weekends ("Jet-Lagged By Your Social Calendar? Better Check Your Waistline").
"Unfortunately, we have caveman's hard-core wiring," Emsellem says, "and insufficient sleep in primitive times was read by the body: Danger, store fat," she says.
Aaaack! So toddlers and the elderly are nature's chosen people, and ... oh, I can't even finish that thought. If I read one more time about the hard-core wiring of cavemen, I'm going to unleash the Morlock horde on these people.
The new research by Tanya Yatsunenko and colleagues examining gut microbiomes in different human populations is just incredibly cool work [1]. I don't have time to write much about it this morning, but Ed Yong's report is an excellent place to start: "Three nations divided by common gut bacteria".
The population genomics of these gut microbes is a great topic also, but what I find most interesting is the parallel ontogenetic changes among populations from infants to adults:
The guts of babies are dominated by Bifidobacterium – the group that’s commonly found in probiotic foods. They’re also loaded with genes for producing folate, an essential B-vitamin that’s involved in creating and repairing DNA. These folate-making genes decline as babies grow up, and get more of the vitamin from their diets. At the same time, the genes for making other vitamins, like B1, B7 and especially B12, become more common. “This similarity across cultures in building up the gut microbiome in childhood has been touched on before but it’s much more convincing here,” says Peer Bork, from the European Molecular Biology Laboratory.
Adam Van Arsdale also has written up some thoughts about the research: "The human gut microbiome".
Michael B. Eisen: "The solution to the ‘serials crisis’ on campus"
The solution is obvious: universities must stop outsourcing vital functions to publishers. They need to shift the currency of academic success from the title of the journal in which a scholar’s works are published to the inherent quality of their research. And they need to immediately stop spending money on journal subscriptions, investing instead in the new forms of scholarly communication appropriate for the Internet age.
On Wednesday, May 16, PBS here in the U.S. is broadcasting a film called "Bones of Turkana".
The astonishing life of Richard Leakey — paleoanthropologist, conservationist, statesman, provocateur —will be the subject of an hour-long special from National Geographic, Bones of Turkana. The program investigates four decades of exploration and discovery around Northern Kenya's Lake Turkana, which have given rise to both breakthroughs and controversy in the contentious field of human evolution.
The film follows Leakey today — along with his wife, Meave, daughter Louise and the world-famous fossil hunters of the Turkana Basin Institute team — striving and exploring along the shores of a mercurial and prophetic lake. It is both a portrait of a remarkable family, as well as a dramatic tale of a place that, despite momentous climate change, has never ceased being the cauldron of human evolution.
Sounds like a lot to squeeze into an hour...
Alon Keinan and Andrew Clark have a short report in the current Science examining the effects of recent human population growth on the expected spectrum of human genetic variation [1]. Population growth skews the variation in a population so that there are many more rare alleles than would be expected in a constant-sized population.
Why is this? In a constant-sized population, individuals have an average of two offspring who survive to have offspring of their own. Many people have no children at all, or only one, while only a small proportion of people have more than four children. In the constant-sized population, a person born with a new mutation would have a 50% chance of passing it on to each child. In such a population, more than a third (36%) of mutations aren't passed on even once. The same fraction are inherited by only one child, and these face the same odds of extinction in the next generation. This isn't natural selection, it is random genetic drift -- and its net result is that most new mutations are lost.
In a growing population, individuals average more than two offspring. Every additional offspring increases the chance that a new mutation will be passed on to the next generation. In other words, more people means less genetic drift. As a population grows, new mutations begin to stack up at low frequencies in the population.
This is a very basic point in population genetic theory, and it interacts in a troubling way with the current generation of sequencing technology. Short-read shotgun sequencing yields a high number of false positive mutations, which must be aggressively filtered out of whole genome data. If we don't filter these out, we will arrive at incorrect conclusions about many aspects of human biology. The simplest means of filtering require some understanding of how many rare mutations you expect to find, in particular how many should be found in only one person in a sample of people. That expectation is different in a growing population, resulting in a potentially large bias.
Despite an improvement in the accuracy of sequencing technologies, some errors remain unavoidable. For example, with a sequencing error rate of 1 in 10,000 bases, in a sample of 10,000 individuals, each base pair will exhibit two errors on average across the sample and the majority of monomorphic sites will appear polymorphic (most often as a singleton or a doubleton; i.e., with the rare allele present in one or two copies in the sample). On the other hand, strict filtering of the data will lead to missing many rare variants because they are not observed as reliably. Hence, any analysis of large sample sizes must account for the uncertainty inherent in sequencing by considering the variant calls probabilistically, and secondary validation of rare variants by an alternate sequencing procedure is essential.
Keinan and Clark present some models that show how much it matters to consider a growing population compared to the usual null model of constant population size.
It's so interesting to me to see human geneticists catching up to where anthropologists have been for a long time. Of course, we wrote about the effects of recent population expansions in 2007, noting the apparent acceleration of positive selection in post-agricultural populations ("Why human evolution accelerated") [2].
Large-scale sequencing projects have moved beyond simply categorizing common genetic variation. They are now at a stage where thousands of individuals need to be examined, to find increasingly rare genetic variations and determine their collective effects on phenotypes. That means that the next version of the 1000 Genomes Project really needs to be involve many of us who are directly concerned with human population history. The growth and dynamics of actual historic human populations are going to matter to how we understand their genetic variation and its effects on phenotypes. Fortunately, archaeology and written history can help -- if anthropologists are involved in this work from the start!
Captive chimpanzees do clever things, but how deep is their planning? Michael Balter describes a research study following how one chimpanzee harasses zoo visitors: "Stone-throwing chimp plans ahead".
The next day, Santino again threatened visitors with stones, but the group again backed away to avoid being hit. Santino was then observed pulling a heap of hay from inside his enclosure and placing it on the island close to where the visitors approached. He put several stones under the hay and waited until the group returned about an hour later. Then, without performing a dominance display, Santino pulled a stone from under the hay and threw it. Later, he pulled a stone that he had apparently hidden behind a log and tried to hit the visitors with that, as well.
This kind of research is a response to Morgan's Canon, the principle that animal behavior should be explained by the lowest-level cognitive process possible. If you want to demonstrate some kind of intentional planning, you have to do very close ethological study of every step in the planning process. The principle is a way of countering anthropomorphism -- animals sometimes do complex-looking things that actually impose very simple cognitive requirements. But it's good to remind ourselves that chimpanzees aren't ants.
Carole McGranahan describes a memorable case where academics shut down public discussion of their work: "Dialogue with the Public: Adam Yauch and Academic Snobbery". The subject of the story is the recently deceased Beastie Boys member Adam Yauch.
Before anyone on the panel could reply, one of the conference organizers—a Harvard professor—stood up and said forcefully that this was an “academic conference” and that “emotional” questions would not be entertained. He made it clear we were here to discuss real politics in an academic, dispassionate manner. That is: in discussing politics we were to be apolitical.
A celebrity unrecognized by the academics, asking a simple question.
Razib Khan comments on the current round of Henry Louis Gates ancestry programming: "Finding fake roots", and "Reification is alright by me! Razib notes that the criteria that tell many subjects that their ancestry is a mixture of different populations are conditioned on assumptions that don't work at all for South Asians. From the latter:
In my post below some commenters argued that obviously implausible inferences from a thin set of reference populations are acceptable considering Henry Louis Gates Jr’s target audience. But that really wasn’t my main point. Rather, it was that he was eliding the distinction between uniparental markers, and the clusters generated by modeled based ancestry assignment algorithms, and ascribing the phylogenies of the former to the latter. It is important to note that categories like “Europeans” are only approximations. But they’re damn good approximations today! Nevertheless, note the qualification of time: they may have basically no meaning at some point in the recent past. They’re powerful when it comes to precisely partitioning modern variation, but they don’t tell us the history of that variation.
The uniparental marker "interpretations" given to people doing genealogical work has become increasingly comical in its distance from what we now know about ancient variation. For example, I carry mtDNA haplogroup H, and here's what the Genographic Project tells me about that history in their "Atlas of the Human Journey":
Around 15,000 to 20,000 years ago, colder temperatures and a drier global climate locked much of the world's fresh water at the polar ice caps, making living conditions near impossible for much of the northern hemisphere. Early Europeans retreated to the warmer climates of the Iberian Peninsula, Italy, and the Balkans, where they waited out the cold spell. Their population sizes were drastically reduced, and much of the genetic diversity that had previously existed in Europe was lost. Beginning about 15,000 years ago -- after the ice sheets had begun their retreat -- humans moved north again and recolonized western Europe. By far the most frequent mitochondrial lineage carried by these expanding groups was haplogroup H. Because of the population growth that quickly followed this expansion, this haplogroup now dominates the European female landscape.
Here, a very common mtDNA haplogroup today is given its own origin myth, complete with a glacial refugium and massive expansion and dispersal. The text goes on to explain how this European haplogroup spread right out of southern Europe into central Asia, where today -- surprisingly -- it is even more variable and shows less sign of expansion. Notice how precise the story sounds, a fleshed-out history for people looking to connect their roots to European prehistoric events.
Why do I say comical? We have ancient mtDNA from all over Europe now, from Neolithic and pre-Neolithic people, showing that haplogroup H was barely there before farming.
I don't mean to single out Genographic for this issue, in fact the whole edifice of genealogical interpretation is built on assumptions about history that are currently known to be false. We can do much better than this, I think. But many of the same characters who failed five or six years ago keep plugging at it, persisting in describing a distorted version of human history.
UPDATE (2012-05-08): The thing that really bugs me, is that the amount of money spent producing a season of one of these programs would be more than enough to get some of us to straighten some of these problems out. Population genetics is a lot cheaper than media. Or, to put it in a more inspiring way: any media organization that is willing to spring for a couple of postdocs along with their program can show some real science instead of making stuff up. Just saying...
Are narrative stories the glue that holds society together? That's the thesis of literature professor Jonathan Gottschall, who has written for the Boston Globe, "Why fiction is good for you". It's a précis of his book, The Storytelling Animal: How Stories Make Us Human.
In Appel’s study, people who mainly watched drama and comedy on TV — as opposed to heavy viewers of news programs and documentaries — had substantially stronger “just-world” beliefs. Appel concludes that fiction, by constantly exposing us to the theme of poetic justice, may be partly responsible for the sense that the world is, on the whole, a just place.
This is despite the fact, as Appel puts it, “that this is patently not the case.” As people who watch the news know very well, bad things happen to good people all the time, and most crimes go unpunished. In other words, fiction seems to teach us to see the world through rose-colored lenses. And the fact that we see the world that way seems to be an important part of what makes human societies work.
I met Gottschall at the Consilience Conference last week and he is an energetic and insightful presenter. Construction of narratives is an important cognitive tool, one that may be fundamental to planning social action. If we consider the oral storytelling in preliterate societies, fictional stories and myth both provide a domain for individuals to learn about the social expectations of other group members. Gossip is another way of communicating about social expectations and intentions, but has a more immediate seriousness as it concerns actual individuals. A fictional story draws attention to intentions and rules in a context that is removed from immediate threat.
Jack Hitt writing in the NY TImes writes some thoughts on the way that online post-publication commentary and review are changing the authority of scientific statements: "Science and Truth - We're All In It Together". He takes as his theme the 2005 "sighting" of the ivory-headed woodpecker. Every piece of evidence that appeared to support this sighting was later debunked by serious naturalists and amateur birders, working in a loose network centered on a blog. Early in the public exposure of the story, more prominent scientists given fuller information than the public had privately expressed doubts, but held their tongues.
Take the case of the ivory-bill. The article in Science has never been retracted. Cornell still stands by its video. The federal Fish and Wildlife Service acted as though the ivory-bill existed, and, in 2008, it asked for $27 million to support recovery efforts. Here’s the thing: The ivory-billed woodpecker is the Schrödinger’s cat of contemporary media — dead to those who’ve looked inside Tom Nelson’s blog but alive to the professionals who can’t bear to.
Adam Van Arsdale considers whether a "bushy", speciose phylogeny is actually evidence of evolutionary "complexity": "Linearity and simplicity in the fossil record". As he points out, there's nothing especially "complex" about looking at two fossils and calling them different names. More complex are evolutionary scenarios that involve reticulate genealogies that cross population or subspecies boundaries.
One thing that is certain is that the fossils generally categorized within [early Homo] encompass a broad range of variation, perhaps providing support for greater taxonomic diversity. But I would suggest that the variation we see in the fossils is more parsimoniously assigned to greater evolutionary complexity – complexity that may come from the rapid development of differentiated niche structures and reproductive barriers in early Homo, but that also might come from the development of a highly structured, geographically dispersed, behaviorally flexible, polytypic lineage. Indeed, most of the changes we observe in early Homo can be interpreted as changes towards a broader, more generalized and flexible ecology.
The null model for early Homo should be the kind of evolutionary pattern that we now know to be true for Late Pleistocene humans. Multiple populations, much more highly differentiated than today's human populations, existed during the Late Pleistocene and exhibited nonuniform patterns of expansion and mixture. The expansions of some groups within and outside Africa were likely driven by gene-culture coevolution, as both technological changes and physiological changes affected population growth. We are beginning to appreciate that similar episodes of expansions and mixture happened throughout the Pleistocene. The origin of our genus, initiating the first expansions of hominins into Eurasia, was surely driven by a similar process.
The Guardian is giving us some pre-London-Olympic buildup, including an interesting article about the impact of strategies to make female athletes more like males: "The rise of performance-enhancing genes".
While not necessarily agreeing with this statement quantitatively, qualitatively it is sound. Female world and Olympic records set prior to random drug testing have been much harder to break. For example, while there is a steady progression in the male Olympic athletic records, there are as many female Olympic records still standing that were set prior to 1990 as those that were set in the last decade. It is hard not to argue with the implication that the steroid doping that was widespread in the 1980s has had a more dramatic effect in female sport than male sport.
I also did not know the story of Dora Ratjen, a gender-ambiguous German athlete and 1938 female European high jump champion.
Blond hair is relatively common in island Melanesia, even though the skin pigmentation of Melanesian peoples is relatively dark. Eimear Kenny and colleagues report in this week's Science that one SNP variant in the gene TYRP1 explains a high proportion of the variance in hair color in this population [1].
Resequencing of TYRP1 exons detected a single previously unknown polymorphism, a C-to-T transition at chr9:12,694,273 (GrCH37/hg19), that corresponds to a predicted arginine-to-cysteine mutation (R93C) in exon 2 of TYRP1 at amino acid position 93 (TT in blond- and CT or CC in dark-haired individuals)...[more on assessing effect in a GWA panel].
We genotyped R93C in 918 Solomon Islanders for whom we had measured hair pigmentation with spectrometry. A recessive model provided the best fit for the data, and R93C genotypes accounted for 46.4% of the variance in hair color (linear regression; P = 2.19 × 10−90; Fig. 1D and table S2). The frequency of the 93C allele in the Solomon Islands is 0.26, and genotyping of R93C in an additional 941 individuals from 52 worldwide populations revealed that the 93C allele is rare or absent outside of Oceania (table S3). Furthermore, we found no evidence for recent gene flow from Europe (i.e., admixture) (figs. S5 and S6) nor a strong signature of recent positive selection for the 93C allele (figs. S9 to S11).
This paper is very short, only a few paragraphs. When I read through it, I got one impression of the results, and that impression changed greatly when I looked into the supplement.
Some underreported facts:
1. The blondness allele is present in all the samples from the Solomon Islands, at a frequency as high as 49% in a large sample from Malaita. In this study, the authors found it at its lowest frequency in "Polynesian outlier" islands near the Solomons.
2. The allele was not found in any of the HGDP samples, even when they were genotyped specifically for this study. That includes the "Melanesian" and "Papuan" samples. These two are relatively small in HGDP (n=14 and n=16 in this study) but even so would probably present this allele were it present at anything like the frequency in the Solomon Islands.
3. The text of the paper reports that a recessive effect model is the best explanation for the relation of hair pigmentation and TYRP1 genotypes. The supplement shows that the recessive model is only very slightly better than a "codominant" model, as it only explains an additional 3 percent of the variance. In the best case considering this allele along with age and geographic origin of the individuals, only 48% of the variation of hair pigmentation can be explained. That leaves 52% to be explained by other genetic and nongenetic causes. There may be a lot of genetic background, which may include more alleles of large effect.
4. Skin pigmentation varies greatly among these Solomon Islands samples, with more than a third of the overall variance in skin pigmentation explained by geography. The tables don't make it clear how pigmentation is patterned by geography. The TYRP1 allele that is the subject of this paper does not explain much variation in skin pigmentation.
5. Sex and age have strong effects on hair pigmentation in this sample, but not on skin pigmentation. Again, these point to background genetic factors. Many populations have sex and age effects on hair pigmentation, so some of the additional causal factors may be widely shared.
I began looking more deeply into TYRP1 R93C for a couple of reasons. The prehistory of human populations in the Solomon Islands goes back more than 30,000 years. Because this allele is not present in mainland Asian populations, as far as we know, but it is present thoughout the Solomons, suggests that it may have become common at or near the initial founding of this population. The LD pattern around the mutation likewise suggests that it has been segregating in this population for a long time. The data are consistent with the idea that blond phenotypes were present in the Solomon Islands as early as the initial colonists who founded the population.
It will be interesting to look further into nearby populations to see if it characterized early colonists more broadly. Blond phenotypes occur very commonly in Aboriginal Australians, also age-dependent in expression, as many children have blond hair that darkens with age. Other Melanesian islands, such as Vanuatu and Fiji, also have a high incidence of blondness. For the islands, I expect that the same allele will be responsible for a similar fraction of the variance. For Australia, I would guess that this allele is also present, but with 40,000 years of evolution, there could well be a more diverse genetic explanation.
Pigmentation variation in Eurasia is clearly a phenotype that has been affected both by recent positive selection and selection on old, standing genetic variants. Europe and East Asia today each have a dozen or more alleles that individually have strong effects on skin, hair, or eye pigmentation. Many of the alleles common in one region are rare in the other. These are well explained by recent selection on pigmentation; if there had been no selection on pigmentation, the populations would not show as extensive a pattern of differences, and new alleles would not have reached high frequencies. But if we had only a single mutation at 30 percent distinguishing one of these populations, which had arisen as early as 30,000 years ago, we would not have a strong case for selection.
In Melanesia, we have just the opening sketch of pigmentation variation. We know that there is substantial variation in skin and hair pigmentation, and that one mutation unique to this part of the world explains a large fraction (but still a minority) of the variance in hair pigment. The other genes that contribute to variation in hair and skin pigmentation are not known. Possibly, skin pigmentation variation among the geographic regions in this study may reflect late prehistoric migration of people through this region, as agriculture moved into the area and Polynesia was settled. But the genetic part of this story remains to be demonstrated.
Both Asia and Europe have a similar pattern of selection which has favored new alleles along with some old, standing alleles. Across the temperate regions of Europe, East Asia, and the Americas, it is plausible that the disadvantages of dark pigment for vitamin D production manifested themselves. It is also plausible across these regions that the advantages of dark pigment as protection from UV radiation would have been relaxed, allowing sexual selection on pigmentation to play an important role.
The evidence here suggests that this allele in Melanesia has not been recently selected from a new mutation. Additionally weighing against recent selection is the observation that the mutation acts recessively on hair pigmentation -- recent selection is much more likely for mutations with dominant or additive effects.
Together, these observations suggest that variation in human pigmentation emerged in stages. Some genes, such as ASIP, have old alleles that explain some of the variation in pigmentation today and are geographically ubiquitous, in Africa, Eurasia, and the Americas. This genetic variation was older than the Late Pleistocene. Such genes (ASIP is probably an example) today have alleles associated with darker pigment that are common in sub-Saharan Africa. Probably many other genes have variation within Africa that are part of the ancestral pigment variation of humanity. As people dispersed throughout the world, mixing with archaic humans, they carried some of these pigmentation variants along with them.
What's interesting is that even though some of these ancient alleles lighten skin pigmentation, they remain segregating in today's light-pigmented populations. They were not selected to fixation, even though there was plenty of time for them to increase toward fixation, and even though strong selection on pigmentation appears to have been present in many high-latitude populations. Later mutations that lighten pigmentation were strongly selected in these same populations, some reaching very high frequencies, while the old mutations still were not selected to fixation.
The story is of course more complex than a simple count of standing and new mutations. Some genetic changes that lighten pigmentation may have countervailing negative effects. Solving the problem of becoming light pigmented in just the right way may really be a different problem in different populations. Founder effects may have shifted the genetic background of early Eurasian populations just enough to create strong path-dependence for later mutations, allowing some to proceed rapidly and blocking the rise of others.
The story of TYRP1 gives a new perspective on the early evolution of pigmentation outside Africa. Here is a novel allele that originated within the earliest colonists to Oceania, which affects hair pigmentation strongly, in a population that was always low-latitude. It did not come from earlier archaic humans as far as we know so far (not in the Denisova genome). It may have become common by a founder effect. We cannot rule out selection, such as social or sexual selection, as a cause of its initial spread or current geographic distribution, but we have no genetic evidence in favor of such selection. We know from the data that there must be many other loci that affect pigmentation in this population.
This may have been much like the original pigmentation genetics of early modern human populations. It may also be much like the pattern that accounts for pigmentation variation within Africa today. It is not a simple story in which a few loci of large effect explain the evolutionary pattern. It is a story in which a substantial store of segregating variation persists within populations for tens of thousands of years.
Why does that matter? Here's one reason: We're looking at possible pigmentation variants in archaic humans, and we have counted many of them. Anyone might begin this project with the presumption that Neandertals and Denisovans had pigmentation variants that were fixed relative to living people. In that context, it would be surprising to find that they had not introgressed.
But if all these ancient populations had a large store of small-effect variants affecting pigmentation, a mutation that we find in one individual might have been rare in the population. The TYRP1 R93C allele varies from 5 to 50 percent in the Solomon Islands samples. We already know that the MC1R coding variant in some Neandertals is not found in the Vindija genomes. Variation in pigmentation loci may have been ubiquitous in human populations, with few fixed alleles separating populations. The ancient landscape was more like ASIP than SLC24A5.
The New York Times has a long profile of developmental psychologist Elizabeth Spielke, whose work with babies has opened a window on early cognition ("Insights from the youngest minds"). The article is wide-ranging and worth sharing. I thought I'd make an note of Spielke's version of the "cathedral" model in which distinct cognitive functions are combined by executive consciousness into synthetic abilities. She denotes language as the functional glue holding the brain's abilities together:
Dr. Spelke is also seeking to understand how the core domains of the human mind interact to yield our uniquely restless and creative intelligence — able to master calculus, probe the cosmos and play a Bach toccata as no bonobo or New Caledonian crow can. Even though “our core systems are fundamental yet limited,” as she put it, “we manage to get beyond them.”
Dr. Spelke has proposed that human language is the secret ingredient, the cognitive catalyst that allows our numeric, architectonic and social modules to join forces, swap ideas and take us to far horizons. “What’s special about language is its productive combinatorial power,” she said. “We can use it to combine anything with anything.”
She's in a position to test that by looking at prelinguistic children. I think there's much truth in the idea, but some functional integration must take place in any conscious organism, even without language. Language allows a complexity of expression, but complexity does not necessarily mean integration.
Today's public service announcement, by Virginia Postrel: "Recycling Eyeglasses Is a Feel-Good Waste of Money".
In a paper published in March in the journal Optometry and Vision Science, four researchers compare the full costs of delivering used glasses to the costs of instead delivering ready-made glasses in standard powers (like my drugstore readers, but for myopia as well). The authors find that recycled glasses cost nearly twice as much per usable pair.
Glasses (which we should probably call "polycarbonates" instead) are pretty cheap to manufacture and distribute in quantity these days. From the linked article, it's amazing how much wastage there is in the process of recycling this kind of product.
Digging through some literature this afternoon, I ran into a 2007 paper by Denise Su and Terry Harrison [1], who mounted several explanations for why Laetoli, Tanzania, has a relatively low abundance of Au. afarensis fossils compared to other sites. They suggest a size-sorting bias due to predation, which would disproportionately have affected postcranial bones:
The evidence supports the inference that, with increasing body size of the prey species, there is a greater chance that skeletal elements will survive complete destruction by carnivore scavenging. This results in a higher representation of postcranial elements relative to craniodental remains as body size increases. However, the converse means that species in the lower weight categories are increasingly susceptible to being entirely destroyed by carnivores. Hominins, which occur in the lowest end of the range for WC II, would be among those large mammals expected to be most heavily affected by the greatest number of species with the ability to completely remove skeletal elements from the skeletal assemblage at Laetoli. If this model is correct, then it is not unexpected that so few postcranial bones of hominins have been recovered. In fact, it is precisely what would be predicted at an open-air site with subaerial deposition in which the skeletal assemblage was readily accessible to carnivore scavengers.
They also point to the variation in the abundance of living chimpanzees and other primates in different ecologies.
Extant chimpanzees occur at a wide range of population densities across equatorial Africa according to habitat. Densities range from 0.08–0.09/km2 in open woodland (Ugalla, Tanzania; Mount Assirik, Senegal) to 3.1–4.7/km2 in closed woodland and forest (Gombe, Tanzania) (Plumptre and Cox, 2006), an almost sixty-fold difference between marginal and optimal habitats. This observation gives us a better appreciation of how different types of habitat can influence the biomass of African hominoids. It can be assumed that similar levels of population-density variation would have characterized A. afarensis across its geographic range. Given this fact, if A. afarensis at Hadar is indeed more common than at Laetoli, then it would suggest that Hadar had habitats that were more optimal for sustaining higher population densities of A. afarensis compared to Laetoli. The magnitude of the difference between the specimen counts between Hadar and Laetoli are equivalent to the difference in population density between modern-day chimpanzees living in closed and open woodland habitats, respectively.
Based on the fauna -- which interestingly include some rat genera now absent in East Africa but present in India and Southeast Asia -- along with other indicators, they infer that Hadar had more woody cover than Laetoli during the period represented by the hominins.
This is cool, from Big Think: "563 - Pop by Lat and Pop by Long".
More details and a map by latitude (even cooler) at the link.
