What traits make us uniquely human? Anthropologists have been occupied with this question for decades in an effort to understand the origins of human evolution and our eventual domination of the planet. Several traits of modern humans-- language, bipedalism, hairlessness, incredibly strong molar enamel, and large brains-- distinguish us from our primate relatives. But the precise story of why and how it all came to be still remains unresolved. Now we can add one more trait to our list of things distinctly human, and its evolution may have pre-dated all others. The evidence comes from a surprising place-- our saliva.
Our saliva contains the enzyme amylase, responsible for cleaving starch molecules into smaller glucose units. Without amylase, we would not be able to digest starch and other complex carbohydrates-- and that means we would not be able to enjoy many of the foods that constitute a large part of the global human diet-- foods such as corn, potatoes, rice, wheat, and sorghum.
Multiple lines of evidence now indicate that the ability to digest large quantities of starch may have been a crucial adaptation in human evolution-- providing the calories needed to grow large, cognitively-sophisticated brains capable of complex language and social cooperation. This idea is a serious departure from the leading hypothesis that carnivory (via hunting) was the dietary shift needed to support large brains in early humans.
The breakthrough study, lead by George Perry of Arizona State University and Nathaniel Dominy of UC Santa Cruz (http://www.nature.com/ng/journal/v39/n10/abs/ng2123.html), first demonstrates that individuals with more copies of the AMY1 gene tend to have higher levels of amylase in their saliva. The researchers then sampled a suite of high- and low-starch populations spanning cultures world-wide-- Hadza hunter-gathers who survive primarily on roots and tubers, and two agricultural populations (Japanese and European Americans) comprised the high-starch sample. Low-starch populations, of which there are considerably few, included rainforest hunter-gatherers (Biaka and Mbuti) and pastoralists (Datog and Yakut). In line with expectations, mean AMY1 copy number was greater in the high-starch compared to low-starch populations.
Notably, there was no geographic pattern in AMY1 copy number to suggest that populations closer to one another have more similar AMY1 copy numbers than populations that are further apart-- this pattern would be expected if variation in AMY1 is driven largely by neutral genetic changes (genetic drift). Instead, the results suggest that variation in AMY1 is related to ecological adaptations in diet. Perry and Dominy hypothesize that natural selection is driving differences in AMY1 copy number. Their results do provide some compelling evidence for natural selection at the AMY1 locus, but the authors cautiously note that the jury is still out on this question-- pending additional data of course.
Shedding some light on the evolutionary history of AMY1, Perry and Dominy also looked at AMY1 variation in chimps and bonobos, our close genetic relatives. Their primary diet-- ripe fruit-- contains very little starch, leading the researchers to predict low numbers of AMY1 in these apes. Indeed, the data indicate that chimps and bonobos have, at most, 2 functional copies of AMY1. The researchers report that humans have 3 times more AMY1 copies compared to chimps, on average-- and bonobos may not have any functional AMY1 copies at all. These findings support the conclusion that elevated AMY1 copy numbers arose in the human lineage, not before it.
If this doesn't convince you, Dominy and colleagues have also found evidence that Homo erectus, an early human progenitor, specialized on eating high-starch corms and tubers. In this sister study, Dominy used stable isotope analysis, a common method to assess diet composition. In a nutshell, the stable isotope signatures of consumers will resemble the stable isotope signatures of their food sources-- after some corrections for fractionation. As it turns out, Homo erectus has a stable isotope signature that is consistent with a high-starch diet, and decidedly not consistent with a carnivorous one.
All of these lines of evidence suggest that having many copies of AMY1 is likely to have evolved early in the human lineage-- indeed it may have been critical to launching humans on our own immensely successful, starch-filled, evolutionary path.
Okay, I need to forget for the moment that L’Oréal unabashedly conducts animal testing in order to provide women with a heap of cosmetics they probably don't really need. Instead, what I need to do is spread the word about L’Oréal's 2008 Women in Science Fellowship for "exceptionally talented young women scientists"-- five of them to be exact. Interested exceptionally talented young women scientists should read on:
L’Oréal USA Fellowships For Women in Science program-- a special fellowship program for exceptional female post doctoral students-- announces the 2008 call for applications (due 10/31/07).
The L’Oréal USA Fellowships for Women in Science grants of $40,000 are awarded each year to five female post docs in the life and physical/material sciences, technology (including computer science), engineering or mathematics.
For more information and application materials, here is their website:
Finally, the second installment of the X Vials... my PLoS pick of the week. But before I get to the paper, I should first explain that I'm a huge fan of PLoS (Public Library of Science) and open access publication. If you haven't heard of PLoS and don't know what I'm talking about, then go to http://www.plos.org/oa/index.html and read up. The short of it is this-- PLoS is a largely internet-based non-profit publisher of original, peer-reviewed scientific literature that is freely accessible to anyone who can access the internet. There is no journal access fee, as is true of most other scholarly journals that restrict access only to those individuals and institutions that can afford it. If you are an academic who has never stepped foot outside a large research university, then you probably don't know exactly how frustrating it can be when you don't have access to the primary literature you need. I spent a whole nine months in such a situation-- it wasn't fun.
So cheers to PLoS for having the vision to start a whole collection of scholarly journals that don't restrict access to select groups of people while excluding those less fortunate! You can download a PLoS paper from any computer, from any institution, in any country, and read to your heart's content. It's a great thing.
I was drawn to this paper because I've been interested in the link between genetic diversity at the major histocompatibility complex (which has its own acronym, MHC, and includes the HLA genes) and sexual selection. Coevolution with disease is one of the leading theories explaining the origin and maintenance of sexual reproduction (aka the Red Queen theory). Parasites and pathogens are good at evolving ways to circumvent our immune defenses. At a molecular level, the pathogen is evolving new surface binding proteins that disguise it's true identity and enable it to pass through the host's immune system. It's analogous to a hacker finding the right password to bypass internet security and access your bank account. So, just as we are all advised to change our internet passwords from time to time to prevent security breeches, our immune systems need to change their locks (antigen-presenting proteins) to keep the pathogens at bay. This process seems to require lots of genetic diversity and recombination of alleles (i.e. sexual reproduction). The MHC is in fact one of the most diverse gene regions of the mammalian genome.
Something so important to an individual's survival, and especially the survival of their future offspring, is bound to play a role in the selection of mates-- and there is evidence supporting this idea in humans and other vertebrates (mammals, birds, and fish). The question is, how do individuals detect another individual's MHC or HLA diversity and what exactly is being selected (maximum HLA diversity in offspring)?
Coetzee et al. focused their study on humans, testing the idea that facial attractiveness correlates positively with HLA diversity and perceived health. While some studies have reported positive correlations between HLA diversity and facial attractiveness (usually more symmetrical faces are judged as more attractive and this may be a useful proxy for sizing up a mate's HLA diversity) other studies have failed to find such a relationship. Coetzee et al. provide an additional study to try and clear up the apparent controversy, and do so using a population with higher expected pathogen loads than previous human populations studied.
As you can glean from their title, they found no evidence for any relationship between HLA diversity and facial attractiveness. Women who were homozygous at their HLA loci (two were examined) were not less likely to be considered healthy and attractive (by a cohort of males of the same ethnic group) than heterozygous women. They even looked at genetic distance, another way to measure diversity, and found no pattern. They did find, however, that women with common HLA alleles considered themselves healthier and reported fewer illnesses than women lacking those common alleles (however this did not affect male perceptions of female facial attractiveness or health).
Before making my own general conclusions, I like to think about the limitations of a study--they all have them. Coetzee et al. point out that they are dealing with a small sample size, which means limited statistical power to detect differences between groups. So maybe there is a pattern there, but they can't detect it. I will add the following-- this study only measured the HLA diversity of the female participants, not the males who ranked female facial attractiveness. My guess is that the HLA diversity of the males involved in the study also matters-- in other words, it's not diversity alone that is being sexually selected, but the particular kind of HLA diversity (alleles) possessed by a mate and how that diversity compares to your own. There's evidence now from multiple sources (mice, humans, sturgeon) suggesting negative-assortative mating with respect to MHC diversity (although not all studies have found this pattern). Translation-- individuals may prefer to mate with partners that have different MHC signatures than their own. Such a preference may lead to novel combinations of HLA genes in offspring that confer fitness advantages.
In my opinion, the question could be addressed more closely by looking for patterns at the individual level and testing whether an individual's HLA sequence predicts the HLA sequences of individuals that they find attractive. So you need genetic information from both sexes and ideally one would want to include an analysis of female preferences as well (anisogamy = choosier females, so if there is a pattern of MHC-based mating preferences, we would reasonably expect those preferences to be stronger in females).
Another point to make: MHC-HLA diversity is probably better known for its effect on individual body odor than facial attractiveness, and this is another mechanism by which individuals can assess each other's MHC-HLA signature (studies in humans and mice support this idea). So, I would also venture to say that facial attractiveness by itself may not be the strongest correlate of an individual's HLA signature. Body odor, or some combination of body odor and physical features, may be a more reliable HLA cue-- this puts a different spin on the perfume industry doesn't it?
So my take-home message from this paper is the following: females with common HLA alleles perceive themselves as healthy and report fewer illnesses than women with rare HLA alleles. Evidence to support a link between facial attractiveness, perceived health, and HLA diversity was not found, but keep in mind the study's limitations. There are still many interesting questions on this topic that remain to be answered-- good news for those interested in deciphering the behavioral and molecular mechanisms of mate choice (and of course eventually we want to link this back to what's going on with those parasites and pathogens that seem to be responsible for this whole sex thing in the first place).
That's all for now. For more info on MHC-dependent mating, there's a nice literature out there. Unfortunately, most of it is published in for-profit journals, so I can't link you to the papers here. For that, you are on your own!
For my first X Vials post, I thought it fitting to blog about one of my favorite evolutionary biologists, W.D. Hamilton. I was reminded of him recently while browsing for something to read during a layover in the Atlanta airport. Inundated with the usual morass of pop culture mags (okay, I admit I bought one of those too-- to gawk at celebrities and feel out-of-touch for not knowing who any of them are these days), my eyes happened upon a National Geographic. On the cover of the July 2007 edition (Malaria: Stopping a Global Killer) is a stunning picture of the mosquito, Anopheles stephensi, carrier of the malaria parasite, a single-celled organism called a plasmodium. I immediately thought of Hamilton, who prematurely left this world on March 7, 2000 six weeks after contracting malaria in the Congo. After being rushed back to England for treatment, Hamilton at first seemed to recover, but then fell into a coma and died of cerebral hemorrhage. Hamilton was described by his colleagues as a brilliant, deep, yet humble scientist (a refreshing combination amongst the egos in academia). He burned brightly, "shine[ing] like a violet ground beetle under a stone"-- the quote from Hamilton's essay, My Intended Burial and Why, in which he described his wish to be buried in the forests of Brazil upon his death. In the end, his body was placed in Wytham Woods, England where, instead of "escaping death" through the violet ground beetle, his essence has perhaps made its way into the many badgers that live there. Hamilton is best known in evolutionary biology for deriving Hamilton's Rule, a simple and elegant mathematical statement predicting when individuals (usually closely related ones, as measured by their coefficient of relatedness, R) should cooperate with one another. In a nutshell, if the indirect fitness benefits (R*B) are greater than the direct fitness costs (C) of cooperation, then kin-based sociality can evolve. It is the basis for understanding kin selection, parental care, and the evolution of complex animal societies (think honey bees, naked-mole rats, etc.).
Hamilton also made significant contributions to the study of sex ratios and the evolution of sex (why do we need males anyway?). Near the end of his life, Hamilton was tackling the origins of the HIV virus in humans, collecting primate scats in the Congo when he contracted malaria. Incidentally, the rise of HIV in Africa in the early 1990s caused an associated increase in malaria due to weakened human resistance. Today, the malaria epidemic is huge, affecting half of the world's population--about a million die each year, primarily children in poor areas of Africa and India. There is no vaccine for the disease, and global warming is expected to extend malaria's range back into the paler regions of the world. In January of 2000, just months before Hamilton's demise, the Gates Foundation pledged 6 billion dollars to developing cures for tropical diseases, with malaria as the front-runner (the Bush Administration has since offered up 1.2 billion). This was driven by a lack of interest on the part of private pharmaceuticals to invest in malaria R&D. Hmm, I wonder why the pharms aren't stepping up to the plate? Perhaps when babies with wealthy parents start contracting malaria... Beyond geographic and economic concerns, the parasite is evolving resistance to the pesticides and medications commonly used to keep it at bay. This is a glaring reminder of why it is so important to understand how evolution works-- parasite populations, having much shorter generation times, can evolve much faster than human populations. We need to be several steps ahead in the coevolutionary game. Religiously-fueled arguments over evolution's legitimacy, whether it should be taught in schools, yada yada, are merely slowing down progress. While we bicker, the parasites are getting better at infecting us. The bottom line is, future generations need to understand evolution better than we do... perhaps even better than both Darwin and Hamilton did. A-hem, I think I will humbly step off my soap-box for now. For the next X Vials, something a little less preachy... my PLoSpick of the week.
But before I sign off, a big kudos to my sis (the Artista!) for designing the X Vials web banner! It looks perfecto....
I'm a postdoc whose research focuses on the ecology and evolution of social and mating systems. This blog is my experiment in using the web to share ideas and network with other science-minded types. My aim is to cover research developments in evolutionary biology (broadly defined) and comment on academic culture, particularly the status of women in science.