Dobzhansky on continuing human evolution
On a bit of a writing junket for his book, Mankind Evolving, in 1963 Theodosius Dobzhansky put an essay in Current Anthropology titled "Anthropology and the Natural Sciences -- The Problem of Human Evolution."
He spends the first half of the essay expositing a dual inheritance theory of human evolution, with both biological and cultural systems included, and puts forward an argument for a synthetic vision of the cultural and biological approaches to studying humanity.
Like any well-written essay, it is really in the second half that this argument builds up steam. This passage concerning the recent force of natural selection as a result of cultural changes is a good example:
The radical changes in the ways of life of our generation compared to those of our parents and grandparents must have been largely cultural rather than genetic. This only proves again the absence of one-to-one correspondence between genetic and cultural changes; this does not prove that the biological evolution of mankind has stopped or that it is irrelevant to the cultural evolution. It is admittedly difficult to prove that mankind has changed biologically since, let us say, the days of the ancient Greeks and Romans, if by "proof" you mean demonstration of sizeable gene differences. We cannot test the genes of Pericles or Caesar or their contemporaries. But neither was Darwin able to "prove" organic evolution in this sense. The evidence is indirect, inferential, but nevertheless, I think, conclusive. Paradoxically, it is precisely because we know that mankind changes so greatly culturally that we can be so confident that it changes to some extent also genetically. When the environment changs, the only other necessary condition for the occurrence of genetic evolutioanry chagne can be defined. This is the presence in human popluations of genetic variants, some of which confer upon their carriers a higher fitness in the older, and other variants in the incoming environments. Despite all the inadequacies of our present knowledge of human genetics, this can scarcely be doubted. What is more, since the environment in which man lives is in the first place his sociocultural environment, the genetic changes induced by culture must affect man's fitness for culture and hence may affect culture. The process thus becomes self-sustaining. Biological changes increase the fitness for, and the dependence of their carriers on culture, and therefore stimulate cultural developments; cultural developments in turn instigate further genetic changes. This amounts to a positive feedback relationship between the cultural and the biological evolutions. The positive feedback explains the great evolutionary change, so great that it creates the illusion of an unbridgeable gap between our animal ancestors and ourselves.... Those who believe that man no longer evolves biologically might contend that our species has entered upon such a period. Here we must, however, proceed with the greatest caution. The potentialities for rapid evolution of the human species have not been depleted, since hte environment continues to change and the genetic variance remains plentiful. Mankind assuredly continues to evolve, both culturally and biologically (Dobzhansky 1963:147, emphasis added).
This really became the conventional view within a certain school of human evolutionists (which ultimately encompassed my own training), although not always so clearly expressed. It is behind the notion that culture is the "human niche," although not going so far as the ultimate expression of the "niche" idea, which came to hold that no other cultural species could have existed alongside ours.
I would say that Dobzhansky represents the rational conclusion about human evolution from the perspective of the neo-Darwinian synthesis. After having begun from the premise that morphological evolution must be explicable in population genetic terms, there is a problem for the synthetist: human behavior (and morphology itself to the extent that it is influenced by behavior) includes a learned component that can induce behavioral stability across genetic variants in time or space. In population genetic terms, this is an environmental effect, but it is clearly a determining effect for much of what interests us about humans. And culture is not readily incorporated into a synthesis in which the population genetic mechanisms are the basis of change.
So Dobzhansky attempts to bring the fields of biological evolution and cultural "evolution" together with three basic assumptions:
(1) Human exceptionalism -- "Man is the sole product of evolution who has achieved the knowledge that he came into this universe out of animality by means of evolution" (p. 148). The effect of this is to cordon off cultural evolution as a special mechanism applying to humans.
(2) Separate causes. By assuming that the causes of cultural evolution are different from the causes of biological evolution, Dobzhansky envisages a feedback process between the two. If they had the same causes (i.e., maximization of Darwinian fitness), then cultural evolution could simply supplant biological evolution. Nor would there be any possibility of a "conflict" between the two, as he goes on to discuss.
(3) Biological variation is value-neutral. This is the anti-racist assumption that marks a strong difference between Dobzhansky and many of his contemporaries.
These latter two claims both reflect the orthogonality of cultural and biological variation. In other words, the factors that cause and maintain cultural variability are not the same as the factors that cause and maintain biological variability, and the two are (potentially) independent. (We may observe that to the extent that a "feedback" process occurs, it is by inducing some correlation between the factors underlying cultural and biological variation). The two assumptions are marked by the following quote from page 147:
The chief reasons why so many people are loath to admit the genetic variability of socially and culturally significant traits are two. First, human equality is stubbornly confused with identity, and diversity with inequality, as though to be entitled to an equality of opportunity, people would have to be identical twins. Human diversity is not incompatible with equality. Secondly, it is futile to look for one-to-one correspondence between cultural forms and genetic traits. Cultural forms are not determined by gnes, but their emergence and maintenance are made possible by the genetically conditioned human diversity. The division of labor in human societies is primarily a cultural rather than a genetic phenomenon, but could it be sustained in a population consisting of persons genetically as similar as identical twins? This is not entirely a vain question, since at least one great geneticist has recently envisaged the possibility of bringing about such genetic uniformity.
I find it interesting that in comparison with most exponents of dual inheritance theory, Dobzhansky does not accept a fourth assumption that cultural evolution applies to rapid change and genetic evolution applies to slow change -- in other words, an assumption of "different rates." He knew all too well that the pace of genetic evolution is often rapid, and follows the implication of that view to quite logically conclude that cultural evolution could induce rapid biological evolution within humans, even asserting the logical necessity of accepting genetic evolution of humanity "since the Greeks and Romans."
After the passage cited above, Dobzhansky goes on to describe the perils of recent cultural and biological evolutionary trends in our species, which have tended toward population explosion and the potential hazards therein. Then he proceeds to point out that worries that evolution has been "suspended" are wrongly directed:
Neither do I need to retell here the story of the alleged relaxation or suspension of natural selection in civilized mankind. THe dangers from this source, although not necessarily exaggerated, have often been presented in a wrong perspective. A notion, which is less frequently stated explicitly than implied in many writings, is that the progress of mankind would be safe and even irresistable if only the natural selection were permitted to operate unobstructed by civilization and its amenities. This notion does not stand critical examination. Natural selection does not even insure that the species on which it acts will survive, let alone that it will improve, in any sense of the word "improvement." Dinosaurs became extinct, despite their evolution having been piloted by natural selection, quite unhampered by culture, medicine, or charity (Dobzhansky 1963:148).
Of all the major population geneticists of the synthesis, Dobzhansky was probably the least sympathetic with the aims and practices of the eugenicists. And he spends several paragraphs in this paper describing -- in not so many words -- why the problems addressed by eugenicists were wrongly posed.
But even in spite of this skepticism of aims, Dobzhansky is more or less accepting of the potential for human controls to deliberately control natural selection on humankind -- as he wrote (p. 148): "Man, if he so choose, may introduce his purposes into his evolution."
The paper ends with this (I would offer, "apocalyptic") vision of anthropology:
Being an anthropologist only by avocation, I may perhaps venture to claim for anthropology more than most anthropologists dare claim for themselves. The ultimate function of anthropology is no less than to provide the knowledge requisite for the guidance of human evolution. Human evolution has arrived at a crossroad from which there is no turning back and no escape. Our animal past is irretrievably lost -- we could not go back to it even had we wished. The choice is between a twilight, cultural as well as biological, or a progressive adaptation of man's genes to his culture, ans od man's culture to his genes. But to fulfill its function, anthropology cannot belong entirely either to biological or to social sciences or to humanities. It must, in the fullness of time, become a synthesis of all three (148).
Well, I think he probably could have predicted that the mantle of planning human destiny was not really what anthropology was about, even in 1963. In fact, reflecting on that date, this is probably about as close to a Kennedy-esque vision of anthropology as ever was expressed!
References:
Dobzhansky T. 1963. Anthropology and the natural sciences - The problem of human evolution. Curr Anthropol 4:138+146-148.
Ewald bird flu spat
Scientific American has an editors' blog, SciAm Observations. I point to it because a series of recent posts has included an interesting exchange among evolutionary biologist Paul Ewald, the editor John Rennie, and an anonymous "senior public health scientist". The exchange developed after an LA Times op-ed by Wendy Orent, which discussed Ewald's views.
Ewald believes on evolutionary grounds that any bird flu pandemic is likely to have a much lower mortality rate from the disease than either the recent cases of the H5N1 variant or the 1918 pandemic. From his letter:
The future that we are debating concerns the evolution of influenza viruses. Being an expert on the molecular biology or epidemiology of influenza viruses does not translate into expert assessments of the future evolution of influenza viruses. One need only peruse the writings of such influenza experts to recognize that they generally fail to incorporate the most essential component of the evolutionary process into their arguments--they talk as though mutation and reassortment were the only processes relevant to the evolution of influenza viruses. To discuss evolutionary processes with any degree of expertise one must focus on natural selection. Mutations and reassortments generate the variation on which natural selection acts. But natural selection molds viral evolution.
...
A second process critical to accurate predictions of the future threat posed by H5N1 is the evolution of virulence. The evolution of virulence is linked to the evolution of transmissibility because high virulence itself curtails transmission unless conditions allow transmission from people who are immobilized with illness. Evolution of increased transmissibility of H5N1 from human to human is bound to go hand in hand with drastic evolutionary reductions in virulence. The history of influenza provides strong evidence for this conclusion. Except for the 1918 pandemic, all the trustworthy evidence from all the years of well documented influenza epidemics and pandemics indicate that influenza viruses maintain themselves evolutionarily at low to moderate virulence when transmission depends on host mobility. Influenza experts who do not understand natural selection--or choose to ignore its implications--fail to realize how powerful this evidence is. The last century represents countless thousands of "natural experiments" involving countless trillions of mutation-prone viruses. If the highly virulent variants were able to spread in competition with strains of low or moderate virulence we would see some evidence of regional outbreaks. Instead we see only epidemics and pandemics of low to moderate virulence.
Essentially, the theory is that a virus that spreads by social contact requires its host to be socially active in order to spread. Make him too sick, and he won't be seeing very many people. Some diseases, like malaria and cholera, don't fit this model because they can spread from inactive hosts --- mosquitoes carry malaria away from a prostrate body, cholera spreads in water fouled by the sick. Ewald argues that the 1918 flu was likewise an exception, because situations like the trenches in Western Europe and the open sick wards of hospitals allowed the virus to spread effectively from incapacitated hosts to many new ones.
A later post carries a reply by the anonymous critic. Here's an excerpt:
But it should be obvious, even to him, that if a very virulent disease becomes transmissible before virulent effects immobilize the host, very virulent diseases can propagate with ease. SARS is not very transmissible until the host is seriously ill. Influenza, on the other hand, is transmissible before and during the early phases of illness. Moreover, Ewald objects that a 2% mortality shows the virus is very virulent. Why? Yes, 2% is high mortality for seasonal flu, whose case-fatality rate is usually on the order of 0.1%, the very figure Ewald predicts will hold for a pandemic strain. What epidemiologists know about pandemic strains, however, is that they tend to have higher mortality than the seasonal ones. Ewald assumes that there will be no difference in mortality from a subtype against which there is no population immunity compared to one where there is substantial population immunity. We know 2% mortality is attainable by influenza. I guess being an expert in evolutionary biology doesn't make you an expert in immunology, public health or infectious disease epidemiology.
If you're interested in the bird flu, the exchange is worth reading in full, along with Rennie's earlier posts. None of the participants is saying (as far as I can tell) that a flu pandemic wouldn't be a terrible thing. They differ on the likely mortality rate in the event a pandemic should occur -- Ewald predicts it won't be greatly above the yearly flu strains that we already see, others predict it will either be much higher or even catastrophically higher.
I don't have a dog in this hunt, but I notice several points:
1. Almost no mainstream press accounts of the bird flu threat discuss anything about the evolution of influenza. This is probably the most important public impact of evolutionary theory today, but we hear almost nothing of the evolutionary modeling of how the virus may change.
2. Ewald is very well known for studying the evolutionary dynamics of disease. He is making an argument that is sound, as far as the dynamics of selection are concerned. Thus, there are good reasons to think that the worst will not happen, and this is a perspective that has been underplayed.
3. So far, the theory has only been tested by a relatively small number of instances -- there just haven't been so many pandemics that we can infer accurately from past events what the future will be like. It could certainly happen that some new influenza strain could violate the model in some unexpected way, and for this reason governments should play it safe rather than assume that no high-virulence pandemic will emerge.
4. A lot of public health scientists are going to be well-employed for as long as the bird flu remains in the public perception. This doesn't mean that they are wrong to convey alarm, but it does mean that they don't benefit by playing down the threat. It's sort of like NASA and the asteroid impact threat --- partly they are more concerned because they know more about the threat and its terrible effects, partly because it's their job to be concerned.
5. There are a lot of biologists who don't use or understand selection.
The genetic networks underlying disease
Last week, the NY Times printed an interesting article by Andrew Pollack, titled "Redefining disease, genes and all." The article explores recent (and ongoing) attempts to map the genetic networks underlying common disease phenotypes.
Many people, including me, have criticized the HapMap and other attempts to catalog disease alleles because they depend on an evolutionary fallacy. These projects are best at finding genetic variations that are relatively common in today's human populations -- common because the number of people surveyed in such studies is ultimately limited. But if an allele were bad in an evolutionary sense -- that is, if it lowers fitness -- then it shouldn't be common. So we really shouldn't expect to find alleles associated with common disease phenotypes.
Naturally, there are exceptions, which we can find if we consider some population genetics. A bad allele may become common if its bad effect doesn't really lower fitness. Disease phenotypes that occur late in life, such as Alzheimer's, have a minimal impact on their victims' fitness, because for the most part the childrearing years are long past.
Or, an allele that yields one unpleasant phenotype may actually increase fitness -- sickle cell and other instances of heterozygote advantage are examples of this.
Or, the disorder associated with the allele may occur only in the presence of some new environmental factor. Obesity is one such phenotype: lately on the increase, it cannot have been common throughout most of our evolutionary past because of resource limitations.
But aside from these exceptions, we can expect that any common allele is likely to explain relatively little of the overall risk of any given disorder. And indeed, so far, this is precisely what genome surveys have found. Many disorders now have known genetic associations, but these are almost always alleles of relatively weak effect on the phenotype.
Another reason to look for risk alleles, even if they are of weak effect, is that they may help to identify the genetic interactions that lead to disease. This idea has been around for a long time. Mapping the genes that cause Mendelian disorders in a given phenotype led to our current understanding of genetic pathways underlying skin color, inner ear function, blood clotting, and many other biological functions. Finding some genes associated with Alzheimer's is helping to unravel the physiological observations on people with the disorder, particularly the role of beta-amyloid plaques in the disease progression.
Many workers are currently trying to facilitate these kinds of discoveries by developing new functional maps of gene-disease associations and interactions. Pollack's article focuses on the growing discrepancy between symptomology and etiology -- the consequences of a disease and its causes:
Scientists are finding that two tumors that arise in the same part of the body and look the same on a pathologist's slide might be quite different in terms of what is occurring at the gene and protein level. Certain breast cancers are already being treated differently from others because of genetic markers like estrogen receptor and Her2, and also more complicated patterns of genetic activity.
"In the not too distant future, we will think about these diseases based on the molecular pathways that are aberrant, rather than the anatomical origin of the tumor," said Dr. Todd Golub, director of the cancer program at the Broad Institute in Cambridge, Mass.
The process is really one of atomizing disease. As Pollack notes, diseases that once were considered different kinds of cases of a single disorder -- like hemophilia -- were later shown to be due to distinct defects in different genes. A diffuse grouping of "like with like" has given way to much greater specificity at the biochemical and genetic level for many disorders.
Complex disease phenotypes that involve interactions among many genes will fall the last, but computational methods are starting to attack them:
Other scientists use data on which genes appear to cause disease or contribute to the risk of contracting it.
Using such data, Marc Vidal, a biologist at Harvard, and Albert-Laszlo Barabasi, now a physicist at Northeastern University, created a map of what they called the "diseasome" that was published last year in The Proceedings of the National Academy of Sciences.
Diseases were represented by circles, or nodes, and linked to other diseases by lines that represent genes they have in common -- something like the charts linking actors to one another (and ultimately to Kevin Bacon) based on the movies they appeared in together.
But obviously if the genetic associations are weak, they do not give great hope of simple effective treatments for such complex diseases. And some genetic similarities may lead people to infer equivalences that do not really exist.
What is lacking from this story -- and in general from the field -- is an understanding of evolution. If there is one thing that can deal with the genetics underlying complex phenotypes, it is natural selection. Population genetics has been dealing with the theory underlying genetic interactions for a hundred years. Now we have empirical observations on gene networks, all of them products of our evolutionary history.
So it is disheartening to see that some prominent figures in the field of human genetics (and who hold the purse strings for so much funding) have little familiarity with the evolutionary dynamics of gene interactions:
"I'm shaking my head with disbelief that two genes would pop up in these two diseases that have absolutely nothing in common," said Dr. Francis S. Collins, the director of the National Human Genome Research Institute. He said another gene, cyclin-dependent kinase inhibitor 2A, seemed to be involved in cancer, diabetes and heart disease.
I'm shaking my head in disbelief that Collins doesn't seem to be aware of pleiotropy. That's another of the exceptions I pointed out above -- the rare instances where a common allele might really be associated with a common disease. In antagonistic pleiotropy, an allele that has a good effect on one function may proliferate despite having a bad effect on some other function. There's nothing at all surprising about a single gene having different alleles that may have adverse impacts on two different bodily processes, and in fact some have been well known for fifty years or more.
Um, could somebody brief Collins about ABO?
Whole-genome studies of viruses: future studies of people?
Viral evolution is different from human evolution chiefly because viruses mutate faster, exist in larger populations, have much shorter generations, and have a sharp multifold population structure, including within-host subpopulations and global (and potentially local, regional, or species-specific) metapopulations.
So maybe we shouldn't read too much into this free PLoS essay by Eddie Holmes, "Viral Evolution in the Genomic Age."
But then again, viral evolution sets the context for much of recent human adaptation, including strong recent selection on genes related to pathogen defense.
If there is a lesson to be learned from the history of population genetics, it is that the more fine-scaled the data available for analysis -- from allozymes to genomes -- the more powerful the biological inference. Not only does the comparison of complete genomes invariably provide greater resolution of the spatial and temporal dynamics of viral spread, but it obviously enables the study of genome-wide interactions. As a case in point, the complex evolutionary processes that underpin the recent dramatic rise of resistance to adamantane drugs in influenza A virus, including the central role played by epistasis, were not revealed until an analysis of complete genome sequences was undertaken [10]. Rather than focusing on single genes in isolation, it is therefore essential that we examine the similarities and differences in evolutionary patterns among all the genes in a viral genome.
Holmes begins his essay by noting that the influenza A virus project has so far generated "around 2,500 complete viral genomes." Of course, such widespread sequencing is essential for studying the processes of virus evolution and the rise of new virulent strains.
But it also gives a hint of what will happen to human population genetics when large numbers of complete genomes start coming online. Considering that humans have rather less genomic diversity than influenza A, SNP surveys already have much of the power to detect polymorphisms. Coming attractions: larger and larger samples of people from different populations.
References:
Holmes EC. 2007. Viral evolution in the genomic age. PLoS Biol 5:e278. doi:10.1371/journal.pbio.0050278
Chicken introgression
Bees, dogs, and cattle have all provided interesting evolutionary stories this week. Now it goes to the chickens: A study by Jonas Eriksson and colleagues finds that introgression from grey junglefowl contributed to the gene pool of domesticated chickens:
This study contradicts the assumption that the red junglefowl is the sole wild ancestor of the domestic chicken [5] and provides the first conclusive evidence that other species have contributed to the domestic chicken genome. We therefore propose that the taxonomy of the domestic chicken should be changed from Gallus gallus domesticus to Gallus domesticus to reflect the polyphyletic origin of chicken [27]. The emerging technologies for total genome resequencing can be readily employed to determine if other parts of the chicken genome also originate from other species of junglefowls. Such regions are expected to be enriched for functionally important variants, like yellow skin, because neutral sequences should have been diluted out during the extensive back-crossing that must have taken place after introgression. It is possible that the introgression of yellow skin was facilitated by the fact that it resides on a microchromosome (only 6.4 Mb in size) with a high recombination rate, which reduces the amount of genetic material affected by linkage drag.
The need to reduce linkage to possibly disadvantageous genes around an introgressive allele is an important thing to consider, although breaking such an allele down to a 6 Mb block wouldn't take an terribly long time. The real question is why this trait in particular was brought into chickens -- whether it was linked to desirable pelage characters, or whether it may have had other advantages in survival or productivity under domestication.
These two species are not known to hybridize in the wild.
(via Blog Around the Clock)
(also Greg Laden)
References:
Eriksson J, Larson G, Gunnarsson U, Bed'hom B, Tixier-Boichard M, Strömstedt L, Wright D, Jungerius A, Vereijken A, Randi E, Jensen P, Andersson L. 2008. Identification of the Yellow Skin gene reveals a hybrid origin of the domestic chicken. PLoS Genet 4:e1000010. doi:10.1371/journal.pgen.1000010
Mice are nice, mice are nice, mice are ... AAARRGHHHH!
Nature has a news report on a problem with seabirds on Gough Island in the South Atlantic. You see, invasive mice are eating albatross chicks. Reuters also has a report (via Panda's Thumb).
From Reuters:
"Gough Island hosts an astonishing community of seabirds and this catastrophe could make many extinct within decades," said Dr Geoff Hilton, a senior research biologist with Britain's Royal Society for the Protection of Birds (RSPB).
"We think there are about 700,000 mice, which have somehow learned to eat chicks alive," he said in a statement.
The island is home to 99 percent of the world's Tristan albatross and Atlantic petrel populations -- the birds most often attacked. Just 2,000 Tristan albatross pairs remain.
"The albatross chicks weigh up to 10 kg (22 lb) and ... the mice weigh just 35 grams; it is like a tabby cat attacking a hippopotamus," Hilton said.
But you have to go to Nature for the good stuff, including video. Who expected a video of mice that warns, "Viewer discretion advised"? But it's no mystery why:
The videos confirm that mice are taking on the chicks, biting them over and over until they die from loss of blood or infection. Wanless, an invasive-species biologist from the Percy FitzPatrick Institute of African Ornithology at the University of Cape Town, South Africa, vividly recalls watching the first videos. "It was carnage. Chicks half alive, with massive gaping wounds and guts hanging out."
Researchers surveyed the incidence of chick attacks on different parts of the island, and inferred that the behavior is probably learned. So the transmission of this behavior may be one reason for the rapid expansion in body size of mice on the island, which are three times the size of normal mice.
Hmm.... Body size expansion? Check. Hunting? Check. Culture? Sound familiar? Yes, it's the "killer mouse" hypothesis!
Heterochrony and island dwarfism
I'm reading through the volume Integrative Paths to the Past (Corruccini and Ciochon, eds.) because of a piece of work I've been doing, and I came across this interesting passage in the contribution by Elizabeth Vrba, titled "An hypothesis of heterochrony in response to climatic cooling and its relevance to early hominid evolution."
Conversely, I suggest that acceleration and hypomorphism often evolve in warmer environments. In fact, the celebrated correlation of dwarfing of mammals on islands may well have less to do with the absence of predators and resource depletion (e.g., Lomolino 1985) than with the fact that island refugia for large mammals come into being in times of global warming and sea level rise--namely, maximal warming periods--and islands at all times enjoy a more mesic climate than the mainland uplands of the ancestors. Prothero and Sereno's (1982) results for North American fossil rhinoceroses is relevant: Dwarf species were associated with mesic forest-swamp "climatic islands" on the Miocene land mass, surrounded by savanna uplands on which larger rhinoceros taxa lived (Vrba 1994:355-356).
In other words, Vrba says that the reason we find dwarf elephants, hippopotamus, and other large mammals on the Mediterranean islands during the past few million years may be climatic. I'm not sure this accounts for the presence of dwarf mammoths on Wrangell Island, or the Catalina Islands for that matter, since full-size mammoths were on the adjacent mainland. On the other hand, migration is a factor affecting the evolution of continental taxa that simply isn't an issue for species trapped on islands. So there may be a combination of climate and the necessity for long-distance movement that makes sense.
In any event, this kind of explanation appears to be closer to the truth for phyletic dwarfs in continental regions than other explanations. Consider the Pygmies of West Africa: their small body size has been variously interpreted as a result of nutritional restrictions, inability to thermoregulate efficiently in the humid atmosphere, the need to maintain small mass for effective climbing, or sexual selection. It is not obvious that any of these explanations are applicable to other human populations with small body sizes, such the Negritos from Southeast Asia. There is obviously much thinking to do here, but I'm not sure that we have a very good explanation for dwarfism in human populations. Vrba's remarks lead to believe that we don't have a very good explanation for dwarfism in mammal populations in general.
References:
Vrba ES. 1994. An hypothesis of heterochrony in response to climatic cooling and its relevance to early hominid evolution. In Corruccini RS and Ciochon RL, eds., Integrative paths to the past: paleoanthropological advances in honor of F. Clark Howell. Prentice Hall, Englewood Cliffs, NJ. pp. 345-376.
Judson on sticklebacks
Olivia Judson's blog, "The Wild Side" has quickly become a worthwhile weekly stop. This week, she describes some stickleback developmental biology.
Now, you may not get that excited about sticklebacks, but there have been a lot of cool parallels between stickleback and human evolution during the past couple of years. For one thing, as sticklebacks invaded the post-glacial lakes of British Columbia after the last ice age, they repeatedly differentiated in parallel into different ecological morphs. Is this like the differentiation of robust and non-robust australopithecines in different regions of Africa? Could be -- it certainly provides a possible model of parallel niche construction.
Judson features a couple of other interesting aspects of their biology. She mentions a pigmentation gene, KITLG, that has undergone adaptive changes in both sticklebacks and recent humans. Most of her story is devoted to a developmental regulation gene, Pitx1:
There are a couple of interesting things about this discovery. The first is that the molecular basis of the change from pelvis to no pelvis does not involve a mutation to the protein-coding region of the Pitx1 gene itself. In other words, the protein made from the gene hasnât changed. What has changed is the way the gene is expressed. This is in contrast to the sorts of mutations one often reads about as being involved in evolution, which typically involve changes to the protein itself.
A second interesting feature of the stickleback pelvis is that -- unlike the armor plates -- the loss is probably due to mutations having occurred independently in the different populations. Whatâs more, changes to the use of Pitx1 are also implicated in pelvic loss in nine-spine sticklebacks (Pungitius pungitius) -- yet nine-spine and three-spine sticklebacks have been going their own evolutionary ways for at least 10 million years.
This "parallel regulatory mutation" story has been told a number of times for different systems in the last few years -- Sean Carroll in particular tells several in his recent book, The Making of the Fittest -- which I recommend. But for a short version, Judson's post is a good read.
From the front lines of the squirrel war
The Sunday NY Times has a long, entertaining article about the defenders of British red squirrels.
"Can I, um, suggest something?" [Baron] Redesdale said to the three women. He was seated on a couch with a red-squirrel throw. "I was thinking . . . it would be great to form a sort of mobile kill group." He explained: "We just knock on people's doors and find out if there's a gray and get them to put the traps in." One person a day, he said, would go around and do the actual killings. The women gave Redesdale a "Candid Camera" look. Was this a joke?
Yes, the leader of the resistance is a real baron, Rupert Redesdale, and the article paints a vivid picture of him along with a looney-sounding squirrel-roasting sidekick. These guys are begging to turn into a Wes Anderson movie.
Writer D. T. Max treats the American gray squirrels as metaphors for everything from Thatcherite fiscal policy to American imperialism. Which, it turns out, is sort of how they got to England in the first place. Of course, the real problem is squirrelpox -- the flesh-eating disease that gray squirrels carry without effect, but that kills red squirrels dead.
But the real treasure in this article is the House of Lords debate:
[B]efore turning his attention to Squirrel Nutkin, Earl Peel proposed conducting "a brief health check" of various other Beatrix Potter characters. "Starting with Tabitha Twitchit and Tom Kitten" -- both cats -- "they are truly on top of their game. . . . Let us now consider the status of Mr. Tod, the fox. On second thoughts, given that he has taken up 700 hours of parliamentary time, it would be somewhat hypocritical of me to prolong the debate." He went on: "That brings me on seamlessly to the other really controversial character that graced the class of 1912 -- and that of course is Tommy Brock," Potter's badger. "Hasn't he done well?"
Peel continued: "Despite suffering from and carrying tuberculosis, he has successfully managed to establish himself in the hearts and minds of the nation as being more important than dairy cows or, indeed, farmers' livelihoods, and like Mr. Tod, has managed to secure his very own legislation."
Peel concluded his health check: "Squirrel Nutkin must look back on his alma mater and think to himself, 'How could it have all gone so wretchedly wrong for me?'"
Can anyone doubt that a hundred years from now, it will be SpongeBob, Patrick and Squidward making an appearance in a debate about coral reef protection?
Razib's interview with Jim Crow
Now I'm back home again, and catching up on some reading. So I direct your attention to this excellent interview with Jim Crow, from Razib's 10 questions series. It touches on the history of population genetics -- in which Crow himself played an important part -- as well as some of the hot-button issues of the present.
Theory or law?
Andrew Sullivan has been posting comments from readers about why evolutionary biology is comprised of "theories" rather than "laws." I found these via Razib, who naturally has more interesting things to say than Sullivan or his commenters. But no one in the conversation has really given an answer to the question, other than some vague idea of what it takes to "qualify" as a "law." I think the answer is historical, and demands that we consider a number of so-called "laws of evolution" and their fates.
As evolutionary biology got underway in the late nineteenth century, its main proponents called many of its major ideas "laws." I give a number of examples toward the end of the essay, but to begin with, Darwin referred to the "Law of Natural Selection." When Mendel was rediscovered, his two main ideas were called "Mendel's Laws of Heredity": the "Law of Independent Assortment" and the "Law of Segregation." Those two have stuck around.
The "Hardy-Weinberg Law" is hardly ever called that anymore; "law" being replaced by "principle."
It seems to me there's an obvious historical reason why evolutionary biologists reject the term "law" -- too many of the so-called "laws" of evolution ended up being false!
The premier example is Haeckel's "Biogenetic Law": "Ontogeny recapitulates phylogeny." The theory of recapitulation came with an entire suite of concomitant mechanisms to explain its exceptions, In the end the idea was conclusively falsified. The mode of evolution of developmental processes can generate similarities between ontogenetic and phylogenetic sequences, but there is no causal mechanism constraining these other than the normal mechanisms of genetics.
There are other outmoded "laws" of a similar vein. The "Law of Orthogenesis" is now rarely referred to as a "law", but its main proponents certainly called it one. Then there was the "Law of Irreversibility" -- the idea that evolution couldn't "go backward" to bring a population to an ancestral morphological pattern.
The empirical and theoretical failure of these so-called "laws" did not suppress evolutionary biology's taste for overarching statements about patterns and process. But their failures did tend to make people skeptical of the idea that "laws" of evolution would really be found. Also, the discovery of actual "laws" of heredity yielded a theoretical interest (enshrined in population genetics) for reducing the overarching pattern of evolutionary history to the mechanisms of heredity.
The influence of recapitulation over embryology has been well-documented, and of course the main detractors from the early development of population genetics as the mechanism of evolution were morphologists -- embryologists, paleontologists, biometricians. This possibly influenced early population geneticists like Fisher to refer to their mathematical formulations as "theories" or "principles" rather than laws -- although this is just a speculation and I would like to see documentary evidence.
What seems clearer is that after the biogenetic law was rejected, empirical generalizations in biology tended to be called "rules" rather than "laws". Consider "Romer's rule", the "Island rule" (also called "Foster's rule"), "Rensch's rule", and (this is a genetic example) "Hamilton's rule."
Maybe the best example is "Cope's rule", which started out as a "law" but was turned into a rule by people who still found it useful at midcentury. I find this sentence from the Wikipedia article on "Cope's rule" quite relevant to the shift:
Note that semantically the "rule" in this context (unproven assumption with exeptions) refers more to a rule of thumb, trend or a belief than to a truth, law, fact or a norm.
That's certainly the way that biologists today think of these "rules." Interestingly, Cope was also responsible for the "Law of the Unspecialized", which is uncommonly enough invoked that the "law" name has stuck.
Still, in physiology and anatomy (biological fields, to be sure), "law" is widely used. "Kleiber's law" relates body mass and metabolic rate. "Sherrington's law" refers to the simultaneous stimulation and inhibition of opposing muscles. "Wolff's law" relates bone growth to mechanical loading. Most of these have just been held over from the nineteenth century, but not all -- Kleiber's law was formulated in the 1930's just as "law" was going out of vogue.
In short, I think that the reasons why evolutionary biologists don't call ideas "laws" are basically historical. It has nothing to do with whether a "mathematical formulation" can be found -- there's certainly none underlying Wolff's Law, which is still called that. It has entirely do do with the rejection of over-ambitious "Laws of Nature" as applied to the outcomes of the evolutionary process. The worst offender was the biogenetic law, but there were others as well.
Ten assertions about evolution
I thought for a long time about how to respond to Razib's challenge:
My post asking to define evolution in less than 10 words elicited a lot of response (some of it outside the parameters I set in regards to length). So I figured I'd give this sort of thing another shot, again, with parameters which all are welcome to violate, but which I set for myself to prune my tendency toward qualifying verbosity. Below the fold are "10 assertions of 10 words or less" which I believe that the public should know about evolutionary science. I did this in 3.5 minutes, typing out what came to mind and checking word count in M$ Word. Obviously the assertions reflect my biases, though if I can get others to bite perhaps we can establish a "core" which we can all agree upon as necessary to a genuine understanding of evolutionary science.
Of course, I cheated and read not only Razib's list but also Robert Skipper's, RPM's, Afarensis's, and John Wilkins's lists.
The problem with compressing things into 10 words is that it always leaves the terms undefined. And since these are supposed to represent what I think the public should know, I certainly can't assume that the terms will be understood already. Which really means that what I think the public should know is what evolution is, and the like -- in other words, definitions of terms.
And definitions of terms are totally boring. Nobody who's reading this wants to read definitions. So they're out, at least mostly.
Of course, the fun of this is writing some assertions that will gin up some controversy. Like Razib's "The difference between micro & macroevolution is semantic." Or Afarensis's "Most people do not understand punctuated equilibria." But the thing is, if I only have 10 things to get the public to remember, do I choose controversial things? The first is plausibly false (insofar as a lot of evolutionary biologists think there are mechanisms driving speciation and the evolution of higher-rank taxa that are never manifested microevolutionarily), the second introduces a controversy without the possibility of explanation (I'm not sure a 10-word explanation is even possible).
And yet, if I avoid all controversial things, it really seems to suck the life out of the science. I mean, imagine 10 assertions about physics today without mentioning string theory. It's controversial, but it's all a whole lot of people care about!
The other question is, how representative should the list be? The other lists are pretty much centralized on population genetics (the first two weeks of my intro class), but have little to say about branches of evolutionary biology like paleontology, evolutionary ecology, agricultural genetics, evolutionary medicine, and (dare-I-say) anthropology. With one exception -- several include "humans are still evolving", which really seems to me like little more than a truism, since it follows from other principles. More interesting would be to convey some notion of how humans are evolving, or in which direction -- although that certainly won't satisfy my "no controversy" condition. More important, stuff we want the public to know about evolution surely includes things like why extinction happens, where all those delicious plants came from, why those antibiotics don't work anymore and why you shouldn't marry your sister.
So I thought three things are desirable. First, the list should be broad, so that it connects to things people are likely to already know, or hear on the news. That makes it relevant. Second, it should not introduce terms needlessly. Natural selection is one of the most important achievements of science, and everyone needs to know about it. Genetic drift is interesting and all, but it is not all that important to ordinary people. To the extent that it is relevant (in conservation, for example), it can be introduced with a concept people already have a vague concept of -- inbreeding.
Third, many of these assertions are reducible to equations. But most people don't relate to equations, and won't remember numbers, so I've tried to be clear about the direction of relationships without quantifying them.
And I admit it, I couldn't get them all to 10 words. I tried very hard, but in the end I thought better to be clear than to make people consult their dictionaries. I added a little cheat by giving each assertion a "category"; that helps to clarify what they refer to.
OK, so here's the list:
- Genetics: Hidden "recessive" genes can cause phenotypic traits to "skip generations."
- Population genetics: Inbreeding increases the risk that offspring will express harmful recessive genes.
- Demography: A slight intrinsic growth rate over many generations causes a population to grow exponentially in numbers.
- Natural selection: A gene that increases the intrinsic growth rate of its carriers thereby increases its representation in future generations.
- Ecology: Selection shapes interactions with other organisms, including mutualism, predation, competition, and parasitism.
- Kin selection: Helping relatives will help an individual's own genes, proportionally with relatedness.
- Species: Selection and interbreeding can make populations more similar; selection and inbreeding can make them more different.
- Paleontology: A species' future is contingent on its history; new adaptations must build on or delete the old.
- Extinction: Rare, inbred, or specialized species have more trouble surviving ecological disturbances and may become extinct.
- Agriculture: Humans changed the ecology of domesticated plants and animals, exerting selection on them.
- Medicine: Pests, parasites, and diseases evolve rapidly, often overcoming human interventions.
Compiling this list really brought home to me how difficult some of the concepts are. So I jotted down some questions as I was doing it, with my thought process about how to answer them:
Boy, why did you wimp out on species? My main problem was that the species concepts familiar to most people (a) don't mention natural selection in any way, and so don't really give an evolutionary account of speciation, and (b) are highly animal-centric. Sure, interbreeding is necessary for species cohesion in sexual organisms, over millions of years at least. But what about asexuals? And what about good "species" that interbreed readily given opportunities? And ring species? I know that my readers know all these problems and many more, and the list of problems never ends. I thought for a long time, but I think I'm just too close to the topic to come up with a one-sentence species assertion that I would foist on anybody. And hey, Darwin wimped out on species, so why shouldn't I?
Why define selection in terms of intrinsic growth rate? For one thing, most short definitions of natural selection are really unsatisfactory. Darwin defined it by analogy. The usual population genetics definition ("correlation between a genotype and reproductive success" or some such) is entirely silent about how this correlation comes about. Fisher's treatment of selection in terms of intrinsic growth rate has the benefit of being very clear, and it can be related to something people are likely to understand. Additionally, it inspired much later mathematical work, including Hamilton's treatment of senescence.
Why waste a whole assertion on defining intrinsic growth rate? Hey, if I thought people actually knew this, I wouldn't. Compound interest generally comes as a surprise to my undergraduates, so I think it's worth explicitly connecting Darwinism to Malthus. But I felt guilty burning an assertion on mathematics instead of biology, so I expanded the list to eleven.
Why is "recessive" important enough to belong on the list? Genes are the chief unobservable entities of biology. Mendel could posit their existence because of the proportion of offspring that exhibited traits that were concealed in their F1 hybrid parents. People are already familiar with the idea of traits "skipping generations", but they generally don't realize that this phenomenon requires the gene theory (that is, it is inconsistent with blending inheritance).
Why "ecological disturbances" instead of "environmental changes"? First, "disturbances" brings to mind human-induced habitat loss, without limiting it to that. Second, "ecology" carries a meaning of intricate relationships, while "environment" is associated by most people with the weather. Not that the weather isn't important, but for the most part its importance is channeled through ecological relationships.
Why "genes" and not "alleles"? I wavered on this, too, but went in favor of genes throughout because it is consistent with the use of many genetics texts and also is a term people are likely to have heard.
Why no adaptation? I kept an assertion about adaptation on the list for a long time. It is a logical intermediate between the definition of selection and the mention of ecological interactions. I guess my attitude came to be very similar to my attitude about "fitness" (which I also ended up not using): it confuses people more than it clarifies. Both "adaptation" and "fitness" are readily misinterpreted as purposive, and ordinary people cannot help but understand them that way. (To my mind, that confusion explains much of the appeal of Dawkins' "Selfish Gene": not that it clarifies adaptation or fitness, which it doesn't, but that it reframes their "purposiveness" in terms orthogonal or reversed from Western moral sensibilities.) For a long time, I had the word "fitness" in the natural selection assertion, but ended up taking it out for simplicity.
"Humans changed the ecology..?" The distinction between natural and artificial selection simply confuses people. Humans certainly did not create their environments from scratch (we sure wouldn't have created brucellosis!), and they remain under non-human-mediated selection for most of their biology. I don't propose doing away with the artificial-natural distinction, but reframing domestication in terms of ecology does allow more interesting thoughts. For instance, humans are mutualists with many domesticated species. Humans work hard to eliminate natural predation on domesticated species, and they still compete with weed species and suffer from diseases.
Well, anyway, that's the list. I think I'll try to come up with 10 paragraphs, which might actually be a great help for my classes. If I were going to add more assertions, I would first add one about senescence and death, then probably something about brain evolution, and possibly mass extinctions. I can think of many more concrete events that people should know before I would add a lot more about genetic mechanisms.
Meanwhile, I've been working on a list that will be a bit more fun...
The (non-)neutral Neandertals
OK, I'm clearly going to have to cut out the beer if I'm going to do anything about stories like this one:
New research led by UC Davis anthropologist Tim Weaver adds to the evidence that chance, rather than natural selection, best explains why the skulls of modern humans and ancient Neanderthals evolved differently. The findings may alter how anthropologists think about human evolution.
Weaver's study appears in the March 17 issue of the Proceedings of the National Academy of Sciences. It builds on findings from a study he and his colleagues published last year in the Journal of Human Evolution, in which the team compared cranial measurements of 2,524 modern human skulls and 20 Neanderthal specimens. The researchers concluded that random genetic change, or genetic drift, most likely account for the cranial differences.
In their new study, Weaver and his colleagues crunched their fossil data using sophisticated mathematical models -- and calculated that Neanderthals and modern humans split about 370,000 years ago. The estimate is very close to estimates derived by other researchers who have dated the split based on clues from ancient Neanderthal and modern-day human DNA sequences.
The close correlation of the two estimates -- one based on studying bones, one based on studying genes -- demonstrates that the fossil record and analyses of DNA sequences give a consistent picture of human evolution during this time period.
"A take-home message may be that we should reconsider the idea that all morphological (physical) changes are due to natural selection, and instead consider that some of them may be due to genetic drift," Weaver said. "This may have interesting implications for our understanding of human evolution."
If you've been reading for long, you might reasonably wonder what I think about this study. My work has shown rapid natural selection in recent humans, consistent with evidence from recent skeletal samples for rapid evolutionary change. So it might seem incongruous that a study could assume that there has been no natural selection on the skeletal traits of recent human populations, and come to any kind of sensible conclusion.
I am actively working on this particular problem, with a manuscript in preparation, so I don't want to comment too extensively. However, I can say a brief word about why I disagree with the analysis.
A model of phenotypic evolution by genetic drift requires an assumption about the effective size of the population (Ne). Weaver et al. (2008) assume a model of "mutation-drift equilibrium." This is an assumption that the effective population size has not changed over time in the populations under consideration -- in this case, the Neandertal and human populations back at least as far as their common ancestor.
In their analysis, Weaver et al. (2008:4647) assume that the effective sizes of the human and Neandertal lineages, throughout the last few hundred thousand years, were equal to 2700 individuals. They wrote this:
The second reference point is the effective population size, PNe, under a mutation-drift-equilibrium model for sub-Saharan African human populations. Zhivotovsky and colleagues (ref. 17) estimated Ne from 271 microsatellites using an equation equivalent to our Eq. 7 as ≈ 2,700 individuals. Once again, we are just assuming that the morphological and microsatellite estimates should match up under the same model, not that this is the most realistic model to use to infer the actual effective population size.
This is an astounding assumption. It is important because a small effective size allows rapid evolution by genetic drift. But it is contradicted by other evidence.
For one thing, most other sets of genetic data indicate a long-term effective size of at least 10,000 for human populations -- four times larger than assumed in this study. All things being equal, this means that the rate of phenotypic evolution by genetic drift should be four times slower than assumed by Weaver et al. (2008). Some of this difference between real and assumed effective sizes may be washed out by their process of calibration -- their equations involve several unknowns that must be simultaneously estimated, and give a lot of wiggle-room to the results. But that points to another weakness of the analysis -- there's so much wiggle room that almost any level of phenotypic difference might look like "drift."
Moreover, the human population has vastly increased in numbers within the last 50,000 years. Weaver et al. (2008) use the phenotypic and genetic divergences of recent humans to calibrate their "clock" of phenotypic evolution. But the phenotypic divergences between recent human populations, with very large effective population sizes (Ne > 100,000) are simply not comparable to those between Middle Pleistocene humans and Neandertals -- at least, not without taking into account the vast difference in effective population sizes.
But please don't take my word for it. I am a clear partisan on the side of natural selection in recent human evolution. Weaver's quote in the press release above implies that we should accept a pluralistic model, in which genetic drift accounts for some changes. I agree entirely. But their analysis assumes that genetic drift accounts for all changes. I don't deny the role of genetic drift, but I do deny that it explains much about recent skeletal evolution in humans. Random chance cannot do much in a very large population in a few hundred generations.
I really don't understand why you would want to use a heuristic value for effective population size, when it is contradicted by genetic and archaeological evidence. I will be writing about effective population size over the next week, introducing some of the importance of the concept for these kinds of analyses. You're welcome to take a look at what I have to say, and take it or leave it.
Sewall Wright and the factors of evolution
Last year around this time, I noted that I happened to be reading Sewall Wright during a TV episode that mentioned Sewall Wright. It's not so unusual for me to be reading Wright, but in this instance I was directed to something I hadn't paid much attention to before.
I'm reminded of the article today because I talked about its basic theme during a lecture, and also because I'm writing up some stuff about effective population size, a concept attributed to Wright.
John Gillespie's 2000 article, "Genetic drift in an infinite population," introduced the concept of pseudohitchhiking, or "genetic draft." An important thing about pseudohitchhiking is that it behaves as a stochastic force very much like genetic drift. The formal difference between the two is that the stochasticity of a pseudohitchhiking locus depends on recombination and selection, while genetic drift depends on neither. Gillespie's paper considered to what extent pseudohitchhiking led to similar predictions for the change in allele frequency. This is a connection he made more explicit in his 2001 article, "Is the population size of a species relevant to its evolution?" by drawing out the first and second moments of neutral evolution under both drift and pseudohitchhiking. For drift, these are (Gillespie 2001:2161, eqs. 1 and 2):
The first equation means that the expected change in allele frequency under drift is zero. This is otherwise known as the deterministic component. Under selection, the expected change in allele frequency depends on the current frequency and the fitnesses of genotypes. Under drift all genotypes have equal fitnesses and the only possible changes are stochastic, therefore the expected change is zero irrespective of the current allele frequency.
The second equation describes the variance of the change in allele frequency. You might think this variance would be zero, since the expected amount of change is zero. But the variance represents the magnitude of possible changes from the expected value due to random sampling a finite number of individuals. This is the stochastic component of allele frequency evolution.
The magnitude of these stochastic changes is directly proportional to heterozygosity and inversely proportional to population size. Larger populations have smaller potential changes in allele frequency due to random sampling. Intermediate allele frequencies (near 50 percent) can change more due to random sampling than high or low frequencies. These relations are embodied by the second equation above -- and if you're keeping score, this second equation is used in defining the variance effective population size.
The two equations help to frame the discussion of effective population size. The size of a population is relevant to its evolution only under certain contexts. If the deterministic change in allele frequencies is the dominant pattern of evolution, then population size is irrelevant to the outcome. In contrast, if random sampling is the most important cause of allele frequency changes, then the outcome (fixation or loss) may be indeterminate, but the population size is very important to the rate of the process.
As Gillespie's article makes clear, genetic drift is not the only stochastic process affecting the evolution of allele frequencies. His mechanism of pseudohitchhiking is one. And there are many others -- all non-deterministic in that their outcomes cannot be predicted from the frequencies of alleles or their phenotypic effects. The rate of these processes depends on different things: some internal to the population and some external. Genetic drift depends on the size of the population and its allele frequencies; genetic draft depends on the rate of recombination, the rate of generation of new favorable mutations, and the relative fitnesses of these mutations. Environmental stochasticity depends on the demography of other species as well as physical factors such as water availability and the weather.
Sewall Wright tried to categorize these stochastic processes, as well as the deterministic ones, making a catalog of of the processes that can cause evolutionary changes. Those of us who teach intro classes are well accustomed to talking about the "forces of evolution" -- selection, drift, gene flow, and mutation. These are important because they constitute different patterns of change in allele frequencies. But Sewall Wright went beyond this four-fold categorization, linking different aspects of these patterns with their stochastic and deterministic effects.
First, he defines the problem in terms of allele frequencies:
As is now generally appreciated, the seemingly very diverse factors that must be taken into account in population genetics can best be brought under a common viewpoint by considering their effects on gene frequency (Wright 1955:17).
Then he provides a full breakdown of different patterns of evolutionary change, or "modes" of change of the gene frequencies in a population:
Modes of Change of Gene Frequency
I. Immediate
1. Directed processes (mean change in allele frequencies determinate in principle)
a. Recurrent mutation
b. Recurrent immigration and crossbreeding
c. Mass selection
2. Random processes (variance in change in allele frequencies determinate in principle)
a. Fluctuations in mutation
b. Fluctuations in immigration
c. Fluctuations in selection
d. Accidents of sampling
3. Unique events
a. Novel favorable mutation
b. Unique hybridization
c. Swamping by mass immigration
d. Unique selective incident
e. Unique reduction in numbers
II. Secular change in system of coefficients
1. From internal causes (control by new adaptive peak)
2. From changes in environment
a. In home territory
b. In colonized territory
This breakdown clearly separates the deterministic factors of evolution (here, category 1, "Directed processes") from the stochastic factors (everything else). I find a couple of things very interesting from this perspective:
1. Wright makes a distinction between recurrent mutation, whose effect is more or less deterministic on allele frequencies, and "novel favorable mutation", each of which is a random, unlikely event. Both are distinguished from "fluctuations in mutation," which might be described as an intermediate between the two -- although writing in 1955 it is plausible that Wright may actually have meant alterations in the propensity toward mutations due to variation in radiational or chemical processes. This is one indication of the difference between Wright and Fisher, who felt that novel mutations might become more or less predictable in large populations.
I also noticed how many of Wright's "unique events" have been marshalled by one or another researcher to explain human evolution.
Another point of interest, reflecting the several instances of interesting evolutionary trends under domestication that I've linked this week, is Wright's accommodation of artificial selection within this scheme:
It may be noted here that artificial selection also imposes a new system of peaks toward one of which mass selection may be expected to drive the population rapidly. Since the peak attained is not a natural one, progress is almost inevitably at the expense of fecundity and viability. On relaxation, the population may be expected to return toward the original peak, or to another, and usually lower one, if the artificial selection has driven it across what was naturally a valley (Wright 1955:17).
This should be amended, in that selection comes at the expense of fecundity and viability in the previous environment, not the new artificially selected one. But the prediction that artificial selection should decrease fitness in the species' natural environment comes straightforwardly considering the nature of selection as a deterministic force. If the species was initially well adapted to its natural environment, any changes resulting from artificial selection would likely make it worse, not better.
Wright's well-known idea was that the stochastic factors might play an important role allowing a population to explore the adaptive landscape. In his "shifting balance" formulation, the division of an abundant species into many small subpopulations tends to maximize the species' ability to evolve toward higher fitness peaks, because a small group might have a fortuitous combination of alleles allowing it to move to a higher fitness peak. This model has been controversial even up to the present day, because of our lack of knowledge about the characteristics of "fitness landscapes".
But it is worth pointing out Wright's definition of the stochastic factors here, each of which might operate in conjunction with genetic drift in the shifting balance model. It is clear from the list that the balance between these different factors might itself change over time -- for instance, in our acceleration idea, the incidence of novel mutations is greatly accelerated in a growing population, ultimately increasing the scope of the deterministic process.
References:
Gillespie JH. 2000. Genetic drift in an infinite population: the pseudohitchhiking model. Genetics 155:909-919.
Gillespie JH. 2001. Is the population size of a species relevant to its evolution? Evolution 55:2161-2169.
Wright S. 1955. Classification of the factors of evolution. Cold Spring Harbor Symp Quant Biol 20:16-24.
Most phenotypic evolution is neutral, er, I
A bee orchid. Photo by Mr. Bov, available on Flickr. Creative Commons Attribution license
Most phenotypic evolution is neutral, er, II
Papilio caterpillar. Photo by scorius, available on Flickr. Creative Commons license
Most phenotypic evolution is neutral, III
Rudbeckia flower, viewed in ultraviolet light. Dark, UV-absorbing nectar guides are not apparent in the visible spectrum. Photo by kds315, available on Flickr. Creative Commons license
Most phenotypic evolution is neutral, IV
Skeleton of an Irish elk (Megaloceros giganteus) at the Carnegie Museum of Natural History. Photo by Via Bulatao, available on Flickr. Creative Commons license
Evolution focus in Science Times
This week's NY Times Science section is devoted to evolution, with articles by:
Carl Zimmer, on microbial evolution
John Noble Wilford, on human paleontology
Nicholas Wade, on recent human genetic evolution
Carol Kaesuk Yoon, on evo-devo
An essay by Douglas Erwin, about evo-devo and Darwinism
A video interview with my UW colleague, Sean Carroll
And several other things. I will be reading through these articles over the next several days and providing some annotation and commentary -- I think they are an interesting compilation of recent (and some older) developments in evolutionary science.
Cane toad invasion and evolution
The Hawaiian cane toad is a classic case of an invasive species, and its genetics have long been a subject of study for those interested in the spread of species into new habitat.
That's why it's so interesting to me that a new study in Nature(subscription) has shown morphological differences (LiveScience) between the initial wave of toads and later populations. The fastest colonizers have the longest legs:
From the 1940s through the 1960s, the toads were invading at a rate of about 6 miles per year; now they're taking over at a rate of about 30 miles a year.
To find out why the toads are spreading so fast, researchers stationed themselves about 40 miles east of Australia's port city of Darwin, in a region where the cane toads had not yet spread.
When the toads arrived, the researchers found that those in the vanguard of the invasion had legs that were up to 6 percent longer than average; shorter-legged stragglers followed. The study showed that newer populations of toads tended to have longer legs than those in long-established populations.
These are BIG toads, by the way -- weighing up to 2 kg. Leg length does lead to faster dispersal:
The morphological trait most often linked to locomotor ability in anurans is leg length, both among and within species8. Our trials (see supplementary information) confirm that cane toads with relatively long legs are indeed faster over a short distance (regressing time taken to cover 1 m against residual leg length: r=-0.44, n=29, P<0.02). But, more important, longer-legged toads moved further over 24 h (maximum displacement of radio-tracked toads versus relative leg length: r=0.46, n=21, P<0.04) and over three days (r=0.58, n=21, P<0.006; Fig. 1a). Longer legs therefore facilitate more rapid dispersal.
Of course, the idea that longer-legged toads would move faster and colonize more quickly makes perfect sense.
The mystery is: Why do leg lengths subsequently decline?
References:
Phillips BL et al. 2006. Invasion and the evolution of speed in toads. Nature 439:803. Full text (subscription)
But was it a tiny-brained dwarf buffalo?
It's a short piece by John Noble Wilford, and there may be little more to say:
Remains of the extinct dwarf buffalo were found 50 years ago in a cave on Cebu, an island in the Philippines, but were not brought to the attention of scientists at the Field Museum in Chicago until recent years. They determined that the animal, which they named Bubalus cebuensis, weighed about 350 pounds and stood only two and a half feet at the shoulders.
The researchers were unable to date the fossils but thought it unlikely that they were more than a few tens of thousands of years old. A different species of dwarf buffalo lives today on Mindoro Island in the Philippines. But at 500 pounds, it is large compared to the extinct Cebu dwarf.
I find the biogeography of the Philippines and Sulawesi to be fascinating. Some mammals got there (notably pigs and monkeys on Sulawesi), while others didn't -- even those that you might expect to have because they are on Java and Sumatra. There are endemic buffalo in the Philippines now (notably the tamarao). It seems interesting that the buffalo of Java are feral, and there the native large bovid is a species of cattle, the gauteng.
I guess the thing is that there were dispersal barriers besides water in the region, so that even dispersing animals did so within relatively limited ranges. Geology is not the only answer with respect to these dispersals, and that is a lesson that is very relevant to the Flores case, although not in the way that Wilford points out.
The Tao of introgression
Like mathematician Terence Tao hasn't heard that one before, hyuk. But he gives a nice account of the Grants' work on introgressive hybridization of ground finches:
This was all very reasonable and predictable, but it led to an interesting puzzle - given the modest genetic pool of the Geospiza scandens population, how was it that both the small-beak genes and large-beak genes survived for millions of years, given that selective pressures tended to strongly favour one over the other every decade or so?
The answer, hypothesised and then confirmed by Grant and her collaborators, was introgressive hybridisation - the occasional sharing of genes between Geospiza scandens and Geospiza fortis due to interbreeding.
We didn't include the finches in our paper on introgression,, but it's a well-documented example. For the finches, the clear importance of reinforcement selection on the species barrier between the forms means that their species difference is greater than it would be in the absence of such selection -- and in my thinking probably greater than species barriers in early hominids.
(via Gene Expression)
Derby day horse physiology
LiveScience has a story about the qualities of good racing horses. It doesn't talk about breeding too much, but it has a lot of interesting stuff about their physiology:
"Horses have what I call a 'natural blood doper' -- a huge spleen that stores a blood supply very rich in red blood cells," McKeever says.
It's a spleen that any elite athlete would envy. When the horse is just standing around, the percentage of oxygen-carrying red blood cells in its circulatory system runs around 35 to 40 percent. Blood in its huge spleen -- 3 to 4 feet long, 8 inches wide, and 4 inches thick--is a whopping 80 percent red blood cells.
When the horse starts its gallop, the surrounding muscles clamp down on the spleen like a bagpipe and squeeze all that extra blood into the circulation system. The blood ferries extra oxygen to the muscles during the run and for about an hour after exercise.
I sure didn't know that. Also, their lungs have nearly double the oxygen-moving potential of humans, and their stride helps to pump air in and out like a bellows.
Horses really are an interesting combination of fast and large, which brings all these energetic and oxygen restrictions to a head.
Inbred mice
At Nobel Intent, Jonathan Gitlin writes about the diversity of lab mice:
Now, scientists don't use just any mice; you couldn't trap one in your attic and then bring it to work. Instead, there are hundreds of inbred strains that are used. Creating such a strain involves mating sibling mice for at least 20 generations. By this point, almost all the genetic loci will be homozygous, that is, each of the two copies of each gene will be identical.
...
[A]ll of the inbred strains, and even the four wild-derived strains, are much closer genetically than previously thought. The study identified 8.27 million different single nucleotide polymorphisms (SNPs). These SNPs are distributed along the genome, but those that are near each other are likely to be inherited together as a group. By creating a map of these groups, or haplotypes, the researchers were able to look at the contributions of each of the four wild-derived strains to the 11 inbred strains, to attribute ancestry. They found that M. m. domesticus contributed the largest part of the 'HapMap,' with 68 percent. The other three wild strains each were responsible for between three and ten percent, with another ten percent of unknown origin, presumably coming from populations of wild mice not represented in the four wild-derived strains.
The whole post is interesting, tracing the development of mouse strains back through breeder Abbie Lathrop to their origins in wild mouse subspecies.
The original research is by Kelly Frazer and colleagues in Nature and Hyuna Yang et al. in Nature Genetics.
Antitrendy mouse evolution
A paper in this week's Science by Hopi Hoekstra and colleagues (DOI link) ends with this provocative paragraph:
This work has specific implications for understanding the evolutionary mechanisms responsible for adaptive phenotypic change. First, the identification and functional characterization of a single amino acid mutation's effect on quantitative variation provides a convincing exception to a growing number of examples demonstrating that variation in morphology is governed by changes in gene regulatory regions (19, 20). Second, the observation that different combinations of alleles can produce similar pigmentation patterns suggests that distinct molecular mechanisms can underlie adaptive convergence even in similar selective environments (but see 21). Finally, Mc1r represents a large effect locus, containing a quantitative trait nucleotide (QTN) contributing to variation in fitness, consistent with the view that adaptation may often proceed by large steps (Hoekstra et al. 2006:104).
That certainly packs in a lot of contrarianism on the main recent strains of "how phenotypic evolution works" literature.
The study itself is about pigmentation in Florida beach mice, which are more lightly colored to blend in to dunes. They found that an amino acid change in Mc1r had a large effect on lighter pigmentation in Gulf Coast mice, and not Atlantic mice (hence the different mechanisms of adaptive convergence).
It is most interesting to see pushback against the "regulatory evolution" story that has been strongly emerging in the past several years.
References:
Hoekstra HE, Hirschmann RJ, Bundey RA, Insel PA, Crossland JP. 2006. A single amino acid mutation contributes to adaptive beach mouse color pattern. Science 313:101-104. DOI link
"Males may rub them together for as-yet unknown sensations"
I'm not into whale-blogging, but with a quote like that, the narwhal has become today's subject.
Here's the story (from LiveScience):
For hundreds of years the purpose of the tusk on the narwhal, or "unicorn" whale, has stumped scientists and Inuit elders alike. It is an evolutionary mystery that defies many of the known principles of mammalian teeth.
A new study suggests the whales use their tusks to determine the salinity of water and search for food.
So it looks like if a mammal wants to develop an antenna, a good bet is to modify a tooth.
After four trips to the Canadian High Arctic to study these whales, Martin Nweeia of the Harvard School of Dental Medicine has discovered that the narwhal's tooth, while seemingly rigid and hard, has remarkable sensor capabilities. With ten million tiny nerve connections tunneling from the central nerve of the tusk to its outer surface, the thing is like a membrane with an extremely sensitive surface and can detect changes in water temperature, pressure, and particle gradients.
Because these whales can detect particle gradients in water, they can discern the salinity of the water, which could help them survive in their Arctic ice environment. They can also detect water particles that hint at the fish that make up their diet.
There is no known comparison in nature and certainly none more unique in tooth form, expression, and functional adaptation.
"Why would a tusk break the rules of normal development by expressing millions of sensory pathways that connect its nervous system to the frigid arctic environment?" Nweeia said. "Such a finding is startling and indeed surprised all of us who discovered it."
Oh, and about that headline:
The findings point to a new direction of scientific investigation. The tusk is also sensitive to touch, and narwhals are known for their "tusking" behavior, when males rub tusks with each other. Because of the tactile sensory ability of the tusk surface, the whales are likely experiencing a unique sensation.
This is exactly why I'm not a marine biologist.
"Darwin stuck snails on ducks' feet"
Who'd'a thunk it? This story from LiveScience explains all.
The study, published in the journal Nature, indicates that Balea snails somehow traveled from Europe to the Azores and evolved into two different species. Then, some packed up and headed 5,500 miles south to Tristan da Cunha, where they further differentiated into eight more species.
Finally, Balea snails from Tristan returned to Europe, where until recently they have been mistaken as the Baleaperversa snails that made that original trip.
The question remains, though, how did these snails cross the ocean?
They're guessing birds, but have no idea which. But the question of snail dispersal to islands evidently interested Darwin enough to experiment a bit with them -- according to the story, at least; I haven't had any luck finding a reference to it in Darwin's writings.
UPDATE (1/30/2006): A reader e-mails a post with the citation! Turns out there's a whole blog devoted to snails! That is cool.
Skittering not included
Who knew?
Termites actually social cockroaches
...
Researchers added that the cockroach penchant for coprophagy, or eating feces, could very well have led termites to evolve in the first place.
Yeeeaaah!
Escaping the male-killer
At the moment, our yard here has many more butterflies than the "butterfly garden" at the zoo. That's mostly attributable to the zoo's complete lack of milkweed (Asclepias), which we've had going strong for around three weeks, supplemented by a huge number of coneflowers (Echinacea). After a quick burst of painted ladies, the monarchs have settled in. We've had phlox for a few days now, so we'll be watching for tiger swallowtails.
So I like this story about the rapid response to selection among Blue Moon butterflies in Samoa:
Sylvain Charlat of the University of California, Berkeley, and the University College London, along with colleagues, studied the sex ratios of Hypolimnas bolina butterflies on the Samoan islands of Upolu and Savaii, where males had dwindled to 1 percent of the populations in 2001.
The likely culprit was a male-killing parasite, Wolbachia, which lives inside the butterfly's reproductive cells, preferably female sex cells. With a female host, Wolbachia can hitch a ride to the next generation aboard the mother's eggs. Since males are "useless" for the bacteria's survival, the parasite kills male embryos.
But the male butterflies found a way to stealthily overcome the parasites. At the beginning of 2006, the scientists found the males made up about 40 percent of Upolu's butterfly population.
On Savaii, females still dominated the Blue Moon butterfly population (99 percent) at the start of 2006, but by the year's end, males made up nearly 40 percent.
Wolbachia may be the best parasites in nature, judging by the diversity of strategies that they exhibit. Killing males to direct resources toward females is the least of these. Here's a passage from a 1995 article by Stephen Hart:
Entomologists had thought that parthenogenetic wasps represented a quirk of nature -- until geneticist Richard Stouthamer of the Agricultural University in Wageningen, the Netherlands, reported in the April 1990 Proceedings of the National Academy of Sciences that he had "cured" parthenogenetic wasps with a dose of antibiotic. Tetracycline exorcises a parthenogenetic female, allowing her to lay viable female and male eggs. Her offspring can then go on to form a sexually reproducing population (Hart 1995:4).
The culprit was Wolbachia, of course, which can spur unfertilized eggs to develop. You may pause to consider whether this is good or bad for the wasps (clearly, it's bad for the male wasps!). But for the females, it leaves them 100 percent related to their offspring.
The rapid response to the high infection rate is quite expected based on the mechanism of male-killing, as long as the few remaining males are necessary, their genes will be represented in all the next generation. So it's an enormous reproductive advantage, in this case causing an allele to go from near zero to 40 percent in only 10 generations.
Still, it raises that question again -- who's better off here, the lucky males or the Wolbachia?
UPDATE (7/21/2007): A tiger swallowtail yesterday -- a dark morph female, which is the first of those we've had around here.
References
Hart S. 1995. When "Wolbachia" invades, insect sex lives get a new spin. BioScience 45:4-6.
EVOLUTION IS OVER...WATCH MORE TV
That was the message that just flashed surreally on my TV screen, from the old U2 "ZooTV" tour. Yes, that's the one where the Edge is wearing a beret.
So, having this excellent 17-year-old advice from Bono, I decided to Google "EVOLUTION IS OVER" to see what I would find.
Here's an old article (2002) in The Observer by Robin McKie:
For those who dream of a better life, science has bad news: this is the best it is going to get. Our species has reached its biological pinnacle and is no longer capable of changing.
That is the stark, controversial view of a group of biologists who believe a Western lifestyle now protects humanity from the forces that used to shape Homo sapiens.
'If you want to know what Utopia is like, just look around - this is it,' said Professor Steve Jones, of University College London, who is to present his argument at a Royal Society Edinburgh debate, 'Is Evolution Over?', next week. 'Things have simply stopped getting better, or worse, for our species.'
There is more, including quotes from Chris Stringer noting the continuing evolutionary change du