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March 31, 2007

Can a selfish gene stop malaria?

A bird that risks her life to lead a fox away from her chicks may be influenced by a "selfish gene" (Dawkins, 1976). Genes can't think, of course. However, a gene causing behavior that risks the loss of one copy of itself (in the mother) will become more common over time, if this same behavior often saves more than one copy of itself (in the chicks). The gene can be considered "selfish", in the sense that the welfare of the mother, her species, or the whole ecosystem only indirectly affect the gene's spread. It's as if each gene were at war with rivals (other versions of the gene, or alleles) for its place on the chromosome.

The selfish gene concept is now being used to design new methods to control the spread of disease. Mosquitoes that resist infection by the malaria parasite can be made by genetic engineering. Unfortunately, the small benefit (to a mosquito) of resistance to this parasite is probably not enough for resistant mosquitoes to take over in the wild, because most of the animals they bite aren't infected. (It would be nice if the laws of nature always favored human welfare, but they don't.)

How can we make such beneficial genes spread through mosquito populations? This week's paper, "A Synthetic Maternal-Effect Selfish Genetic Element Drives Population Replacement in Drosophila" by Chun-Hong Chen and colleagues at Cal Tech and UCLA, published on-line in Science, demonstrates one interesting approach.

The proposed method would use a cluster of genes that are tightly linked (close together on the chromosome), so that they would usually be inherited together. One gene, if present in the mother, tends to kill her babies at the embryo stage. Call this gene K, with k being the nonkilling variant. A second gene, if inherited from the mother, makes the babies resistant to killing by the mother's K gene. Call this second gene R, with r the nonresistant variant. The third gene (M) is the one that prevents infection by the malaria parasite.

Suppose a female mosquito has genotype Kk (two different versions of the K gene from her two parents). Because the genes are so closely linked, she would also probably have genotype Rr (and Mm). Roughly half of her eggs would receive the r gene from her. The resulting embryos would all die (unless they happened to receive an R gene from their father), because they wouldn't be resistant to the mother's K-gene activity. But half of her eggs would get the R gene from her and survive. Because these would also have the M gene (due to linkage), her only surviving offspring would all be resistant to infection by the malaria parasite.

Chen et al. cite theoretical analyses showing that linked genes with these properties would take over an insect population, so long as they are "introduced into the population above a threshold frequency, determined by any associated fitness cost." Losing half of ones offspring seems like a major fitness cost, but this may not be the case. If a mosquito lays a bunch of eggs in a puddle with only enough food for 100 baby mosquitoes, it may not matter whether she lays 1000 eggs or 2000.

So much for the theory. To test this approach, Chen et al. made fruit flies (Drosophila) with a maternally expressed gene (encoding an interfering RNA, not a protein, in this case) that prevents hatching in normal ("wild-type") embryos. They linked this to a mutant version of the interfering RNA's target. Presence of this mutant gene allowed normal embryo development even in the presence of the interfering RNA.

They started with a mix of wild-type and transgenic genotypes, and allowed the Drosophila populations to evolve in cages. As predicted by "selfish-gene" theory, the wild-type genes disappeared from the population after 10-12 generations, in replicated experiments.

How soon will we see the deliberate release of genetically engineered mosquitoes bearing selfishly propagating genes linked to malaria resistance? This question really has two parts: would it work, and would (politically powerful elites in) malaria-infested countries accept this approach?

Possible technical problems include mutations in the malaria-parasite-killing gene. Because this gene is not very beneficial to the mosquitoes (partly because most of the animals they bite are malaria-free), we could end up with a population of mosquitoes that have the interfering RNA "poison" and its "antidote", but which still transmit malaria. This problem and possible solutions are discussed in the paper.

There is also wide-spread public suspicion about genetic engineering. This is, in my opinion, partly a reaction to the reckless arrogance of some early proponents of genetic engineering ("don't worry, herbicide-resistance genes won't spread to, or evolve in, weeds!"), and partly irrational public hostility to unfamiliar science and technology.

There are other possible ways to guide the evolution of the malaria parasite and/or mosquitoes in ways that reduce the prevalence and severity of malaria. As mentioned in a previous entry, window screens favor the evolution of reduced virulence in the malaria parasite, because only people with mild cases go outside where they can be bitten. Indiscriminate spraying of insecticides selects for resistant mosquitoes, but spraying only the inside walls of houses selects for mosquitoes that stay outside. Of course, this should only be considered with insecticides that have low toxicity to humans, such as, I hope, the one we were all sprayed with last year when our plane landed in Beijing.

I wouldn't rule out a genetic engineering approach, however. Malaria kills millions and makes millions more sick every year. The important thing is that any such program be evaluated and discussed by a wide range of experts (including disease ecologists and evolutionary biologists) before deciding whether the benefits of transgenic selfish-gene mosquitoes will exceed the risks. Then perhaps it could be tested first on a remote island. Before tourism boards around the world clamor to be the test site, remember that the introduced gene wouldn't stop mosquitoes from biting tourists, only from giving them malaria.

Selfish genes have been used for other practical purposes in the past. For example, some plant genes that are inherited only in seed, not in pollen, suppress pollen production, freeing up resources for more seeds (Trends in Ecology and Evolution 10:412). The resulting "male-sterile" plants have been useful in plant breeding. However, reliance on only one such genetic system for maize (corn) breeding led to widespread damage by Southern Corn Leaf Blight. There's a lesson here about not putting all your eggs in the the same basket, but it doesn't necessarily indicate that practical applications of selfish gene theory all involve similar risks.

Other recent discoveries:

Dinosaur extinction wasn't so important to the diversification of mammals.

Experimental evolution of robots shows selection at the level of groups, rather than individuals, favors evolution of within-group cooperation. We already knew this, from experiments with chickens, for example (Poultry Science 75:447; thanks to Richard Dawkins for calling my attention to this paper). The question is whether the right kind of group selection happens in the natural world often enough to overcome the evolutionary effects of within-group competition, especially when migration between groups is possible. Probably not.

Two papers in Nature show how experiments with microbes can be used to explore roles of competition, predation, and migration in evolutionary diversification.

March 27, 2007

Evolution of color vision: transgenic mice see red

This week’s paper, "Emergence of novel color vision in mice engineered to express human cone pigment", by Gerald Jacobs and colleagues at UC Santa Barbara and Johns Hopkins Medical School (Science 315:1723), is yet another experimental study that increases our understanding of how repeated cycles of natural selection, each producing a fairly small change, can lead to adaptations that may seem irreducibly complex.

Most humans have three different photopigment color sensors, as do our closest relatives. Many other mammals, including mice, have only two. Three-color vision is useful for many purposes, from identifying higher-protein leaves to eat (Nature 410:363) to telling which wire to cut to disarm the nuclear bomb buried under the stadium. But eventual usefulness isn’t enough for a trait to evolve. If a series of steps is required, each step must be beneficial, or at least not lethal. Such a series of steps has been worked out for the evolution of optically sophisticated eyes from light-sensitive spots (Proc. Roy. Soc. B 256:53), but what about color vision?

New World monkeys have a form of color vision that may have been a stepping stone between the two-color vision of other mammals and the three-color vision we apes enjoy. One of their photopigment genes is on the X sex chromosome; another is on a nonsex chromosome. Males have one X chromosome (and one Y sex chromosome), so two different color receptors. Females with the same photopigment on both X chromosomes also have only two different color receptors. But "heterozygous" females (with two different X chromosomes), can have two different photopigments on their X chromosomes, plus one on the nonsex chromosome, for a total of three photopigments, each sensitive to different colors of light.

How could this form of three-color vision evolve from the two-color version in other mammals? Although mutation of the photopigment gene on the X chromosome would yield some heterozygous females with three photopigments, I would have thought that three-color vision would have additional requirements (special neurons, etc.). But apparently I would have been wrong.

Jacobs and colleagues genetically transformed mice, adding a human gene for a photopigment not normally present in mice. They then tested color vision in heterozygous females, which had three different photopigments: the two normal mice versions (X and non-X), plus the human version on their second X chromosome. These mice varied in the proportion of the two X-linked photopigments. Those with roughly equal proportions were usually able to tell the difference between colors that looked the same to normal mice. The tests involved distinguishing between differently-illuminated color panels, presumably in exchange for mouse treats.

So specialized neuronal circuitry for each photopigment apparently isn’t essential for at least simple three-color vision. The authors suggest that inactivation of different X chromosomes in different cones in the mouse eyes may have helped the mouse brains learn to distinguish nerve signals linked to photopigments that respond to different colors of light.

Once this simple color vision system was established, further evolution of the nervous system could lead to further improvements, so it seems likely that monkeys have better color vision than these transgenic mice. But why haven't monkeys evolved an ape-like color vision, which works for males as well as females? The required evolutionary changes in the nervous system may be trickier for photopigment genes on nonsex chromosomes. Or maybe the benefits of three-color vision aren’t great enough for natural selection to favor allocation of more brain cells to processing additional color information, except in species with large brains. Or, for monkeys living in troops, maybe there are always enough heterozygous females around to serve as color consultants.

The same issue of Science has 1) a paper showing that fewer genes have been transferred from mitochondria (respiratory organelles descended from intercellular symbionts, and retaining some of their own genes) to the cell nucleus in plants that out-cross (produce seeds with another plant rather than by self-pollination), perhaps because out-crossing can scramble interactions between nuclear and mitochondrial genes, and 2) a report on a virus-defense system in bacteria in which viral DNA from a previous infection is used against new infections, analogous to the vertebrate immune system but using a very different mechanism. As in previous weeks, I haven't seen any papers on "intelligent design" this week, maybe because I've only been looking in scientific journals.

March 21, 2007

Splitting species: sneak attacks from strategic hamlets

This week's paper is "Colour pattern as a single trait driving speciation in Hypoplectrus coral reef fishes?" by Oscar Puebla (Smithsonian Tropical Research Institute, Panama) and colleagues in Canada and the UK, published on-line (no volume or page number yet) in Proceedings of the Royal Society. (I was planning to review a paper on the evolutionary history of genetic differences between chimps and humans, suggested by a reader, but decided I didn't understand it well enough myself to explain it clearly. Is there a volunteer guest blogger out there?)

Actually, there's a bit of a connection between the two papers. At some point, the ancestors of humans must have stopped having babies with the ancestors of chimps. Otherwise, we'd still be one species. We might have evolved a lot from our common ancestor, but we'd be evolving together, not separately. Interbreeding is a problem for the production of new species in general; the resulting "gene flow" can prevent differentiation into separate species.

One easy solution is geographic separation. Finches on different islands in the Galapagos group rarely interbreed with each other, and never with their ancestral species on the mainland. So natural selection, working in different directions on the different islands, isn't swamped by interbreeding. This eventually produced enough change that the finches would at least hesitate to mate if brought back together.

But can species separate without being physically separated? There are already a few known examples of this, but the authors of this week's paper may have caught "sympatric" speciation in reef fish known as hamlets red-handed. Uh, finned.

Hamlets have a variety of color patterns (morphs) on the same coral reef. From the picture in the article, I would have guessed that they were several different species, just as I would have guessed that brocolli and cabbage are different species, but in both cases the different morphs sometimes produce offspring together, as if they were all one species.

Puebla and colleagues collected several individuals of each of three different morphs for genetic analysis. There were significant genetic differences among morphs. In particular, one gene (or one region of a chromosome, anyway) differed consistently among fish with different color patterns. Field observations showed that the fish usually mate with another of the same color pattern (247 out of 251 observations). Within-species mating of like with like is is known as "assortative mating." This behavior and the genetic differences were enough to classify the morphs as "incipient species."

Assortative mating based on color morph would favor eventual speciation, although you might think this would require one gene for being blue, and another gene for mating with blue. But there's more to the story.

Hamlets are predatory fish, so their prey should avoid them. But apparently some mutants arose that somewhat resembled various nonpredatory fish. The hamlets exploit this resemblance. When divers followed 12 individuals of one of the morphs, the hamlets spent a lot of time following nonpredatory fish that they resembled -- if you have access to this journal, e.g., via a university library, check out the video! -- and were most successful in catching prey when in this nonthreatening company.

But we seem to be swimming into a sea of troubles here. Do the blue morphs now need a gene for being blue, a gene for mating with blue, and a gene for associating with blue nonpredatory fish, while yellow morphs need a gene for being yellow, a gene for mating with yellow, and a gene for associating with yellow nonpredatory fish?

Maybe not. It seems to me that there are at least three hypotheses consistent with the data in this week's paper:

1) Maybe color, mating preference, and mimicry behavior are indeed controlled by separate genes at present. How could this system of genes have evolved? Here's one scenario: the original genetic variation among the ancestors of today's morphs was variation in a gene that influenced which type of nonpredatory fish they associate with. That would lead to some assortative mating, through propinquity, even without preference for a mate that shows a particular color pattern. Differences among hamlets in the nonpredatory fish they associate with would then drive divergent natural selection, favoring mutations making each mimic look even more like its model. There would also be selection for mating preferences that would strengthen assortative mating, since hybrids between two incipient morphs wouldn't resemble either of the nonthreatening model species and would therefore be less successful predators and less likely to survive to reproduce themselves.

2) Or maybe morphs initially varied only in appearance; each individual hamlet learned which nonpredatory model fish to hang out with by trial and error (based on hunting success), and then mated with others associating with the same model. These behaviors could subsequently have been strengthened by natural selection, as in hypothesis 1.

3) If all of the hamlets share a gene for "following nonpredatory fish that look like me" and another gene for "mating with fish that look like me" (or genes for associating with fish, of whatever species, that look like themselves and for mating with nearby members of their own species), then as few as one gene, controlling color pattern, would need to vary among morphs. This assumes, among other things, that each individual knows what it looks like. They don't have access to mirrors, but maybe their fisheye-lens eyes have a sufficiently wide-angle view that they can see themselves. My impression is that this is the hypothesis preferred by the authors.

I hope we will be seeing more research on these interesting fish. For example, mate-choice experiments under laboratory conditions, where the fish wouldn't have the opportunity to associate with any nonpredatory fish, could potentially disprove the "mate with those who associate with the same nonpredators" hypothesis. (Alexandra Basolo uses clever three-part aquaria to study the mating preferences of female swordtail fish. Crossed polarizing glass in the two dividers lets the female see and approach males on each side, while they can see her but not each other.) It would also be interesting to interbreed morphs in the laboratory and see how the hybrids behave, both with respect to mating preferences (including with nonhybrids) and with respect to associating with different nonpredatory fish.

The same issue of Proceedings of the Royal Society has a review article on the evolution of "family living" in birds, experiments on the evolution of mutation rate in bacteria by Angus Buckling (an evolutionary biologist mentioned last week), a new fossil of a dinosaur that dug underground dens, research on mate choice in birds, and a computer modeling paper that tries to explain some aspects of human mating behavior, including societies that consider children to have more than one biological father. This seems unlikely, but maybe we should teach the controversy?

March 12, 2007

Less-vicious viruses evolve in viscous cannibal populations

This week’s paper is “Local interactions select for lower pathogen infectivity? by Michael Boots and Michael Mealor, University of Sheffield, published in Science (vol. 315, pgs. 1284-1286) and suggested by my wife.

The evolution of greater or lesser infectiousness in pathogens has important implications for health of plants and animals, including humans. Evolution is a process that follows its own rules and humans can’t control it completely, but we can sometimes influence it, just as we may be able to constrain the course of a river or limit the spread of a forest fire.

One factor over which we have some control is the ease with which a pathogen spreads from one host individual to another. For example, a bacterium on the skin of one patient in a hospital can’t jump to another patient in a different room, but it may be able to hitch a ride with a doctor or nurse who forgets to change gloves between patients. Intestinal bacteria reach new hosts easily if untreated sewage is dumped into the same river used for drinking water, even if the bacterium is so virulent that the host is too sick to walk around and infect others.

Paul Ewald has suggested that easy transfer between hosts favors the evolution of greater virulence (Oxford Surveys in Evolutionary Biology 5:215-245). For example, cholera spreading through South America in 1991 evolved greater virulence in countries with poor water supplies, but lesser virulence in countries with better water supplies. So not only were more people infected in countries with polluted water supplies, but the infected people were sicker.

Virulence (disease severity) isn’t the only trait that can evolve, of course. What about transmission, which depends on the number of bacteria or virus particles released by a host, the chances that each will reach another host, and infectiousness (the chance that contact will lead to infection)? What we need is an experimental system that lets us control the ease of pathogen movement between hosts while measuring evolution of all these traits. Any volunteers to "host" this experiment? I didn’t think so, and anyway it would take a village.

So Boots and Mealor used caterpillar larvae that get infected with a virus, mostly by eating dead infected larvae. They controlled movement by controlling the viscosity of the medium in which the larvae lived. (A “viscous population? is one that doesn’t mix with neighbors much, for whatever reason, but in this case movement was controlled by physical viscosity of the medium.) After about eight generations, they harvested virus from high- and low-viscosity populations and measured their ability to infect a standard caterpillar population. The virus populations in low- and medium-viscosity media hadn’t evolved, but those swimming in oobleck had evolved much lower infectivity.

Boots and Mealor suggested that, when movement is limited, more infective viral genotypes would quickly run out of uninfected (and therefore susceptible-to-infection) hosts. (The caterpillars and viruses in a local area might all die out before another host wanders by, just as measles died out in the rarely visited Faroe Islands between 1781 and 1846.) A less-infective mutant, on the other hand, would make the limited local supply of hosts last long enough for a ship – I mean a caterpillar – to arrive from elsewhere.

Can we extrapolate from one study with cannibal caterpillars to humans or wheat? Not with much confidence. On the other hand, if a large number of experiments, conducted by different scientists, using different species and different methods, find the same general pattern, then the results might apply to our crops and perhaps to ourselves. Another study consistent with that of Boots and Mealor was published last year in Nature (442:75-78) by Benjamin Kerr and others, here at the University of Minnesota. It’s past its “use-by date? for This Week in Evolution, but maybe I’ll discuss it in my other blog, The Comedy of the Trojans, since it's about a "tragedy of the commons" for viruses.

Even if there were no effects on the evolution of infectiousness and/or virulence, reducing pathogen transfer between hosts is usually something we would want to do anyway. In the case of humans, this could involve hand-washing, face masks, and monogamy or condoms rather than restrictions on travel per se. Adding in the evolutionary benefits could make improvement of public water supplies, screening windows against mosquitoes, and enforcing glove-changing rules in hospitals even more cost-effective.

The same issue of Science has a good discussion of Boot’s and Mealor’s paper by Angus Buckling (we’ve both published with Stuart West, but hasn’t everyone?), an article on brain evolution, an experimental molecular biology paper on the evolution of a membrane protein that confers antibiotic resistance in bacteria (gene duplication is involved, as in the hormone-receptor paper discussed last week), and newly discovered 500-million-year-old fossils from the Burgess Shale that apparently shed light on the evolution of mollusks.

Next week: "Adaptive evolution in humans revealed by the negative correlation between the polymorphism and fixation phases of evolution"

March 10, 2007

Troll refuge may prevent local extinction

I reserve my blog-given right to delete off-topic comments -- except in this Troll Refuge. "Comments" whose only purpose is to link to a commercial or crackpot site will generally be deleted everywhere. This is a free service to people who may not realize they are crackpots.

Comments immune from deletion outside the Troll Refuge are either:
1) comments on the particular paper-of-the-week, or
2) suggestions for papers to discuss that meet the criteria in my first post.

"But", you may say, "I've got this great proof that evolution is all wrong! This scientist said something that could be interpreted as inconsistent with some aspect of evolutionary theory! That proves that both versions of the creation story in Genesis (cattle and trees created before and after humans) are literally true, doesn't it?"

If the scientist said it in a peer-reviewed paper published in the last month and containing new data, you can suggest it as a paper of the week. Otherwise, post your proof here in the Troll Refuge.

The comments section for this entry is also the place to whine about censorship, or to complain about my failure to delete someone else's comment that you think is off-topic. Off-topic comments attached to other entries are subject to deletion, or, if particularly amusing, transfer to this troll refuge, possibly with appropriate editing. Trolls repeatedly posting outside the refuge will be banished.

Troll hunters are welcome in the refuge, too. This may seem cruel, but we need to keep the population below carrying capacity. However, no firearms will be allowed, only sticks and stones. And words, of course.

March 8, 2007

Experiments with "fitness landscapes" explain evolution of interacting genes

A reader asked an interesting question about the difficulty of coordinated evolution of groups of genes. Although I welcome comments and questions, I won't usually have time for detailed responses. and I'd already discussed one paper this week. But then Huxley brought in a recent issue of Nature he'd been chewing on, and there it was: "Empirical fitness landscapes reveal accessible evolutionary paths" (Nature 445: 383-386). So I guess I should take this dog-given opportunity to talk about the evolution of multiple interacting genes. The Nature paper is a review article with no original data, so isn't eligible for my regular weekly paper discussion, but maybe it's OK as a bonus paper, especially since the most interesting papers it discusses were published within the last year and they do contain original data.

The exciting thing about these papers is that people are starting to use molecular methods in experiments that solve "you can't get there from here" problems in evolutionary biology.

Let's start with a one-gene example, the paper by Weinreich et al. (Science 312:111-114). They looked at the evolution of antibiotic resistance involving a beta-lactamase gene in certain bacteria. Even with only one gene, evolution of resistance required five mutations. The odds against all of these mutations happening to any one bacterium are really small, even though there are lots of bacteria. So evolution of resistance probably required five successive steps. The problem is, what if one of the intermediate genotypes (step 3, say) were less fit than earlier genotypes in this evolutionary path? The intermediates might die out before any of them mutated to the next step. They didn't know what order the mutations occurred in; there are 32 possible intermediate genotypes (2 to the fifth power) and 120 possible 5-step paths from susceptibility to resistance (5 factorial). So Weinreich et al. made all 32 genotypes and compared their antibiotic resistance. Then they were able to calculate which of the 120 possible pathways involved a decrease in antibiotic resistance at one or more steps, and which pathways, if any, had increasing resistance at each intermediate step. 102 of the possible pathways involved intermediates with lower resistance. Therefore, evolution by any of these pathways would be unlikely, if the only mechanism was natural selection driven by the presence of the antibiotic. The 18 remaining pathways didn't involve intermediates with decreased resistance, but some were still considered more probable than others, for various reasons. Note that there's no doubt about whether this gene evolved; both "before" and "after" versions are out there. Rather, these experiments let us assign relative probabilities to different pathways by which the evolution occurred.

You might think that evolution of interacting genes would be much harder. As the review put it, "if the lock is modified first, the intermediate is not viable because the old key does not fit, and vice versa." Bridgham et al. (Science 312:97-101) looked at the problem of how one hormone and one receptor could evolve into two hormones and two receptors. In this case, evolution involved duplication of genes, a common event also responsible for innovations like color vision. Once there were two copies each of hormone and receptor gene, one copy of each could evolve a new function without losing the original function. Before molecular methods were widely available, we might have speculated about this mechanism, but now it can be tested experimentally. Bridgham et al. used DNA sequences of existing animals to infer ancestral sequences, synthesized genes with the inferred sequence, and tested hormone-receptor interactions in cultured cells containing the synthesized sequences, etc., confirming "recruitment of an older molecule, previously constrained for a different role, into a new functional complex."

There are some other nice examples in the Nature review, including experiments by my colleague Tony Dean and collaborators that let them draw inferences about complex evolutionary events (different enzyme substrate and different cofactor) over a billion years ago. But that's enough for now. I expect we'll be seeing more of this sort of study, further clarifying the evolution of interacting groups of genes.

The same issue of Nature has a neat paper about a microbe that eats chloroplast-containing prey. Rather than digest the chloroplasts, it keeps them, thereby benefiting from ongoing photosynthesis. Chloroplast function requires some genes in the prey nucleus, but fortunately the predatory microbe keeps the nuclei, too, for up to 30 days. It would be fun to come back in a million years and see how this interaction evolves. Or maybe try a little experimental evolution, setting up conditions that select for longer retention of the prey genes?

Thanks for all the comments, especially the chimp movies and suggestion for a paper to discuss!

I made up the part about Huxley.

March 7, 2007

Teenage chimps with spears and hammers

Two related papers this week: “Savanna chimpanzees, Pan troglodytes verus, hunt with tools? by Jill Preutz and Paco Bertolani, published in Current Biology (17:1-6), and “4,300-year-old chimpanzee sites and the origins of percussive stone technology? by Julio Mercader et al., published in Proceedings of the National Academy of Science (104:3043-3048).

Preutz and Bertolani report field observations of chimpanzees in Senegal making simple wooden spears and using them to kill bushbabies (sleeping in hollow trees) for food. Several individuals were seen making and using the spears, although apparently they only saw one successful “hunt.?

Some press reports have said that most of the chimps making and using spears were female, but what the abstract of the paper actually says is “females and immature chimpanzees exhibited this behavior more frequently than adult males.? Table 1 shows one adult male, one adult female, and eight immatures (four male and four female) making and/or using spears. So it might have been more informative to say that “immature chimpanzees exhibited this behavior more frequently than adults.? But apparently they wanted to contrast hunting with spears with “chimpanzee hunting in general, a predominantly [adult?] male activity.?

What can we conclude about tool use in human ancestors? Both humans and chimps are separated from our last common ancestor by a few million years of genetic and cultural evolution. Because other chimps have not been seen making spears, maybe “spear culture? arose in this particular chimp lineage some time after it diverged from our own. Is it possible that the first chimp to make a spear was copying a human spear-maker?

Mercado et al. found stones at three nearby sites in Cote d’Ivoire that had apparently been used by chimps to crack nuts thousands of years ago. Experts classifying the stones by their appearance as having been used for pounding. To avoid bias, these tests were done "blind" (experts weren't told which stones were which), with natural stones included as controls, including some with “natural modification that gives them the appearance of artifacts.? (The Far Side cartoon “Cow Tools? illustrates the problem.) Starch grains on some of the stones were identified as coming from nuts eaten mainly or exclusively by chimps and not by (modern?) humans. Carbon-14 dating of charcoal from forest fires showed that the layer where the stones were found was 4300 years old. This “predates the advent of settled farming villages in this part of the African rainforest?, making it less likely (though still possible) that the first chimps to use stones as “hammers? were imitating humans. Maybe the last common ancestor of humans and chimps used stone hammers and passed this cultural trait on to both lineages, or maybe the two species invented hammers independently.

Preutz and Bertolani endorse an earlier suggestion that “the earliest tool technology likely consisted of pounding or throwing rocks and hitting and jabbing sticks at about 6 million years ago.? Both of these studies, and other reports of chimps using sticks to collect termites, etc., show that animals with chimp-size brains can make and use rudimentary tools. If the last common ancestor of chimps and humans was using sharpened sticks as spears and stones as hammers several million years ago, humans have certainly made a lot more technological progress than chimps have. Maybe technologically innovative adolescent chimp nerds had more trouble finding mates?