This Week in Evolution

If you don't believe in evolution, you might not want to listen to this next story. Scientists reported this week on a new fossil, possibly a human ancestor, older than Lucy. The good news is, we're not descended from chimps after all. The bad news is, chimps and humans are descended from the same ancestor.

That's a paraphrase of how our local TV news covered Ardipithecus ramidus, the fossil hominid discussed in a series of papers in this week's issue of Science. Read all about it on Carl Zimmer's blog. The TV anchor didn't say which scientists claimed we are descended from chimps, perhaps because no scientist has made that claim. Chimps have evolved over the six million years or so since our last common ancestor, including their split with bonobos. Can we expect the story below on the TV soon?

Startling breakthrough in human genetics! You aren't descended from brother after all, or even from your cousin. You and your brother still have the same parents, and you and your cousin have the same grandparents, though. I hope that doesn't upset you too much.

We don't know for sure that present-day humans are descended from Ardipithecus . It's a reasonable hypothesis, but any hypothesis is, by definition, subject to possible disproof. For example, if we found another fossil that was clearly much more similar to modern humans, dating from the same time or earlier, then we'd conclude that Ardipithecus probably has no surviving descendants.

But this species probably isn't too far from the direct line of descent between our common ancestor with chimps and modern humans. Suppose you wanted to know what your great grandmother looked like, but there was no surviving picture of her. If you had pictures of her sister or her daughter, that would give you some idea, even if all her living descendants are descended from a son.

Of course, much of what we know about our ancestors now comes from analyzing DNA in humans and closely related species. We can figure out when vitamin C synthesis was lost or adult lactose tolerance gained, for example. But we don't yet understand development enough to predict height, foot shape, etc., from inferred DNA sequences of ancestral species. So keep those fossils coming!

Posted by R. Ford Denison at 4:32 PM | Permalink | Comments (1)

"This new forage has great insect resistance", effused a former colleague, "we just need to eliminate the toxins that keep sheep from eating it."

Genetically engineered drought-tolerant crops are introduced with great fanfare, only to disappear when they turn out to have low yield under nondrought conditions.

When natural selection falls short of perfection, it may be because "you can't get there (some desirable adaptation) from here (current genotypes)" without passing through a series of intermediate generations that would have lower fitness. Natural selection favors genotypes best-adapted to current conditions, which are not necessarily steps towards any long-term improvement.

But natural selection often seems to miss even "simple" improvements, that might be achieved by changing as little as one DNA base. Such small changes are often enough to increase or decrease expression of key genes, for example. This sort of evolutionary progress may be blocked by tradeoffs, e.g., between seed production under different conditions (e.g., wet vs. dry), or between the competitiveness of individual plants and their collective seed production.

So what are we to make of two recent papers (in Science and Nature, respectively, discussed in Science News) on extending lifespan, one using calorie restriction and the other using the antibiotic, rapamycin?

Calorie restriction has been shown to increase longevity in model species like nematode worms and mice, but this latest study shows clear benefits in monkeys. The obvious question -- at least, it was obvious to me -- is why has past natural selection given monkeys (and fruitflies, and nematodes, and mice...) appetites that make them eat more than is good for them?

At least, that seemed to be the question, until it was shown that food odors can reverse the beneficial effects of calorie restriction, at least in fruitflies and nematodes. In humans, soft drinks with artificial sweeteners turn out to be just as likely to cause "metabolic syndrome" (related to diabetes) as those with sugar. So apparently our lives can be shortened by a perception of abundance, not just by actually eating too much. What is going on here?

In this case, the evolutionary tradeoff seems to be between current and future reproduction. As discussed in last week's post, delaying reproduction usually decreases fitness (representation in the next generation, relative to others) when population is increasing, but delaying reproduction can increase fitness when population is decreasing. Calorie restriction predicts population decline, triggering physiological responses that delay reproduction and thereby increase longevity. So do bitter-tasting foods, traditionally eaten only during famines. Food odors or sweet tastes have the opposite effect, because they predict population increase.

But what about life extension by rapamycin? One known tradeoff is suppression of the immune system, so we might get longer lives only in a hypothetical germ-free environment. But could the protein target of rapamycin (TOR) also be important to reproduction? Is this yet another example of a longevity-vs.-reproduction tradeoff?

Posted by R. Ford Denison at 7:08 PM | Permalink | Comments (0)

If you could choose a longer, healthier life, but only by having fewer kids, would you? What if you could eventually have the same number of kids, but only by having sex more often, and with no possibility of becoming a parent as a teen-ager?

Is this really possible? Based on the paper we published last week, we are pretty sure it is, although we don't yet know how much of an increase in lifespan is achievable, nor how much it will "cost" in reduced fertility.

A key assumption is that there are tradeoffs between longevity and reproduction, especially early reproduction. There is plenty of evidence for this antagonistic pleiotropy hypothesis: some gene variants that increase longevity nonetheless stay rare, because individuals with those variants have fewer kids. There are many possible reasons for this tradeoff. Calories used for reproduction aren't available for maintaining our bodies. Blood pressure and insulin levels optimal for reproduction are unlikely to be exactly optimal for longevity. Other risks associated with reproduction include sexually transmitted diseases and direct risks of childbirth. When there is a conflict between reproduction and longevity, natural selection will often favor reproduction.

There are, however, two ways we may be able to choose differently, increasing longevity at the expense of (potential, but maybe not actual) reproduction. First, once germ-line gene therapy is perfected and available (initially, perhaps, only in one or two "outlaw states"), maybe we could reverse some of the effects of past natural selection. We might be able to produce genetically engineered kids who would reach puberty later and with low enough intrinsic fertility that occasional unprotected sex would rarely lead to pregnancy, but who would still be healthy at age 100.

Second, what about people already born? Is there some biological "switch" we can throw, that tilts the longevity-vs.-reproduction tradeoff more towards longevity? Or has past natural selection welded the switch in the "reproduce now" position?

We think the switch is free to move, depending on environmental cues that affected our ancestors' survival and reproduction. Our paper shows that the switch position that maximizes Darwinian fitness depends on whether the overall population is increasing or decreasing. If population is decreasing, then individuals that live longer and reproduce later can contribute a larger fraction to their species' (shrunken) gene pool than those that reproduce earlier, on average, even if a few of them die before they get a chance to reproduce, and even if their lifetime reproduction is less than they might have achieved earlier.

Therefore, even though gene variants that always sacrifice early reproduction to increase longevity may not have persisted in the gene pool, variants that delay reproduction (thereby increasing longevity) only when populations were decreasing are likely to be with us, in each of our DNA molecules, today.

If this is true, all we need to do to increase our longevity is to give our bodies (false) cues that, over our evolutionary history, usually predicted population declines. To the extent that population declines were caused by food shortage, eating less may work, as it does in most species tested. Eating "famine foods" (leaves rather than meat, maybe) may also trigger physiological responses that reduce fertility but extend lifespan. On the other hand, if population declines were usually caused by cold winters, is there some reasonably comfortable way to trigger similar responses?

Delaying reproduction can only increase fitness if it increases the chances of surviving the famine or cold winter and reproducing later. So stresses that often predicted the death of the stressed individual (those associated with violent conflict, perhaps) won't necessarily delay reproduction or increase longevity. But there are lots of examples of mild stress increasing longevity. These stresses presumably trigger health-and-longevity-promoting mechanisms, but we may be the first to explain why such beneficial mechanisms aren't turned on all the time: they tend to reduce fertility.

Now, here's a question for you: would increasing human longevity be a good thing? I've seen this issue discussed in various places, but rather superficially. Assume that this option was made available to everyone, given that the cost could be quite low: inexpensive drugs or lifestyle changes that might even save money. Death rates would go down, in the short run, but so would birth rates, especially in countries where birth control is now rare. Death from old age is a fairly small component of overall population trends in these countries (relative to birth rate and infant mortality), so their rate of population increase might actually slow. But, if people expected to live longer, would they have more children (despite lower intrinsic fertility) or fewer, and at what age? Assuming some increase in population, we might need to grow more food -- a significant challenge -- but how would the overall impact of two healthy 90-year-olds who are still working (perhaps as doctors or nurses) and driving compare to that of one 90-year old who doesn't drive but needs expensive medical care? If professors keep working into their 90's, will that slow the spread of good new ideas, or only of stupid ideas that younger faculty may not know were debunked long ago? Would a longer-lived population produce too many bloggers?

Posted by R. Ford Denison at 7:31 PM | Permalink | Comments (0)

"When stress predicts a shrinking gene pool, trading early reproduction for longevity can increase fitness, even with lower fecundity." That's the title of a paper that Will Ratcliff, Mike Travisano, Peter Hawthorne and I just published in PloS-One. This was a spin-off from Ratcliff's work on the timing of reproduction in bacteria, but our main conclusions should apply broadly to plants and animals, with important implications for human health. Our entire paper is available on-line, but here is some additional background and explanation.

Earlier, I blogged about our research at UC Davis showing that tomatoes grown using organic methods have higher concentrations of a specific chemical (Mitchell, et al. 2007). Plants make this chemical to defend themselves against insects, which may be why there was more of it in tomatoes not protected by artificial pesticides. Surprisingly, this chemical actually seems to benefit human health. At the time, I thought this might just be coincidence, and wrote that "some of the natural insecticides plants make... are likely to be harmful to humans, rather than beneficial."

Now, I'm not so sure. It turns out that many toxins, including natural insecticides, can have health benefits in low doses, a phenomenon known as hormesis (Mattson & Cheng. 2006). Other forms of mild stress, such as dietary restriction (calorie restriction, intermittent fasting) or high temperature, have also been shown to increase longevity.

How can stress be beneficial? Some stresses trigger various protection mechanisms, such as antioxidants or heat-shock proteins, which may increase lifespan, even relative to individuals not exposed to stress. But why aren't these protective mechanisms turned on all the time, rather than only under stress? Don't individuals with longer lifespans leave more descendants than those with shorter lifespans? Not necessarily.

What if some mechanisms that increase lifespan also delay sexual maturity or decrease the rate of reproduction? For example, what if the blood pressure that maximizes lifespan is lower than that which maximizes reproduction? Then a gene for lower blood pressure would not necessarily increase in frequency over generations. A trade-off between early reproduction and longevity (and later reproduction) was central to the "antagonistic pleiotropy" hypothesis of Williams (1957). Our paper builds on this widely accepted hypothesis.

Given trade-offs between early and late reproduction, when will natural selection favor genes that potentially increase longevity but delay reproduction? Sometimes, resources not used for reproduction can be invested in growth, increasing reproduction in future years. Also, more experienced individuals may care for their offspring better. But what if delaying reproduction doesn't increase either the number of offspring or their survival?

We showed that delaying reproduction can still increase Darwinian fitness, that is, proportional representation in the gene pool, provided that overall population size is decreasing. Hamilton (1966) pointed out that an offspring added to a smaller population represents a larger fraction of the total gene pool. Therefore, if total population is increasing, offspring produced earlier have a larger effect on fitness. But if population size is decreasing, then offspring produced later have a larger effect on fitness. This means that delaying reproduction can sometimes increase fitness, even if delay does not increase the number of offspring.

Most populations will alternate between increasing and decreasing in numbers. If the population is stable or increasing, delaying reproduction can only decrease fitness. This is especially true if there is a high risk of death from causes unrelated to reproduction. But if the size of the gene pool is likely to decrease, delaying reproduction can increase fitness. This is especially true if risks directly or indirectly associated with reproduction are large relative to other risks.

Our mathematical models show that the best strategy is to delay reproduction only when an individual's chance of surviving to reproduce later is high, and only when an individual has reliable information predicting a decrease in overall population size. This is where stress comes in.

Past population declines were often caused by shortages of food, which can affect both the amount and types of food eaten. For example, natural insecticides in plants often have an unpleasant taste. Over most of our evolutionary history, therefore, these plants may have been eaten only when preferred foods, like meat or fruit, were not available. Consumption of these "famine foods" would therefore have been a reasonably good predictor of population decline, so they may trigger physiological changes (lower testosterone, etc.) that increase longevity while tending to delay reproduction.

A remarkable result, seen in both nematode worms and fruit flies, is that food odors can reverse the beneficial effects of dietary restriction on longevity (Libert, et al. 2007). If an individual smells food, others may be eating that food, so population size may be increasing. In that case, delaying reproduction would be a losing strategy, even if reproducing now increases the chance of an early death.

What about humans? Our models assumed that individuals reproduce only once, then die, like salmon or soybeans. However, we expect that some of our results will apply to species, like humans, with more complex life histories. One result for humans that is consistent with our hypothesis is that artificially sweetened soft drinks are just as likely to cause metabolic syndrome (related to diabetes) as sugared soft drinks are (Lutsey, et al. 2008). Like food odors, sweet foods may have been correlated, over much of our evolutionary history, with abundance, and therefore with impending increases in population size. If we want to live longer, maybe we should instead eat foods whose chemical composition or flavor remind our bodies of past famines. The health benefits we get from eating vegetables like kale may be due, in part, to the chemicals that give them their slightly bitter taste.

High levels of toxins, including natural ones, are still presumably harmful. But low doses of plant toxins, perhaps especially those found in traditional famine foods, may often improve health. This assumes that our hypothesis is correct, so you might want to wait for the results of experiments we are planning before making major changes in your diet.

We are also assuming that most people would consider some decrease in potential reproduction to be acceptable. For the many humans that already choose to limit their own reproduction, this need not result in any decrease in actual family size. For example, if people don't expect to marry until after college, the risks of early fertility may outweigh the benefits, even apart from health effects of hormone levels etc. in the teenage years on health later in life. Delaying puberty might, however, result in larger adults, with possible negative implications for automobile fuel economy and other resource issues.

Another popular hypothesis has been that individuals benefit from delaying reproduction in a bad year and waiting until conditions are better. This may increase the number of offspring produced, but we show that it does not increase proportional representation if the entire population also reproduces more in the good year.

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"How is putting our entire kingdom to sleep for 100 years better for my family than losing one daughter, however much we love her?" asked the queen. "In 100 years, our other children would have had countless grandchildren. Meanwhile, those in neighboring kingdoms will multiply. By the time the impenetrable thorn forest you put around our kingdom dies and we awake, our enemies will vastly outnumber us."

"Not necessarily", replied the fairy scientist, "My computer models predict 100 years of wars, famines, and plagues. It's true that your population won't grow, but those of your enemies will shrink. This would have been a winning strategy, even if there were another way to save your daughter's life."


Ratcliff, Travisano, Hawthorne, and Denison. Can you spot the model?

LITERATURE CITED

Hamilton WD. 1966. The moulding of senescence by natural selection. Journal of Theoretical Biology. 12 : 12-45

Libert S, Zwiener J, Chu X, VanVoorhies W, Roman G, Pletcher SD. 2007. Regulation of Drosophila life span by olfaction and food-derived odors. Science. 315 : 1133-7

Lutsey PL, Steffen LM, Stevens J. 2008. Dietary intake and the development of the metabolic syndrome: The atherosclerosis risk in communities study. Circulation. 117 : 754-61

Mattson MP, Cheng A. 2006. Neurohormetic phytochemicals: Low-dose toxins that induce adaptive neuronal stress responses. Trends in Neurosciences. 29 : 632-9

Mitchell AE, Hong YJ, Koh E, Barrett DM, Bryant DC, et al. 2007. Ten-year comparison of the influence of organic and conventional crop management practices on the content of flavonoids in tomatoes. Journal of Agricultural and Food Chemistry. 55 : 6154-9

Williams GC. 1957. Pleiotropy, natural selection, and the evolution of senescence. Evolution. 11 : 398-411

Posted by R. Ford Denison at 3:23 PM | Permalink | Comments (2)

Where to publish a paper on the genetics of altruism? In an open-access journal, of course! One day after publishing the fossil primate paper that's creating so much excitement -- it's a great fossil, but too old to tell us anything about our recent ancestors, shared with other apes, or the less-recent ones shared with monkeys -- PLoS One published "The Oxytocin Receptor (OXTR) Contributes to Prosocial Fund Allocations in the Dictator Game and the Social Value Orientations Task", by Salomon Israel and colleagues. Like all papers in open-access journals, the full text is available on-line.

These researchers measured altruism in 200 students, based on how each chose to divide a pool of money with another unknown individual. Their hypothesis, based on various past studies, was that the hormone oxytocin is important for social interactions in general and for human altruism in particular. For example, Zak and colleagues showed that sniffing oxytocin made people offer a more generous split when the recipient had the chance to retaliate for a low offer (the "Ultimatum Game"), although not when there was no chance to retaliate, as in the Dictator Game used in the current study.

The researchers tested for statistically significant relations between and different variants of the oxytocin receptor gene, which codes for the protein that responds to this hormone signal in the brain, and "prosocial responses" (generosity) in the Dictator Game and a more-complex version, the SVO. Interestingly, none of the genetic differences they looked at were in the protein-coding part of the gene (orange). Most were in an intron, which would be transcribed from DNA into messenger RNA but then cut out before the mRNA is translated into protein. So I assume these genetic differences could affect how much oxytocin receptor protein is made where and when, but not the structure of the protein itself.

Continue reading "Oxytocin and the genetics of altruism" »

Posted by R. Ford Denison at 6:00 PM | Permalink | Comments (0)

Which animals kill the most humans? Lions and tigers and bears? Oh no, malaria-transmitting mosquitoes! The risks of using insecticides to kill mosquitoes may be outweighed by the benefits, but those benefits only last until mosquito populations evolve resistance. Careful use (insecticide-treated bed-nets, for example, rather than spraying wetlands) can slow the evolution of resistance, but we haven't yet achieved a goal I recently saw on a bumper sticker, namely, to "Stop Evolution Now!"

Can we do better? A paper published today suggests a new approach. "How to make evolution-proof insecticides for malaria control" was written by Andrew Read and colleagues. It's in the open-access journal, PLoS Biology, so you can read the whole article for details, but here's my summary:

Continue reading "Evolution-Proof?" »

Posted by R. Ford Denison at 5:43 PM | Permalink | Comments (2)

Here are some links to some papers that looked interesting this week. I hope I will have time to write about one of them this weekend.


Market forces affect patterns of polygyny in Uganda

Harmonic Convergence in the Love Songs of the Dengue Vector Mosquito


Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation

A “crown of thorns” is an inducible defense that protects Daphnia against an ancient predator


The feeding biomechanics and dietary ecology of Australopithecus africanus

Isotopic Evidence for an Aerobic Nitrogen Cycle in the Latest Archean


Risk assessment in man and mouse

Duplicate genes increase expression diversity in closely related species and allopolyploids

Posted by R. Ford Denison at 6:47 PM | Permalink | Comments (0)

Last week I discussed one of many papers that use the ratio of protein-changing to "neutral" genetic changes, along the branches of an evolutionary tree, to infer past natural selection. This week's paper presents data calling that approach into question. This does not necessarily undermine the overall conclusions of last week's paper, which were based on a variety of methods, including testing the actual performance of mutant proteins.

"Hotspots of biased nuclear substitutions in human genes" was published in PLoS Biology by Jonas Berglund and colleagues. I am not a molecular biologist, so will just summarize their main points. The paper is open access.

Most of our DNA does not code for proteins. Some of the noncoding DNA is known to have important regulatory functions. But there is lots of DNA whose function, if any, is unknown, but which is nonetheless highly similar among species, as if any change was lethal. Except, when someone tried deleting this DNA, a bit at a time, most of the deletions were not lethal or even (as far as they could tell) harmful. I discussed this work earlier.

Anyway, much of this noncoding DNA that differs little among most species is different in humans. Could these differences be what makes us different from other apes? Quite possibly. But are all these human-vs.-chimp differences important? Maybe not. An unexpectedly high fraction of the changes from the ape ancestor we share with chimps involved a change from A bound to T (a weak bond) to G bound to C (a strong bond). Unless noncoding DNA with stronger bonds is consistently better somehow (and only in humans!), this suggests that these changes are caused by some DNA-specific process and not by natural selection. In other words, these changes occurred whether or not they were beneficial, just as mutations do. Could similar AT=>GC changes have changed protein-coding sections of DNA?

The researchers compared 10,238 genes in humans, chimps, and macaques...

Continue reading "Inferring details of past evolution from DNA is tricky" »

Posted by R. Ford Denison at 5:21 PM | Permalink | Comments (2)

This week's paper uses molecular methods to reveal new details of the evolutionary arms race between primates, including humans, and viruses. "Protein kinase R reveals an evolutionary model for defeating viral mimicry" was published in Nature by Nels Elde and colleagues in Seattle.

Protein kinase R (PKR) is an important defense against viruses in many species, from humans to yeast. When it detects a virus inside a cell, it activates eIF2-alpha, which shuts down protein production in that cell. With protein production blocked, the virus can't replicate and spread to other cells. Viruses, however, have evolved counter-measures. These include molecules that resemble eIF2-alpha. These molecular mimics interact with PKR and prevent its normal defensive activity.

Viral epidemics can be a major cause of death, so we expect populations to evolve PKR resistant to the eIF2-alpha-mimics produced by viruses. Can we find evidence of such evolution in primates?

Continue reading "Staying ahead in the evolutionary arms race with viruses" »

Posted by R. Ford Denison at 5:32 PM | Permalink | Comments (0)

This is the most amazing thing I've seen in awhile. Vaults are abundant in our cells and bigger than ribosomes and apparently I'm not the only biologist who had never heard of them. They seem to be important in defense against bacteria, but nobody understands them in detail yet, apparently.

Posted by R. Ford Denison at 8:19 PM | Permalink | Comments (0)

My NSF grant will run out soon, so I get to spend the year in which we celebrate the 200th anniversary of Darwin's birth and the 150th anniversary of The Origin of Species as an amateur scientist, like Darwin himself. I'm not as smart or as rich as he was, but I do have imaginative and hard-working students and much better equipment.

I'm working on two grant proposals and several papers while dreaming of getting back to writing my book, so no detailed paper analysis this week. But Nature is highlighting 15 major papers on evolution they have published in the last few years.

Posted by R. Ford Denison at 5:11 PM | Permalink | Comments (0)

I usually only discuss papers with original data, but I'm going to make an exception this week.

"Battle of the sexes may set the brain" was published in Nature by Christopher Badcock and Bernard Crespi. It's labeled "Opinion" but it is based on facts as well as theory. Their central hypothesis is that mental illness in humans is often the result of conflicts between genes inherited from the mother and father.

Imagine a gene -- let's call it IGF2, since that's it's name -- that causes a fetus to grow faster, resulting in somewhat higher birth weight. Babies with slightly higher birth weight tend to be healthier, up to a point, but they may endanger the health of the mother, at least a little. So most women shut down the copy of IGF2 in their eggs. Therefore, most babies get an active copy from their father and an inactive copy from their mother. Occasionally, though, the mother's copy is also active in the fetus, resulting in larger-than-normal babies. It turns out that these babies have a higher risk of autism.

Continue reading "Evolution of mental illness" »

Posted by R. Ford Denison at 11:51 PM | Permalink | Comments (1)

I was going to write about this paper about a gene that evolved rapidly in humans since our lineage split from that leading to chimps. But Ed Yong at Not Exactly Rocket Science has already done a great post on it, including a picture showing its likely link to thumbs.

Comments on Ed's blog and a more complete treatment on Carl Zimmer's "The Loom" (both favorites of mine) point out the fallacy of some popular press coverage claiming this is the first evidence that "junk DNA" isn't junk after all. They both make the important point that we've known for decades that some DNA that doesn't code for protein is nonetheless very important.

On the other hand, lots of our DNA really does seem to be junk. Much of it is the product of "jumping genes" that copy themselves and insert themselves into existing DNA. These are common because they copy themselves, not because they do us any good (although, just by chance, they may occasionally be beneficial).

About 5% of DNA that doesn't code for protein is nonetheless "highly conserved", as if it were somehow beneficial and therefore maintained by natural selection. But a paper I reviewed earlier showed that much of this conserved noncoding DNA can be deleted without apparent ill effects. So if it's beneficial, it's not very beneficial. Or maybe it's beneficial only under special circumstances.

Posted by R. Ford Denison at 6:19 PM | Permalink | Comments (0)

Not enough people voted on the Reader’s Choice, so this week’s paper is “Phylogeny and geography predict pathogen community similarity in wild primates and humans�? by Jonathan Davies and Amy Pedersen, published in Proceedings of the Royal Society.

Many humans diseases, from flu to AIDS, come from other species. Similarly, diseases from dogs are an increasing threat to lions, while cat diseases kill sea otters. Are there general rules that predict how likely two species are to share diseases?

To find out, the authors analyzed several large data sets on diseases of humans and 117 other species of primate (apes, monkeys, etc.). They hypothesized that species are more likely to share diseases if they live near each other and/or if they are more closely related, that is if they share a more recent common ancestor. This is similar to how we define relatedness in humans: brothers and sisters have more recent common ancestors (parents) than cousins do (grandparents). Fortunately, the family tree for primates is relatively uncontroversial, at least among scientists.

Continue reading "Sharing diseases with relatives and neighbors" »

Posted by R. Ford Denison at 6:53 PM | Permalink | Comments (0)

"A struggle for existence inevitably follows from the high rate at which all organic beings tend to increase... It is the doctrine of Malthus applied with manifold force to the whole animal and vegetable kingdoms" -- Charles Darwin, Chapter 3, The Origin of Species

Although this paper focuses on Easter Island, it also discusses many of the same societies in Jared Diamond's 2005 book "Collapse." The book includes much that is not in the paper, but the paper has the advantage of being shorter and of supporting specific points with specific citations, in contrast to the diffuse "Further Reading" approach used in Collapse.

Continue reading "Oestrus Island" »

Posted by R. Ford Denison at 10:34 PM | Permalink | Comments (0)

Punishing cheaters selects against cheating, but what selects for punishing? Are the answers different, depending on whether the species involved have brains? A recent internet experiment suggests that altruistic punishment, perhaps unique to humans, doesn't promote cooperation as effectively as previously thought.

My own research focuses on cooperation in species without brains. We showed that “sanctions�? imposed by legume plants limit the evolution of “cheating�? rhizobium bacteria (those that divert more plant resources to their own reproduction, relative to other rhizobia, by investing less in fixing the nitrogen needed by the plant). We think individual plants help themselves by imposing sanctions that limit wasteful resource use by less-beneficial rhizobia – they don’t do it for the benefit other legumes.

In theory “altruistic punishment�? (paying some cost or taking some risk to punish noncooperators) could help explain why there is more cooperation among unrelated humans than might otherwise be expected. (Cooperation among relatives is explained by kin selection.) But how much are individuals willing to pay to punish noncooperators?
The latest experiments attempting to answer this question were just published on-line in Proceedings of the Royal Society, by Martijn Egas and Arno Riedl: The economics of altruistic punishment and the maintenance of cooperation.

Continue reading "Altruistic punishment? Maybe not." »

Posted by R. Ford Denison at 11:46 PM | Permalink | Comments (0)

There are enough examples of ‘‘cheating’’ in bacteria ... that mindless obedience to such [quorum-sensing] chemical signals cannot be assumed. Mindlessness can be assumed, but not obedience. -- Denison et al. (2003) Ecology 84:838-845

Quorum sensing, an exchange of chemical signals among bacteria, can solve the coordination problem. But this week's paper Cooperation and conflict in quorum-sensing bacterial populations shows that quorum sensing doesn't automatically solve the problem of cheaters. The paper is by Stephen Diggle, Ashleigh Griffin, Genevieve Campbell, and Stuart West and published in Nature.

Continue reading "Communication doesn't automatically prevent cheating" »

Posted by R. Ford Denison at 11:08 PM | Permalink | Comments (0)

Ed Yong beat me again, this time discussing an interesting paper in Nature on the evolution of language, but I'm going to comment anyway. Actually, there are two papers in the same issue, both showing that frequently used words change more slowly. For example, irregular past tenses of rarely-used verbs (bide, delve, etc.) have tended to disappear, but we still say "came and saw" not "goed and seed." Lieberman et al. (Nature 449:713) note that:

It is much rarer for regular verbs to become irregular: for every ‘sneak’ that ‘snuck’ in there are many more ‘flews’ that ‘flied’ out.

Languages evolve, but analogies with evolution of genes may be misleading. Genes pass only from parent(s) to offspring and their frequency changes over generations. Words and ideas can spread much more rapidly, including from child to parent. Cultural evolution seems more analogous to the spread of viruses, only some of which come from our parents.

Some ideas (e.g., religions) come packaged with explicit instructions to proselytize, like the rabies virus making its victims bite others. But the desire to spread our tastes in music, for example, seems intrinsic to us, not to the music. So cultural evolution seems similar enough to epidemiology that analogies will sometimes be useful, but only sometimes.

Posted by R. Ford Denison at 6:11 PM | Permalink | Comments (0)

Why do women, in contrast to our closest relatives, stop giving birth while they are still relatively young and healthy? This week's paper. "Testing Evolutionary Theories of Menopause", by Daryl Shanley and coauthors, published in Proceedings of the Royal Society, uses data from people living in The Gambia to test two different hypotheses.

Continue reading "Menopause trade-offs" »

Posted by R. Ford Denison at 7:12 PM | Permalink | Comments (2)

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Posted by R. Ford Denison at 4:14 PM | Permalink | Comments (3)

Usually, those alleles (versions of a gene) that become more common over generations are those that are most beneficial to the organisms in whose cells they live. But not always.

The latest issue of PLoS Biology has an open-access article on a particularly selfish gene responsible for Apert syndrome in humans.

Continue reading "Selfish sperm cells" »

Posted by R. Ford Denison at 5:13 PM | Permalink | Comments (0)

This week's paper, published in Science (317:679) is "Immune-like phagocyte activity in the social amoeba" by Guokai Chen, Olga Zhuchenko, and Adam Kuspa of the Baylor College of Medicine.

Cells of the social amoeba, Dictyostyleium discoideum forage individually, but eventually group together into a "slug", which crawls through the soil for days before eventually forming a spore-tipped stalk. Previous work with this species has looked at conflicts of interest over which cells have to sacrifice future reproduction (as spores) and become part of the stalk. This week's paper uncovers another example of apparent altruism in Dictyostelium, which may shed light on the evolution of a key part of our immune system.

As a Dictyostelium slug crawls through the soil, some cells are left behind. Are these just random sluggards? Or do they function like human phagocytes, the immune system cells that gobble up bacteria?

Continue reading "Left behind: social amoebae" »

Posted by R. Ford Denison at 6:25 PM | Permalink | Comments (5)

This week's paper is "Palaeogenetic evidence supports a dual model of Neolithic spreading into Europe" by M.L. Sampietro and others, published online in Proceedings of the Royal Society. The paper is interesting both for its findings and for its methods.

We know that agriculture spread from the Near East -- do people in Asia call this the Near West? -- to western Europe, starting around 10,000 years ago. But did this mostly involve farmers moving, or the spread of agriculture without major movement of people?

People have tried to figure out past population movements using genetic differences among modern populations, but it would help to have genetic information from people who lived thousands of years ago, as well. This is technically challenging, however...

Continue reading "Tracing the spread of agriculture with stone-age human DNA" »

Posted by R. Ford Denison at 4:51 PM | Permalink | Comments (0)

I have written about evolutionary trade-offs before, starting with early posts about trade-offs between seed size and seed number in plants, and trade-offs between the ability of insects to escape predators by flying away, versus the ability to hide from them by playing dead. I have also given some examples of the increasing use of sophisticated experimental (often molecular) methods in evolutionary biology. This week's paper combines both themes.

The paper is "Restriction of an extinct retrovirus by the human TRIM5-alpha antiviral protein" by Shari Kaiser, Harmit Malik, and Michael Emerman, published in Science (vol.316 p.1756).

Retroviruses are made of RNA, but make DNA copies of themselves that can insert into the DNA of host cells they infect. HIV, the cause of AIDS, is a well-known example, but there are many others. If DNA copies of the retrovirus are inserted into cells giving rise to sperm or eggs, they can be passed to the next generation, as endogenous retroviruses. If the DNA inserts somewhere where it turns an important gene on or off, it may kill the host. Or, once in a while, this change may turn out to be beneficial. The few beneficial changes are the ones that survive and spread, just as the few mutations that are beneficial are the ones that persist.

VWXYNot has an interesting discussion of how a creationist web site misused one of her papers as evidence of "intelligent design." She shows how shared endoviruses can be used to infer shared ancestry, providing yet more evidence that we share a recent ancestor with apes, less-recent ancestors with monkeys, etc. But that's not what this week's paper is about....

Continue reading "Trade-offs in defense against retroviruses" »

Posted by R. Ford Denison at 8:28 PM | Permalink | Comments (4)

What did our early ancestors and related species eat? Different data seemed to give different answers. This week’s paper may have helped to solve this mystery.

Isotope data suggest that tropical grasses were a big part of the diet of the hominins Australopithecus africanus and Paranthropus robustus. These grasses have CO2-concentrating C4 photosynthesis. As a result, they have a little more of the rare carbon-13 isotope, and a little less C12, relative to most other plants. So do the fossil teeth of these early human relatives, as if they ate these grasses. But the shape of their teeth, and wear patterns, are wrong if they mostly ate grass leaves or animals that ate grass. What about roots, or underground storage organs? These are an important food for some human foragers today, especially in dry climates. If our early relatives mostly ate these “USOs�?, then the isotope ratios in their teeth should be like those of other species with a similar diet. Mole rats, for example.

Continue reading "Roots" »

Posted by R. Ford Denison at 5:48 PM | Permalink | Comments (0)

Last week, I was at a meeting in the Netherlands on “Darwinian agriculture: the evolutionary ecology of agricultural symbiosis.�? Topics included: the effects of cows on human evolution, the independent invention of “agriculture�? by ants and termites, and some disadvantages of diversity. As promised, here are a few highlights.

Continue reading "Darwinian agriculture II" »

Posted by R. Ford Denison at 6:15 PM | Permalink | Comments (5)

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?

Continue reading "Evolution of color vision: transgenic mice see red" »

Posted by R. Ford Denison at 4:15 AM | Permalink | Comments (8)