This Week in Evolution

"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 (0)

I will be visiting in-laws in Hawaii and then at the International Congress on Nitrogen Fixation, so may not post again until late June.

Maybe by then I will be able to write something about our recently accepted paper on the evolution of aging.

Or maybe I'll have good news about an NSF grant. One grad student has a little money left in his own small grant, but the other two are also doing interesting and important work and need to pay for supplies, flow cytometer use, etc.

Posted by R. Ford Denison at 6:32 PM | Permalink | Comments (0)

Bacteria known as pseudomonads produce and release chemicals (defensive toxins) that protect plants from fungi that would otherwise attack their roots. In return, the roots release various organic compounds that serve as food for the bacteria.

The "in return" part has always bothered me. Each root system is associated with millions of bacteria. In a 2003 paper (Cooperation in the rhizosphere and the "free rider" problem. Ecology 84, 838-845), we pointed out that this system is a potential tragedy of the commons. Mutant bacteria that don't make root-protecting chemicals free up resources for their own reproduction, so we might expect them to out-compete more-beneficial strains. If these "cheaters" become common enough, the host plant might be killed by fungi, but that would hurt the beneficial strains around that root system just as much as it hurt the cheaters. We suggested that the bacteria make these toxic chemicals to protect themselves, with protection of roots as a side effect. Research by others, including some of the authors of this week's paper, has provided data consistent with this hypothesis. For example, toxins made by pseudomonads protect them from predators.

More recently (in Annual Review of Ecology, Evolution, and Systematics), Toby Kiers and I suggested that cooperation between microbes and plants is better understood as cooperation among microbes. For example, by providing their host plant with the nitrogen it needs to grow, rhizobia (root-nodule bacteria) help all the other rhizobia infecting the same plant.

This week's paper shows that defensive toxin production by pseudomonads is similar. Toxin production by pseudomonads may benefit the plant and may benefit individual cells, but it also benefits other pseudomonads nearby. "Predators promote defence of rhizosphere bacterial populations by selective feeding on non-toxic cheaters" was published in The ISME Journal by Alexandre Jousset and colleagues in Germany and Switzerland. These pseudomonads produce various toxins, especially when there are many of them in close proximity. This dependence of toxin production on bacterial density is an example of quorum sensing. Mutants "defective" in quorum sensing have been shown to grow (i.e., reproduce by dividing) faster, because they save the cost of toxin production. Can these "cheaters" free-load on defensive toxin producers nearby, essentially hiding behind their chemical defenses?

Continue reading "Whom do cheating bacteria cheat: host plants or other bacteria?" »

Posted by R. Ford Denison at 1:09 AM | Permalink | Comments (0)

My wife bought me a Livescribe Smartpen for my birthday. It's an amazing device, but I can't recommend it at this point. First, the positive: as advertised, it records handwritten text (using special notebooks), displays the text on a computer, and recognizes hand-printed text well enough to search through stored pages for keywords. It can also record sound. It doesn't work with Windows 2000, so I switched to Windows XP, something I haven't had to do for any other program. But I thought my planned uses justified the switch:

1) lab notebooks. I often need to refer to something I wrote months or years ago. With Livescribe, it should be possible to find it quickly.
2) taking notes in seminars. The audio recording is good enough I can can just write keywords and make sketches of graphs, knowing that I can refer back to the audio for details I didn't get written down.

But, after only a few days of use, the program suddenly informed me that it was:

"Unable to access your database folders. Please contact customer support."

Apparently other people have had the same problem.

Update: I got a reasonably prompt generic ("what operating systems are you using?", etc.) response but no actual help so far. I was able to install on a different computer, but worry that the same problem could arise there at some random time in the future, meaning I would lose any files that weren't still on my pen.

Update2: After a few days, "customer service" sent me another generic request for information. Maybe they figure repeatedly asking for more information and just hoping users will solve the problem themselves can be outsourced, whereas they would have to hire someone competent to actually figure out what was wrong. The reason I suspect this is that they didn't seem to do anything with the information they asked for the first time, and they didn't answer a very specific question I asked when I sent them the first bunch of information they asked for, namely, whether it might help to copy the (hidden) MyLivescribe directory from another computer where I'd gotten it to work. Anyway, I went ahead and tried it and that seems to have fixed the problem. So I guess backing up the MyLivescribe directory periodically would be a good idea. There's apparently some way to back stuff up on the company web site, but what happens to the data when the company goes out of business?

I agree with comments on their website: until there's a way to send Livescribe files to colleagues without going through the Livescribe website, they will lose millions of potential customers. For example, this system would be great for notebooks used to document patentable inventions, but nobody working on a patentable invention is going to trust their notes to an outside company.

Posted by R. Ford Denison at 8:28 PM | Permalink | Comments (3)

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)

I once heard PZ reply to this popular creationist question by pointing out that, although many Minnesotans are descended from Norwegians, there are still Norwegians. This isn't really a good analogy, however, because Minnesotans and Norwegians aren't separate species. We know this because they can interbreed, producing healthy children. At the end of this post I suggest a better answer, indirectly inspired by this week's paper.

Two of evolutionary biology's central questions are: how do species change over generations? and how does one species split into two? We have many detailed examples of small evolutionary changes occurring over days (in bacteria) or years (in animals and plants), so one would have to be very close-minded to deny major evolutionary change over millions of years. But major evolutionary change is not enough, by itself, to split one species into two. One subpopulation within a species must change, while the rest of the species either stays the same or changes in different ways. This divergence cannot happen if the two subpopulations continue to interbreed at high rates. In other words, speciation requires some reproductive isolation.

Often, reproductive isolation is a byproduct of geography. After a few individuals (or a pregnant female) cross a mountain range or are blown from the mainland to an island, they no longer interbreed with their ancestral population. Over many generations, random genetic drift or nonrandom natural selection can change the isolated population enough that they can no longer produce healthy offspring with the original population, even if they come back into contact.

Sometimes speciation can occur without a major geographic barrier, but reproductive isolation is still required. This week's paper shows that this has happened and is still happening in Europe.

"A continuum of genetic divergence from sympatric host races to species in the pea aphid complex", by Jean Peccoud and others, was just published online in the Proceedings of the National Academy of Science.

Photo by Jean Peccoud

Continue reading ""If evolution is true, why are there still chimps?"" »

Posted by R. Ford Denison at 10:45 PM | Permalink | Comments (8)

This week I will discuss two papers, both dealing with plants and competition, in the context of genetic relatedness that might be expected to moderate competition:
"Growing with siblings: a common ground for cooperation or for fiercer competition among plants?" by Ruben Milla and colleagues (Proceedings of the Royal Society), and
"Do plant parts compete for resources? An evolutionary viewpoint" by Victor Sadras and me (New Phytologist).

Earlier I discussed a paper by Susan Dudley and Amanda File showing that some plants grow less root when interacting with related than with unrelated neighbors. Spending less resources on roots could have freed resources for more seed production, but they didn't measure that. Now Milla and colleagues have.

Continue reading "Sibling rivalry in plants" »

Posted by R. Ford Denison at 8:10 PM | Permalink | Comments (0)

Mark Taylor, a professor of religion, has observed (in the New York Times) that

"graduate programs in American universities produce a product for which there is no market (candidates for teaching positions that do not exist)…[with] sometimes well over $100,000 in student loans."

But programs in the sciences do collectively graduate more PhD's than they hire, so a PhD is no guarantee of a faculty position. I have discussed this before.

Taylor's proposed solutions? Several ideas whose effects on the stated problem are hard to predict but probably small (restructuring curriculum, abolishing departments, accepting video games and such as substitutes for traditional written dissertations), one that would make the job shortage worse but might have other benefits (eliminating programs and substituting internet courses), and two that might help new PhD's find jobs (preparing students for nonacademic careers and abolishing tenure). Preparing students for nonacademic careers is something that has been discussed for years and Taylor doesn't offer any new ideas on how to do this. But what about abolishing tenure?

Continue reading "Abolish tenure?" »

Posted by R. Ford Denison at 6:24 PM | Permalink | Comments (5)

Suppose, in an average year, that weather is best for survival of young seedlings in early June. If a plant could make only one seed, it should make one targeted to germinate at the beginning of June. (Plants have some control over when their seeds will germinate, based on plant-hormone concentrations, seed-coat thickness, etc.)

Given variability among years, however, a plant that produces many seeds may have more descendants if those seeds germinate at various times, rather than risking everything on one date. On the other hand, too much variation in germination time may be as risky as too little. For example, seeds germinating really late may be killed by frost. How does actual variation in germination timing among seeds of individual wild plants compare with the optimum amount of variation? This week's paper is apparently the first to answer this question.

"Fluctuating natural selection accounts for the evolution of diversification bet-hedging" was published in Proceedings of the Royal Society by Andrew Simons, of Carleton University in Canada.

Continue reading "Optimal bet-hedging?" »

Posted by R. Ford Denison at 10:14 PM | Permalink | Comments (0)

This week I'll discuss a recent paper from our lab. But first, here are links to three other papers that look interesting:

Evidence from the domestication of apple for the maintenance of autumn colours by coevolution Some insect pests avoid trees whose leaves turn red in autumn and do poorly on those trees, but can trees "lie" or is there an unbreakable link between red color and poor quality as a host, perhaps because "aphids grow better on trees that drop their leaves later [because they have enough nitrogen they can risk losing high-N leaves in frost?], which are known to have fewer autumn colours [because, by the time they lose chlorophyll, UV levels are too low to require the protection provided by red anthocyanins?]."?

Functional morphology of the ankle and the likelihood of climbing in early hominins Modern chimps use their ankles, when climbing trees, in ways some early hominins (1-4 million years ago) probably couldn't, based on fossils.

Cooperation and virulence of clinical Pseudomonas aeruginosa populations
Patients with pneumonia are sicker when bacterial cells cooperate by producing individually costly virulence factors, but bacterial populations evolved "cheaters" that don't make these factors within 9 days.

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In our paper, "Rhizobitoxine producers gain more poly-3-hydroxybutyrate in symbiosis than do competing rhizobia, but reduce plant growth", published online in The ISME Journal, my PhD student Will Ratcliff describes experiments showing how symbiotic nitrogen-fixing bacteria can manipulate their plant hosts.

Continue reading "Mindless manipulation" »

Posted by R. Ford Denison at 7:53 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)

Experimental populations of hermaphroditic plants evolved a significant increase in male function in only three generations.

Many plant species are hermaphrodites, with each individual producing both pollen and seeds. Others species have separate sexes, as mammals and birds do, while still others have mixtures of unisexuals and hermaphrodites. Based on the distribution of these traits in the family tree of life, evolutionary transitions among these "lifestyles" appear to have been fairly common. This week's paper shows how hermaphrodites can evolve to be more female or, in this case, more male. Hermaphroditic Sex Allocation Evolves When Mating Opportunities Change was just published in Current Biology by Marcel Dorken and John Pannell.

Continue reading "How fast can sexual traits evolve?" »

Posted by R. Ford Denison at 3:24 AM | Permalink | Comments (0)

“But if you believe that primates and guinea pigs [both of which have mutated, nonfunctional versions of a gene for making vitamin-C] were specially created, these facts don’t make sense. Why would a creator put a pathway for making vitamin C in all these species and then inactivate it? Wouldn’t it be easier simply to omit the pathway from the beginning? Why would the same inactivating mutation be present in all primates, and a different one in guinea pigs? Why would the sequences of the dead gene exactly mirror the pattern of resemblance predicted from the known ancestry of these species? And why do humans have thousands of pseudogenes [DNA sequences very similar to genes that are functional in other species, but with mutations that make them inactive] in the first place?” – Jerry Coyne, Why Evolution is True

I have been reading and enjoying “Why evolution is true”, by Jerry Coyne. Here are some thoughts on what I’ve read so far.

Continue reading "Facts and theory in Coyne’s “Why evolution is true”" »

Posted by R. Ford Denison at 9:04 PM | Permalink | Comments (1)

With a species using cryptic resemblance [camouflage] for its protection, the very existence of neighbours involves a danger to the individual, since the discovery of one by a predator will be a step in teaching it to recognize the crypsis. With an aposematic [bad-tasting, warning-coloration] species, on the other hand, the existence of neighbours is an asset, since they may well serve to teach an inexperienced predator the warning pattern. -- William Hamilton, 1964

Continue reading "No butterflies were harmed by this research" »

Posted by R. Ford Denison at 10:36 PM | Permalink | Comments (0)

...according to the New York Times. Although private ownership is one way to prevent degradation of the commons, this is going too far, in my opinion.

Posted by R. Ford Denison at 7:53 PM | Permalink | Comments (1)