I just read a disturbing post on the amusingly-titled serious-science blog "Mystery Rays from Outer Space", discussing two examples of human pathogens that apparently escaped from laboratories. The key evidence, in each case, is evolution... or rather, lack of evolution....
Ants that grow fungi for food have to control other fungi that attack their gardens, but what about fungi that attack the ants themselves? Two papers published recently reveal surprising sophistication in both ants and fungi.
Sandra Anderson and colleagues discuss "The life of a dead ant: the expression of an adaptive extended phenotype" in American Naturalist. Richard Dawkins coined the term "extended phenotype" to refer to a consistent effect of a gene inside an individual on something outside that individual. For example, it might be possible to link differences in the shape of webs made by different spiders to genetic differences among those spiders. This week's paper shows that ants infected by certain fungi show complex behavior that benefits the fungi. Ants infected by fungi with different genes would probably not show this behavior, but the genes involved have not yet been identified.
Before the fungus-infected ants die, they attach themselves (by biting) to the underside of leaves that are ideally located for fungal reproduction: on the cooler and moister north side of trees, near (but not on) the ground. The researchers showed that these locations were favorable for fungal reproduction by moving infected ants higher in the canopy or down to the ground. Ants on the ground mostly disappeared, but fungi grew abnormally in those that remained. Fungi were unable to compete their life-cycle on ants moved higher in the canopy.
I can imagine a fungus producing an ant hormone (or perhaps destroying a particular neuron) to make its ant host bite a leaf, but getting ants to bite leaves in a particular humidity and temperature range and then hold on until dying seems pretty sophisticated. It would be easier if the ants spent most of their time in that zone anyway, but the one ant colony they found was much higher, about 15 meters.
The second paper shows greater sophistication on the part of the ants. "Adaptive social immunity in leaf-cutting ants" was published by Tom Walker and William Hughes in Biology Letters. The paper is freely available on-line.
These social ants protect each other from fungal infection by grooming each other, much like meerkats or baboons. Ants exposed to the fungus got groomed about twice as long as ants exposed to a control solution without the fungus, or about three times as long if their nest had been exposed to the same fungus two days before. (Another example of learning in insects.) Ants placed in nests that were previously exposed to the fungus were twice as likely to survive for two weeks after they were inoculated.
Just as I was starting to dip into retirement savings to keep my lab going, we got word that both of the grant proposals we sent to the NSF in the latest round were funded, one of them with money from Obama's stimulus funding. We won't be paying ourselves any billion-dollar bonuses, but I may be able to get two months salary this year after all. Both proposals are resubmissions, significantly improved based on suggestions and criticisms from past reviewers. Both projects will use rhizobia, bacteria best known for providing legume plants with nitrogen, but the second project may have eventual applications in medicine (e.g., curing persistent infections) rather than agriculture. The summaries below are intended for a nonscientific audience, such as members of Congress.
"Suppression of rhizobial reproduction by legumes:
implications for mutualism"
(with Prof. Michael Sadowsky, largely based on ideas and preliminary results from grad student Ryoko Oono -- see this recent review article we wrote with Toby Kiers)
Rhizobia are bacteria that can live in soil, but also symbiotically, inside root nodules on plants like soybean or alfalfa. Although many rhizobia provide their host plants with nitrogen, saving farmers billions in fertilizer costs, less beneficial strains cause problems in some areas. Some hosts, including alfalfa and pea, make rhizobia swell up as they start to provide nitrogen. Unlike the nonswollen rhizobia from soybean or cowpea nodules, swollen rhizobia apparently lose the ability to reproduce, but does rhizobial swelling somehow benefit the plant?
To find out, the investigators will map this trait on the family tree for crops and wild plants that host rhizobia, to see if causing swelling evolved more than once, suggesting a positive benefit to the plants. Three dual-host rhizobia (plus mutants that differ in their ability to hoard resources) will be used to measure effects of rhizobial swelling on costs and benefits to the plants. Plant defenses against rhizobia that provide little or no nitrogen, already demonstrated in soybean, will be tested in species that impose bacterial swelling.
This research will increase understanding of a symbiosis that supplies nitrogen to agricultural and natural ecosystems, with implications for other important symbioses. Results could guide the development of crops that selectively enrich soils with the best rhizobia, decreasing future fertilizer requirements. Educational opportunities will be provided for undergraduates, at least one graduate student, and a postdoctoral researcher. Two female high school students have already won trips to the International Science Fair for research done in the principal investigator's laboratory, where such mentoring will continue to be a priority.
Evolution of persistence in the model bacterium, Sinorhizobium
(with Prof. Michael Travisano, largely based on ideas, preliminary data, and writing by grad student Will Ratcliff, with some ideas from Andy Gardner and colleagues -- see the second paper discussed in this post -- and possible relevance to our work on evolution of aging.)
Some bacteria can enter a nongrowing "persister" state that allows them to survive antibiotics and other treatments that normally kill them. By suspending growth, they may also free resources for their genetically identical clonemates.
Most species form only a few persisters. This makes persisters hard to study, despite their importance in long-term infections. However, certain harmless bacteria from plant roots can form up to 40% persisters. These will be used to determine whether persisters benefit mainly from enhanced stress resistance or by increasing the growth of their clonemates.
Successful completion of this research will provide two main benefits: First, this research will determine the conditions that favor the spread of persister-forming bacterial strains over nonpersister strains, and the genetic basis of persistence. This can provide direct medical benefits by aiding the development of novel management strategies, drug targets, and eventually treatments for patients infected with persister-forming bacteria. Second, some conclusions may apply to other species that are difficult to eradicate because they, too, form dormant, stress-resistant stages. These include many agricultural weeds and some species of mosquito. One key advantage of the proposed approach is speed: experiments that would take decades with weeds or mosquitoes can be conducted in months with bacteria. This research will provide training opportunities and jobs for undergraduates, high school students, and a post doctoral researcher.
I am planning to accept another grad student for autumn 2010.
"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?
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:
If being infected is bad, is being infected by two different pathogens at once even worse? Not necessarily, as this week's paper shows. "Quorum sensing and the social evolution of bacterial virulence" was published in Current Biology by Kendra Rumbaugh and colleagues. Their results contradict an earlier prediction, although not the fundamental evolutionary principle behind that prediction.
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" »
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.
About 1500 scientists attended Evolution 2008 here last week. The four-day meeting was filled with 15-minute talks (usually ten at once, in different rooms), plus two evening poster sessions (like a science fair, for grownups, with discussions rather than judging), scenically located on a pedestrian bridge over the Mississippi. Reports that “scientists are abandoning evolution�? appear to be exaggerated.
Here are summaries of some of the talks I enjoyed.
Continue reading "Evolution 2008: sexy plants, battling bacteria, durable cooperation" »
(Top) A small leafcutter worker atop a leaf guards her sister against attacks by parasitic flies. Ants carrying leaves cannot use their mandibles for defense, so they carry hitchhikers to ward off the parasites. (Bottom) The fungus garden in a nest of Atta leaf-cutter ants. Notice the diversity of ant sizes within a colony, from the large red soldier ants to the minute orange ants tending to the garden. Atta ants have some of the most sophisticated caste systems among the social insects. -- photos and captions from Alex Wild (mymercos.net)
I’ve never done research on the fungal “farms" of ants and termites, but I’ve been interested in them every since a camera company bought a close-up photo (not Photoshopped like this one) of an ant carrying a leaf along a barbed wire “bridge" on its way back to its nest, from my mycologist father, William Denison. Dad was best known for pioneering research in the tops of tall trees, but never had to fight a shaman, as far as I know.
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" »
Summary: A 39-year record of host-parasite interaction, recovered from sediment layers in a pond, is consistent with rapid coevolution.
Link: Host-parasite /`Red Queen/' dynamics archived in pond sediment
As I've discussed previously, archival samples often prove useful for answering questions that weren't being asked when the samples were collected. But what if nobody collected and preserved the samples you need for your research? Maybe you can find a "natural archive" that has what you need.
Continue reading "The ghost of infections past, present, and future" »
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?
This week's paper is "HIV-1 proviral DNA excision using an evolved recombinase" by Indrani Sarkar and others, published in Science (vol.316, p.1912). This paper is yet another example showing that selection (natural or artificial) can outperform design.
To illustrate the point, let me start with a well-known example from plant breeding. Suppose you wanted to make broccoli, starting with its ancestor, wild kale? You could cross them, identify which genetic differences are most responsible for the large edible inflorescence, and transfer those genes to the wild kale. But what if broccoli didn't exist?
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.
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.
Continue reading "Less-vicious viruses evolve in viscous cannibal populations" »