To those who are new to my web log, thanks for checking it out. To those who have come from my old site, thanks for clicking through.
This week, while a sickly laptop robbed me of the opportunity to blog, a steady stream of interesting papers were published. Three struck me as particularly fascinating, because they illustrate the different ways evolutionary changes alter our world.
1. Scourges in waiting
When SARS failed to take hold in the United States, it was easy to feel smug about our defences against new epidemics. The nasty influenza strain now spreading across the United States should puncture that arrogance. We face outbreaks the same way people faced hurricanes in the 1800s–they sweep over us without warning, and we are pretty bad at predicting what will come next. What we need is a kind of evolutionary forecasting, in order to know how to head off the next disaster. Humans got HIV from chimpanzees, for example, but there are dozens of related viruses lurking in chimps and monkeys that might–or might not–also make the leap. Of all the pathogens that seem harmless at the moment, which one will become a killer?
Understanding the evolutionary fortunes of diseases is not easy. Earlier this year I wrote a piece in Science about the debate going on these days over exactly what combination of forces can make a disease deadly or harmless. This week in Nature, a group of scientists reported some important discoveries about what it takes to be a major killer. The work is disturbing, because it suggests that even a pathogen that doesn’t seem capable of much harm could swiftly evolve into an epidemic.
A disease is in a continual state of birth and death–the pathogen infects new hosts where it can reproduce and spread to other hosts; meanwhile sick people either get better or die. Epidemiologists get most worried about diseases where the rate of new infections outpaces the end of old ones. They reason that a disease where the opposite is the case will either die out or just cling to a bare existence. A mathematical model of diseases suggests otherwise. It seems that if a pokey pathogen has even a slight rise in its rate of new infections, there’s an opportunity for rapid evolution. A few lineages of the pathogens will have the opportunity to infect a chain of people, and that will offer the chance for it to evolve into a fast-spreading strain.
The researchers propose a way to test low-level diseases to see whether they are at or near this dangerous level. And they also point out that their results mean that some diseases that haven’t caused all that much concern may be poised to strike. A couple generations ago, many more people were protected from smallpox by vaccines than they are today. That vaccine also protected them from other viruses that are still pretty much limited to other animals, particularly monkey pox. Today monkeypox is not spreading fast, but the slow decline of immunization to smallpox may nudge monkeypox up into the breakout zone.
2. Shrinking Trophies
The same issue of Nature also included a report of some unintended evolution brought about by mountain-sheep hunters in Canada. For decades at Ram Mountain in Alberta, the hunters have shot the biggest rams with the biggest horns. There were two reasons for this pattern–hunters want a good trophy for their efforts, and wildlife managers believed they were conserving the population by allowing younger rams to survive and have lambs of their own before getting shot. But the researchers found that the hunters have altered the gene pool in the process. Genes that help produce big horns and big bodies are vanishing from the population. Meanwhile, rams that produce smaller horns and grow to smaller sizes were favored. The horns have shrunk 25 percent as a result.
The title of the paper is “Undesirable evolutionary consequences of trophy hunting” and Living Code’s Richard Gayle rightly asks what exactly is so undesirable about the change if you’re not a hunter. But this burst of evolution may have some other side-effects that could threaten the well-being of the ram population. Horns are an example of the many kinds advertisements that males use to attract females. Roosters have combs, peacocks have tails, crickets have chirps. While television ads may not be particularly honest, these biological ads often reflect the quality of a male’s genes. Good genes can confer bigger size or a stronger resistance to diseases to offspring–things a female prefers in a mate. As hunters shift the balance of the ram population to males with smaller horns, they may also be shifting it to smaller, more disease-prone lambs that are less likely to live long enough to have offspring. The entire population may become maladapted to the tough habitat of the Canadian Rockies.
Rams are not the only animals whose evolution we’re altering even as we try to manage them wisely. Earlier this year in Science, I wrote another article about how fishing has driven the evolution of smaller fish. If we want to conserve these animals, we have to take into account the way we can change the rules of natural selection.
3. Chimp genomes and human nature
Evolution can produce quick changes in a few years, but with a few million years it can produce far more complex changes. One example of this emerged this week inScience , which published some of the early fruits of the ongoing chimpanzee genome project. Researchers were able to pinpoint 1547 human genes that appear to have undergone intense natural selection since our ancestors diverged from other apes.
I described the approach behind this kind of research in an essay that appeared in Natural History last December. In the new research, scientists were able to scan the entire chimp genome for genes that they could find good counterparts in both the human and mouse genomes–a little less than 8000 all told. By tallying up the differences between the different copies, they could pick up signs of natural selection.
The fast-evolving genes were a grab bag. Some are linked with hearing, which may suggest that our ability to listen to language coevolved with our ability to speak. Weirdly, some genes that build olfactory receptors in the nose were evolving fast, too. It’s weird because over half of these receptor genes are broken in humans, a reflection of our shift away from relying on smell. It’s possible that a preference for certain sexy odors in the opposite sex drove the evolution of certain receptors.
Like most early work in genomics, this paper’s net is cast wide but shallow. These genes do not tell us what made us uniquely human; they really just lay out thousands of new research projects to figure out what they do. At the same time, the signal of natural selection will become much clearer when scientists finish some more genome projects, like that of a monkey or a gorilla and can throw them into the comparison.
And it’s likely that the proteins these new genes make are only part of the story of human origins. It’s not just what your genome makes, but when and where, that makes a difference. Some preliminary work is showing that many genes that chimps and humans share are made at high rates in the human brain. They may help us fire more neurons without damaging our brains.
We live in remarkable times, when the inner workings of our closest living relatives are being unveiled and giving us insights into our own history. Unfortunately, in 20 years, this information may all that’s left of chimpanzees. As they are hunted and their forests are logged, they will fade like a genomic Cheshire Cat, leaving behind a string of As, Ts, Cs, and Gs in databases around the world.
(Update, December 15, 10:30 pm: Thanks to Richard Gayle for further insights on the rams.)