By John Timmer 
His election to the Academy gives him the right to publish a paper of his choosing, and he chose a good topic. The bacteria are growth-constrained by low levels of glucose, and most lines have evolved so that they burn through the glucose as quickly as possible, then wait for the next daily infusion. About 33,000 generations in, however, one line of bacteria did something else entirely: it began to digest the large amounts of citrate present in the media. This is more startling than it sounds, as E. coli is sometimes defined by its inability to metabolize citrate.
A quick look into the frozen stocks revealed the citrate-eaters first appeared at about 31,000 generations. They began to grow at the expense of their normal cousins, but then dropped again as the sucrose-eaters adapted a bit. By 33,000 generations, however, a further adaptation sent the citrate-eaters on the road to dominance.
The figure of 31,000 generations suggested something complex was going on, as by that time, every single base in the E. coli genome should have, on average, undergone mutation several times. The bacteria farmers tested two possibilities: either a single mutation that was very rare, or a set of mutations that accumulated over the history of the culture, enabling further adaptation. They tested this by selecting for citrate-eaters from cultures derived from many points in the line’s history. It turns out that their tests never produced a citrate eater from anything frozen before 20,000 generations had passed. They remained extremely rare until the 27,000 generation point, after which they were only rare.
To the authors, this suggested that the history of the strain was key; a mutation that was silent for tens of thousands of generations was necessary for citrate utilization to evolve through later mutations. This, they argue, supports a role for historical contingency in evolution, so that if life were run as an experiment twice, it wouldn’t produce the same results. In this case, the researchers identified three distinct mutations: the enabler at around 27,000 generations, the initial citrate adaptation at 31,000, and then a further adaptation that lets the E. coli rapidly activate citrate metabolism.
What are these mutations? The researchers plan on sequencing the entire genome of the bacteria, pre- and post-citrate adaptation, in order to find out. Meanwhile, the evolution study has become a matter of population genetics. The sucrose-eaters are still around, struggling along at one percent of the population. It’s possible that the competition will spur some further adaptation.
PNAS, 2008. DOI: 10.1073/pnas.0803151105
A new study finds that a change in a single gene has sent two closely related bird populations on their way to becoming two distinct species. The study, published in the August issue of the American Naturalist, is one of only a few to investigate the specific genetic changes that drive two populations toward speciation.
Speciation, the process by which different populations of the same species split into separate species, is central to evolution. But it’s notoriously hard to observe in action. This study, led by biologist J. Albert Uy of Syracuse University, captures two populations of monarch flycatcher birds just as they arrive at that evolutionary crossroads.
Monarch flycatchers are small, insect-eating birds common in the Solomon Islands, east of Papua New Guinea. Uy and his team looked at two flycatcher populations: one found mostly on the large island of Makira, the other on smaller surrounding islands. Besides where they live, the only discernable difference between the two populations is the color of their feathers. The birds on Makira have all black feathers. Birds on the smaller islands have the same black feathers, but with a chestnut-colored belly.
The question of whether these two populations are on the road to speciation comes down to sex. When two populations stop exchanging genes-that is, stop mating with each other-then they can be considered distinct species. Uy and his team wanted to see if these flycatchers were heading in that direction.
It would be all but impossible to try to catalog every occasion on which an all-black flycatcher mated with a chestnut-bellied. So Uy and his team used another test.
Flycatcher males defend their mating territories. If a potential rival male enters another’s territory, fights often ensue. If all-black males react less violently to chestnut-bellied males and vice versa, that’s an indication that the two don’t recognize each other as reproductive rivals. If they don’t see each other as rivals, then one can assume that mating between members of the two populations is rare.
So Uy and his team made all-black and chestnut-bellied taxidermy models. They used the models to invade mating territories in each population. As expected, when all-black birds were presented with all-black models, they attacked. But when all-black birds encountered chestnut-bellied models, they were much less likely to go on the offensive. The same scenario held for the chestnut-bellied birds.
That males from the two populations no longer view the other as a reproductive threat is a good indication that not much mating is taking place between the two groups. Their evolutionary paths are diverging, Uy and his team found-all because of a change in plumage.
We humans have 46 chromosomes – 23 pairs. All of the other great apes have 24 pairs of chromosomes. So how is it that we are missing a pair of chromosomes that all these recent relatives actually have?
Is it possible that a pair of chromosomes just got lost in our lineage? Well, no. There are so many important genes on every chromosome that the loss of both members of a homologous pair would be fatal, wouldn’t even get past embryonic development. So the only possibility is two chromosomes that are still separate in other primates must have gotten accidentally stuck together to form a single fused chromosome in us. And that’s the explanation that exists in evolution. Here is why evolution is science and not conjecture. If that’s true, we want to be able to find that fused chromosome. So if we can, that is a powerful confirmation of an evolutionary prediction.
Well, can we find it? It turns out it is much easier to recognize a fused chromosome than you might think. The tips of all chromosomes are covered with a very special DNA sequence, in a region called the telomere. It is really easy to recognize. Near the center of every chromosome is an equally recognizable region called the centromere. If one of our chromosomes was formed by the fusion of two primate chromosomes, you know what it would have? It would have telomere DNA at the center, and it would have two centromeres. Should be very easy to recognize.
We scanned the human genome. Do we have a chromosome like that? The answer is, you bet we do.
It is called human chromosome number two. Our second chromosome has telomere DNA at the center. It has two centomeres. We have placed it as being from primate chromosomes 12 and 13 and so exact is the correspondence that people who work on the chimpanzee genome now call the chromosomes they used to call 12 and 13 2A and 2B, because they correspond to those two halves of the human second chromosome.
Is there any question, to explain these facts – and these are facts, this is not hypothesis or conjecture – any way to explain these facts in light of the view that our species was uniquely designed or intelligently created? The answer is no. You can only explain this by evolutionary common ancestry. About the only thing you could say is maybe the designer wanted to fool us into thinking we evolved and he rigged chromosome number two to make it look that way.
And the only thing I can tell you is if that was his intent, he did a heck of a job. Because the marks of evolution are literally all over our chromosome.