[M.D. Holloway]

It’s the postapocalyptic survivors that interest Finkel. As 99 percent of their comrades die off, the surviving bacteria feed on the carcasses of the dead and on metabolic by-products of other survivors. Thus the bacteria change the environment in which they live. It doesn’t take long for the cultures in each flask to go their own ways. Within a month, the bacteria in the various flasks convert the light honey color of the broth into a spectrum ranging from light amber to dark amber,

Finkel says. And his nose tells him the cultures are different as well. Microscope examinations reveal that the originally rod-shaped bacteria take on a wide variety of shapes; in one flask, some of the cells never cut the apron strings during cell division, forming long strands resembling linked sausages.

Yet as different as the bacterial populations appear, they also have something in common. All of the cells that have gone through the valley of death and come out the other side are tougher than naive bacteria. And the older the cells get, the more competitive they are, so that 20-day–old cells will drive 10-day–old cells to extinction, and 30-day–old cells beat 20-day–olds. Finkel calls that phenomenon “growth advantage in stationary phase,” or GASP.

On the surface it appears that the number of surviving cells stays constant. But underneath, different mutants rise and fall in number, like waves crashing on the beach, Finkel showed in a 2006 review published in Nature Reviews Microbiology.

The ability for older cells to compete better has been traced to mutations in four genes. Three of the genes allow the bacteria to feast more readily on certain amino acids. One of the genes encodes a key protein, RpoS, needed to turn on stress-response genes. The protein gives the green light to turn on genes under certain conditions. When cells are under stress — for bacteria, stress means high salt, low or high temperatures, broth that is too acidic or alkaline, or other environmental extremes — RpoS turns on genes that help the bacteria cope. But the protein is not necessary when cells aren’t under stress. In fact, it takes resources away from the cells’ main “go” signal, RpoD, a protein critical to normal function. Inactivating or handicapping RpoS makes more resources available for other genes.

Many of the GASP cells contain changes in rpoS, the gene for RpoS, but they don’t all have the same change, Finkel and colleagues reported in 2003. Nearly all of the changes reduce activity of RpoS to 1 percent or less of its normal activity but don’t abolish it entirely. Low levels of RpoS are a fixture in bacterial populations that have GASP.

But just because a mutation serves an organism well under some conditions doesn’t mean it’s always beneficial. Thomas Ferenci, a microbiologist at the University of Sydney in Australia, reviewed what happens to rpoS mutants under a variety of environmental conditions in the May 2008 Heredity. Depending on a cell’s genetic background, an rpoS mutation might give the strain a big boost in fitness or make an undetectable difference. And even if the mutations are beneficial under most conditions, the changes hold the bacteria back when the environment changes. If salt concentrations go up, the temperature drops, bacteria lack oxygen or encounter a toxin, then rpoS mutants, less able to cope with certain types of stress, don’t become established members of the community as quickly as they do under other conditions.

Natural selection works for rpoS mutants in some environments and against them in other conditions. “Selection is a deterministic force pushing relentlessly in one direction,” says Michael Lynch, an evolutionary biologist at Indiana University in Bloomington. That direction is toward ever-greater adaptation for the environment in which a population finds itself. But most environments are in a constant state of flux and, as Darwin was careful to point out in his introduction to the Origin of Species, selection isn’t the only evolutionary force at work.