Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [46]
Meanwhile, in England, another young biologist, William Hamilton, realized that something important had been ignored in the debate over natural selection and group selection: family. Natural selection favors mutations that spread genes through a population, and one way to spread those genes is by having a lot of healthy children. Hamilton demonstrated, however, that an individual can spread its genes by helping its relatives breed.
Hamilton made his point mainly with social insects, such as ants and bees. A sterile female worker ant may have no hope of reproducing, but that does not mean the genes she carries have no chance of getting into the next generation. Every female worker in an anthill is the offspring of the queen, as are the eggs she helps to raise. That means the worker is helping to rear ants that share some of the same genes she carries. In fact, thanks to a quirk in insect genetics, a worker ant shares more genes with the eggs of the queen than she would with her own offspring. Hamilton put together a mathematical model of genes passing from one generation to the next. If altruism is more likely to pass a set of genes to the next generation than is reproducing oneself, it could be favored by natural selection. Group selection is indeed possible, Hamilton argued, if the group is an extended family.
Williams and Hamilton had a staggering impact on biology. It’s as if they had passed out decoder rings that allowed scientists to decipher many mysterious patterns in nature—why some animals dote on their offspring while others abandon them at birth, for example. They could make predictions about the intimate details of species with mathematical precision. As zoologists, Williams and Hamilton didn’t have much to say about the evolution of a microbe such as E. coli. But it turns out that in many ways E. coli supports their view of life as well.
There may be nothing terribly mysterious, for example, about why cheating E. coli haven’t completely taken over. Cheaters can exploit their fellow bacteria in the stationary phase, but only at a cost. The mutation that turns ordinary E. coli into cheaters occurs on a gene called rpoS. Normally rpoS acts as a master control gene, responding to signs of stress by turning on hundreds of other genes. Starvation and other kinds of stress cause rpoS to put E. coli into the stationary phase. If a mutation disables rpoS, the microbe will not shut down its metabolism but instead will begin to feed and grow.
Like many other genes, rpoS has many roles to play in E. coli’s life. When the microbe enters our stomachs and senses that it has entered an acid bath, rpoS responds by switching on acid-resistance genes. Cheaters cannot marshal these defenses, and so they are more likely to die before they can pass through the stomach. Although cheaters may thrive in one state, they lose out over E. coli’s entire life cycle.
Even E. coli’s biofilms, those lovely cooperative ventures built on self-sacrifice, may not be quite the models of altruism they seem to be. Joao Xavier and Kevin Foster, two biologists at Harvard, have found evidence that conflict can help produce biofilms. Xavier and Foster built a complex mathematical model of a biofilm to compare how well two kinds of bacteria would fare: one kind produced a biofilm glue (technically known as extracellular polymeric substances), and the other did not. Xavier and Foster seeded an empty surface with both kinds of bacteria and let them grow by eating glucose and consuming oxygen.
At first, Xavier and Foster found, the glue-making bacteria lost out to the others