Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [49]
After several generations, the scientists doused the bacteria with a potent antibiotic. Most of the E. coli died, but the persisters remained. Balaban and her colleagues found that the persisters grew far more slowly than normal cells, although they had not stopped growing altogether. By looking back at their earlier measurements, Balaban discovered that the microbes had become slow-growing persister cells before the antibiotics arrived.
Balaban concluded that every E. coli has a tiny chance at any moment of spontaneously turning into a persister. Once it makes the change, the microbe has a small chance of reverting to a normal fast-growing cell. All the bacteria Balaban studied, persisters and growers alike, were genetically identical, which meant that mutations were not the source of persistence. Yet persisters gave rise to more persisters, as if persisting were a hereditary trait.
Persisters are born of noise. That’s the theory of Kim Lewis, a leading expert on the phenomenon at Northeastern University. Lewis and his colleagues have found a way to compare the proteins produced by persister cells with the ones made by normal E. coli. One of the major differences between the two kinds of bacteria is that persister cells make a lot of toxins. Scientists have long puzzled over these toxins, which lock on to E. coli’s other proteins and stop them from doing their normal jobs. In most of the bacteria, these toxins don’t cause any harm because E. coli also produces their antidotes—antitoxins that grab the toxins before they can interfere with the microbe’s physiology.
It’s these toxins, Lewis argues, that turn E. coli into persisters. Normally E. coli churns out a tiny stream of toxins, along with another tiny stream of antitoxins. But thanks to the noisy workings of its genes, the microbe sometimes hiccups, releasing a burst of toxins. The extra toxins that aren’t disabled by E. coli’s small supply of antitoxins are free to attack proteins. They don’t do any permanent damage, but they do bring E. coli’s growth nearly to a halt. After the outburst, E. coli’s toxins gradually dwindle as E. coli produces more antitoxins. Once its proteins are liberated, it can go back to being a normal microbe again.
This noisy network acts like a roulette wheel, randomly picking out a few individuals to stop growing at any moment. It’s usually a bad thing for an individual microbe to get stuck with extra toxins, because a persister will fall behind the other, fast-growing E. coli. But there’s also a small chance that a disaster will strike while the microbe is a persister. That disaster might come in the form of a pencillin pill, or it might be a naturally produced poison released by another microbe. In either case, the persister will turn out to be the big winner. For the entire population of E. coli, it doesn’t matter which individual wins as long as its individuality-generating genes continue to get passed down to new generations.
SPITEFUL SUICIDE
Persister cells make a sacrifice for their companions, giving up the chance to multiply quickly. But when E. coli produce colicins, the chemical weapons for killing rival strains, they pay a far bigger price. In order to let their kin thrive, they explode in a suicidal blast.
The chemical warfare practiced by E. coli is the dark side of altruism. William Hamilton originally argued that natural selection could favor sacrifice if it meant an individual could help its relatives reproduce more. In 1970, he recognized that natural selection could also favor sacrifice if it meant that nonrelatives suffered—a nasty sort of altruism he called spite. Hamilton always argued that spite was rare and inconsequential, because his equations suggested it would be favored only when populations were very small. But in 2004, Andy Gardner and Stuart West at the University of Edinburgh demonstrated that if unrelated individuals compete fiercely with their immediate neighbors spite can also evolve.