Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [48]
E. coli’s gamble consists of choosing a response to a particular situation. In some cases, the choice is clear. A population of microbes should all respond in the same way. But in other cases, it pays for the population to hedge its bets. In other words, it pays for some individuals to respond one way and others to respond in another.
Which way E. coli should bet depends on how much information it can get. If E. coli can get a lot of reliable information, it makes sense to put all its money on one bet. But in other cases, it may be hard to determine the best choice. Conditions may be changing quickly and unpredictably. E. coli may be better off hedging its bet in these cases, allowing individuals to respond in different ways.
Lactose, for example, causes E. coli to hedge its bets. A supply of lactose may allow bacteria to survive when other kinds of sugar have been devoured. But in order to feed on lactose, a microbe first has to clear away all the proteins it was using to feed on other sugars and begin making the proteins it needs to eat lactose. That’s a lot of time and energy for a microbe to invest. The investment may pay off or it may be a waste of effort—the lactose may disappear quickly or a more energy-rich sugar may turn up.
E. coli hedges its bets by using its unpredictable bursts of proteins to create both eager and reluctant individuals. If the colony happens to encounter some lactose, the eager microbes will be ready to seize the moment, while the others respond more slowly. If the surge of lactose never comes, the reluctant microbes will grow faster because they haven’t wasted energy preparing for a feast that never arrived. Either way, the colony benefits.
E. coli hedges many bets, scientists are finding, and some of those bets make us sick. Strains of E. coli that infect the bladder need to make sticky hairs to attach to host cells, but the hairs draw the attention of the immune system. To balance this trade-off, the bacteria hedge their bets by randomly switching on and off the machinery for making the hairs. At any moment some individuals in a colony will sprout hairs and others will remain bald.
Bet hedging may also help E. coli defend itself against antibiotics. Many antibiotics kill E. coli by attacking the proteins the microbes use to grow. When antibiotics encounter a population of susceptible E. coli, they kill it off with staggering swiftness. Or at least they kill most of the microbes off. About 1 percent of the E. coli in a biofilm can survive an attack of antibiotics for hours or days. The survivors can rebuild the biofilm and make a person as sick as before.
This resilient minority carries no special genes for resisting antibiotics. They are genetically identical to their dead relatives. Scientists can isolate the survivors and allow them to multiply to form large colonies. The new colonies will be just as vulnerable to antibiotics. Once again, about 99 percent of the microbes die and 1 percent persist.
Scientists discovered so-called persister bacteria in 1944, and for the next sixty years they remained almost entirely baffled by them. Some researchers suggested that antibiotics drive a few microbes into a mysterious dormant state in which they can escape damage. A team of scientists led by Nathalie Balaban of the Hebrew University of Jerusalem tested this idea in 2004 by building a device to spy on persister cells. The scientists placed E. coli in microscopic grooves just wide enough to hold a single microbe. When an individual E. coli divided, its offspring remained in a