Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [69]
Other viruses use a different strategy to survive, but one that’s no less cruel to E. coli. Rather than destroying their host when times are bad, they hold it hostage. One of these viruses, known as P1, carries a gene that makes a protein called a restriction enzyme. Restriction enzymes are able to grab DNA at specific sites and slice it apart. Yet P1 normally does not kill E. coli. That’s because the virus also makes a second protein that protects the microbe from the restriction enzymes. Known as a modification enzyme, it builds shields around E. coli’s DNA at exactly the sites where the restriction enzyme can grab it.
Why should P1 bother building both a poison and its antidote? Like many viruses, P1 lives on a plasmid. Each time E. coli divides, it usually makes new copies of both its own DNA and the P1 plasmid. Sometimes E. coli makes a mistake, however, and all the plasmids end up in one offspring with none in the other. Those plasmid-free bacteria might be able to outcompete the ones that still carry the P1 virus, because they don’t have to use extra energy to make virus proteins and copy their DNA. So the P1 virus kills them—even though it’s not actually in the bacteria. The deadly beauty of restriction and modification enzymes is that restriction enzymes are durable, whereas modification enzymes are short-lived. If E. coli loses the P1 virus, it quickly loses its shields and cannot make new ones. Eventually its DNA becomes vulnerable, and the restriction enzymes move in for the kill. Once E. coli is infected with P1, in other words, it can’t live without the virus.
Genes for restriction and modification enzymes aren’t unique to P1. E. coli carries many of them on its chromosome. Ichizo Kobayashi, a geneticist at the University of Tokyo, has argued that they also got their start as selfish genes holding their host hostage. He points out, too, that restriction and modification enzymes could have allowed viruses to battle other viruses trying to take over their host. A new virus invading E. coli does not have the shields made by the resident virus, leaving it open to attack by restriction enzymes. While restriction and modification enzymes may have gotten their start as ways to let a parasite thrive, some of them appear to have been harnessed by their E. coli hosts. By killing incoming viruses, they have become a primitive sort of immune system for the bacteria.
Genes come into similar conflict in all species. Many insects are infected with a microbe called Wolbachia, for example, that can only live inside their cells. It relies for survival almost entirely on being passed down from one generation to the next. This strategy has one major shortcoming: Wolbachia cannot infect sperm, and so males are a dead end for its posterity. In other words, the success of Wolbachia’s genes and those of its male hosts are in conflict.
Wolbachia has evolved many ways to win this struggle. In some species of wasps, for example, Wolbachia manipulates infected females so that they give birth only to females, and it alters their offspring so that they have no need to mate with males to reproduce. In other species, Wolbachia kills an infected mother’s male eggs. The bacteria in the male eggs die as well, but the strategy ensures the overall success of Wolbachia genes: the Wolbachia-infected female eggs survive, and when they hatch the female larvae don’t face competition for food from their brothers. In fact, their brothers become their food. Wolbachia, in other words, has hit on some of the same strategies that viruses use to thrive in E. coli.
These murky struggles between parasite and host, these blurrings of species, may seem profoundly alien. Yet we are not above the shaping forces of viruses. Most viruses simply invade our cells, which produce new viruses that move on to the next host. But some viruses insert their genetic material in a cell’s genome. If they manage to infect a sperm or an egg, these viruses will