Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [61]
Roth and Andersson’s gene amplification, on the other hand, may not be limited to a few lactose-starved E. coli. Making extra copies of genes may help many organisms adapt to new challenges.
Imagine that a microbe encounters a new kind of food that its ancestors had never tasted. All of the enzymes it uses for feeding have been honed by natural selection for feeding on other molecules. That doesn’t necessarily mean the microbe can’t eat the new food. Enzymes are actually not all that finely tuned. An enzyme that can slice up one molecule very efficiently may slice up other kinds of molecules, too, albeit more slowly and clumsily. If mutations give a microbe more copies of the gene, it may be able to eat more of the new food.
Ichiro Matsumura, a biologist at Emory University, used E. coli to demonstrate just how promiscuous enzymes can be. Matsumura and his colleagues created 104 strains of E. coli, each missing a gene that is absolutely essential to the survival of the microbe. They then created thousands of plasmids, each carrying several copies of another E. coli gene . After adding these plasmids to the crippled strains, they waited to see if the plasmid genes would be able to pinch hit for the essential gene Matsumura had knocked out. Matsumura found that he could revive 21 out of the 104 strains.
Matsumura’s experiment exposed a hidden versality in E. coli that may let it adapt to new conditions. Other species may depend on the same potential in their DNA. As mutations make extra copies of those genes, they can do an even better job of feeding on a new food, or detoxifying some poison, or coping with unprecedented heat. In time, one of the copies of the gene may evolve into a far more efficient form. The other genes may then fade away.
Gene amplification may be a creative force, but it can also put us in mortal danger. Like E. coli, the cells in our bodies sometimes mutate. On very rare occasions, mutations in our cells put them on the road to becoming cancerous. They no longer obey the controls that keep the growth of normal cells in check. As they continue to divide and mutate, new mutations help them become more aggressive and better able to evade the immune system. Like E. coli starving for lactose, these cells face many challenges, and any mutation that helps them overcome these is favored by natural selection. Mutations can create extra copies of genes, which can allow tumor cells to grow faster or escape chemotherapy. Some of these extra genes can evolve new functions of their own that make the tumor even more dangerous.
Sometimes E. coli is a little too much like the elephant for the elephant’s comfort.
A GIFT OF GENES
World War II, like all wars, provided E. coli with a ripe opportunity for slaughter. Its dysentery-causing strains, then known as Shigella, stormed across battlefields and invaded cities, killing beyond counting. At the end of the war, Shigella retreated from countries that rebuilt their sewers and water supplies. However, in places where water remained dirty—much of Africa, Latin America, and Asia—Shigella continued to thrive. The one exception to the rule was Japan. Japan cleaned up its water, and for two years dysentery rates fell. But then, inexplicably, Shigella surged back. There were fewer than 20,000 cases in 1948 but more than 110,000 in 1952.
Japanese microbiologists had been very familiar with Shigella ever since Kiyoshi Shiga discovered it in 1897. During the postwar outbreak of Shigella, they gathered thousands of samples of the bacteria from patients and searched for the cause of its resurgence. Antibiotic resistance, they discovered, was on the rise. At first, microbiologists discovered Shigella strains resistant to sulfa drugs. Within a few years, resistance to tetracycline also emerged, then resistance to