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Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [53]

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its forerunners.

That was what scientists thought until Eric Stewart, a microbiologist now at Northeastern University, decided to take a very close look at E. coli. He and his colleagues built a sort of voyeuristic E. coli paradise. They injected a single microbe onto an agar-coated slide, covering the little shelter with glass and sealing the sides shut with silicon grease. The microbe carried a light-producing gene, making it easy to film through the top of the slide. The scientists mounted the slide on a microscope, and the entire apparatus was put in a box that was kept as warm as a healthy human gut.

The single E. coli feasted and divided. Its descendants spread out in a layer one cell deep. At regular intervals a camera mounted on the microscope took a picture of the glowing colony. Comparing one picture with the next, Stewart could track the fate of every branch of his E. coli dynasty. He could time how long it took each microbe to divide and then how long its two offspring needed and then its four grandchildren. Given that all the microbes were genetically identical and all were living in the same perfect conditions for growth, they all should have grown at the same rate. But they didn’t. Some individuals grew more slowly than their siblings, and over time their descendants lagged farther and farther behind.

Some bacteria, Stewart discovered, were getting old. Each time a microbe reproduces, it builds itself a ring in order to cut itself in half. At the same time, it builds two new caps to cover the new ends of its daughter cells. When those two daughter cells split, each will build new caps as well. After several generations, some bacteria will have old poles and others will have new ones. In the diagram below, the numbers show how many generations have passed since a cap has been created:

Stewart discovered that as the caps on microbes got older, the microbes grew more slowly. He estimates that the aging E. coli were slowing down so quickly that after a hundred generations they would stop dividing altogether.

Once more the Williams-Hamilton decoder ring can help. Old age must have some evolutionary advantage over immortality for E. coli. Its edge may come from the inescapable damage that strikes the bacteria. Proteins become snarled; genes mutate. When a microbe divides, it may pass down its defective proteins and genes to one or both of its descendants. Over the generations, more and more damage can pile up like a cruel, compounding legacy. Of course, E. coli can fix this damage, and it does fix a lot of it. Yet that repair doesn’t come free. A microbe must use up a lot of energy and nutrients to repair itself. If it spent all its resources on repair, a more careless microbe would outcompete it.

There is another way to cope with damage: push it all into one place. In E. coli’s case, the dumping grounds are its poles. E. coli does not put much effort into repairing them, and when it divides, each of its descendants gets an old, damaged pole along with a new one on the other end. Over the generations, some of the poles can get very old—and presumably accumulate a lot of damage to their proteins. Instead of trying to be a perfectionist, Stewart suggests, E. coli may just turn its poles into garbage cans. A microbe that lets some of its descendants get old while the rest stay young may have found the best strategy for evolutionary success.

What once seemed like a major exception to Monod’s rule has now vanished. Once again E. coli has hit on the same strategy we humans have. When a fertilized human egg begins to grow into an embryo, it soon develops into two types of cells: cells that can become new people (eggs and sperm) and all the others. We invest a great deal of energy in protecting eggs and sperm from the ravages of time and much less on protecting the rest of our bodies. From this unconscious choice, we allow our progeny to live on while we die. For both humans and E. coli, the privilege of life must be paid with death.

Seven

DARWIN AT THE DRUGSTORE

LIFE AGAINST LIFE

THE BACTERIA

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