Microcosm by Carl Zimmer Page B

destroyed by
E. coli’
s molecular garbage crews. If the stress does not return in time, the microbe will run out of FliA, and the circuit will shut down. The good times have truly returned.
    Scientists are now starting to map the circuitry of genes in other species as carefully as Alon and his colleagues have in
E. coli.
But it will take time. Scientists don’t yet know enough about how the genes and proteins in those circuits build good models. In many cases, scientists know only that gene A turns on gene B and gene C, without knowing what causes it to flip the switch or what happens when it does.
    But Alon has discovered a remarkable lesson even in that tiny scrap of knowledge. He and his colleagues have surveyed the genes in
E. coli
and a few other well-studied organisms—yeast, vinegar worms, flies, mice, and humans. The arrows that link them tend to form certain patterns far more often than you’d expect if they were the result of chance.
E. coli’
s noise filter, for example, belongs to a class of circuits that engineers call feed-forward loops. (The loop in the noise filter goes from FlhDC to FliA to the flagella-building genes.) Feed-forward loops are unusually common in nature, Alon and his colleagues have shown. Nature has a preference for a few other patterns as well, which also seem to allow life to take advantage of engineering tricks like the noise filter.
E. coli
and the elephant, it seems, are built not only with the same genetic code. They’re also wired in much the same way.
    LIFE ON AUTOPILOT
    An orange winter dusk has settled in. Out my window I can see the webs of bare maple branches. Photons stream through the window and patter on the photoreceptors lining my retina. The photoreceptors produce electric signals, which they trade among themselves and then fire down the fibers of my optic nerves into the back of my brain. Signals move on through my brain, following a network made of billions of neurons linked by trillions of branches. An image emerges. I get up from my desk to turn on the lights. At first I can see nothing outside, but after a moment my eyes adjust. I can still see the trees, down to their twigs.
    I must remind myself how remarkable it is that I can still see them. A moment earlier my vision was exquisitely tuned to perceiving the world at dusk. If it had stayed that way after I turned on the light, I would have been practically blinded. Fortunately my eyes and brain can retune themselves for the noonday sun or a crescent moon. If the light increases, my brain quickly tightens my irises to reduce the light coming in. When the lights go out, my pupils expand, and my retinal neurons boost the contrast between light and dark in my field of vision. An engineer would call my vision robust. In other words, it works steadily in an unsteady world.
    Our bodies are robust in all sorts of ways. Our brains need a steady supply of glucose, but we don’t black out if we skip dinner. Instead, our bodies unload reserves of glucose as needed. A clump of cells develops into an embryo by trading a flurry of signals to coordinate their divisions. The signals are easily disrupted, but most embryos can still turn into perfectly healthy babies. Again and again life avoids catastrophic failure and remains on course.
    Until recently, scientists had no solid evidence for where life’s robustness comes from. To trace robustness to its source, they needed to know living things with a deep intimacy—the same intimacy an engineer may have with an autopilot system, using its plans to carry out experiments. But the blueprints of most living things remain classified. Among the few exceptions is
E. coli.
    E. coli
faces threats to its survival on a regular basis. Set a petri dish on a windowsill on a sunny day and you bring the microbes in it to the brink of disaster. In order to work properly, a protein needs to maintain its intricate origami-like folds. Overheated proteins shake themselves loose. They can no