College students know that cramming for exams will take its toll later on, when they have to sleep off the hours of snoozing they missed. But scientists have found a genetic mutation that allows fruit flies to sleep considerably less without any apparent setbacks. If researchers can pinpoint the equivalent gene in humans, they could be on their way to finding the ultimate nonsleeping pill, experts say.
Sleep takes up a third of our lives, yet researchers don't fully understand why people snooze. Scientists do know that most animals need a siesta, and that in humans, the amount of slumber required by an individual is partly genetic. To determine what genes dictate sleep requirements, molecular biologist Chiara Cirelli and colleagues at the University of Wisconsin, Madison, turned to fruit flies, which catch shut-eye--even without eyelids—every night.
The team soaked 6000 flies in a chemical that mutates DNA, ultimately identifying a line of flies that dozed for only 4 to 5 hours a day but developed properly, flitted normally, and were fertile. Timing the bugs' sleep-wake cycles, the researchers determined that the flies' lack of sleep was due to shorter duration of slumber rather than fewer naps. To find out if less shut eye made the mutants tired during their waking periods, the team tested whether the flies responded to heat with as much vigor as if they'd gotten a full night's rest. After 24 hours of sleep deprivation, normal flies reacted slower to heat in their cages, but the mutants reacted as if they were fully rested, indicating that they didn't need to make up for their slumber loss.
Further testing revealed that the short sleeping flies possessed a mutation in a gene called Shaker, which encodes an ion channel that turns neurons on or off. Although the researchers have yet to test whether the mutation affects higher functions such as memory, they are excited because people have about a half-dozen Shaker-like genes: A drug that facilitates the normal function of Shaker might induce restorative sleep, while one that blocked it could keep people awake for late night driving or to study for exams, posits Cirelli, whose team reports its findings 28 April in Nature.
In contrast to the identification of gene mutations that shift the timing of sleep, this is the first isolation of a mutation that affects how long organisms need to slumber, says neurophysiologist Irene Tobler of the University of Zurich, Switzerland. "This could be the basis to understand the cellular mechanism" of sleep, she says, and ultimately why humans need their nightly zzzzs.