Sleep deprivation, as any new parent or college student can attest, leads to considerable impairments in behaviour. Even fruitflies need to sleep, but a study published in Nature shows that a mutation in a potassium channel can allow them to function normally on just a third as much sleep as wild-type flies.

Clearly, sleep serves some essential function, in species from humans to Drosophila melanogaster. Remarkably, however, it remains unknown what this function is, or how sleep is homeostatically controlled so that the pressure to sleep increases with time awake.

The study by Cirelli and colleagues describes a mutant line of D. melanogaster named minisleep (mns). These flies sleep for only about one-third of the duration for which wild-type flies sleep (4–5 h compared with 9–15 h). Despite this dramatic reduction in the length of each sleep episode, the number of bouts of sleep and general periodic locomotor activity were similar to those of wild-type flies. The authors conclude that the mutation does not influence the circadian clock system, which ensures that animals sleep at appropriate times.

Surprisingly, the mutant flies seem to behave normally despite this lack of sleep, and, unlike their wild-type relatives, are not impaired by further sleep deprivation.

The mutation that leads to this unusual phenotype was found to be in a conserved region of the well-studied Shaker gene, which encodes a voltage-dependent potassium channel that is involved in membrane polarization and presynaptic transmitter release. Taking advantage of the powerful tools available in D. melanogaster genetics, the authors showed that the phenotype is specific to the Shaker locus and does not depend on genetic background. Furthermore, other ion channel mutations did not cause abnormal sleep phenotypes.

The results might pave the way for a greater understanding of how the need for sleep is measured and controlled, much as early genetic studies of period and other mutations in D. melanogaster led to an understanding of the circadian clock. Clearly this is just the beginning of an interesting story. Do mutant flies simply need less sleep, or do they sleep more efficiently? Are the effects central or peripheral? It will also be important to determine whether the results are relevant to mammalian sleep regulation. Cirelli et al. suggest that this might be the case, on the basis of evidence that potassium channels are involved in mammalian sleep rhythms. In addition, some tantalizing hints come from a rare autoimmune disorder, Morvan's syndrome, in which sleeplessness might be associated with autoantibodies against voltage-dependent potassium channels.

There is one crucial caveat for anyone who reads this paper with hopes of a drug that could lead to a reduced need for sleep: compared with controls, the mutant flies had reduced lifespans.