Short Sleep Gene

The latest issue of Science has this interesting report on how the transcriptional repressor DEC2 regulates sleep length in mammals. Here is the abstract:

Sleep deprivation can impair human health and performance. Habitual total sleep time and homeostatic sleep response to sleep deprivation are quantitative traits in humans. Genetic loci for these traits have been identified in model organisms, but none of these potential animal models have a corresponding human genotype and phenotype. We have identified a mutation in a transcriptional repressor (hDEC2-P385R) that is associated with a human short sleep phenotype. Activity profiles and sleep recordings of transgenic mice carrying this mutation showed increased vigilance time and less sleep time than control mice in a zeitgeber time– and sleep deprivation–dependent manner. These mice represent a model of human sleep homeostasis that provides an opportunity to probe the effect of sleep on human physical and mental health.

And a brief excerpt from the "perspectives" piece on sleep:

Sufficient sleep is necessary for optimal daytime performance and well-being, yet there is a large difference in how much sleep people need, ranging from less than 6 to more than 9 hours. People at all points along this range exhibit no noticeable differences in health and waking performance. Those of us who envy short sleepers would like to reduce sleep duration to the minimum necessary for normal functioning, but do we know what this minimum is? Short sleepers are found in families, as are long sleepers, which suggests a genetic basis for sleep duration. On page 866 of this issue, He et al. (1) add new evidence by showing that a mutation in a transcriptional factor, DEC2, is associated with short sleep in humans and mice.

....Sleep amount, like weight and height, is a quantitative phenotype normally distributed in the population. Total daily sleep duration has an estimated heritability of ~50% in humans and mice, suggesting complex underlying genetics with contributions from numerous genes. But mutations in single genes that yield dramatic effects cannot be excluded.

....The question "How much sleep do we need?" is not only of practical interest for obvious societal reasons, but is also of major importance for understanding sleep function. Recent hypotheses in the field favor a role in memory and/or synaptic plasticity. However, an unbiased approach may turn out to be more efficient. Molecular genetic approaches remain our best hope to find, without a priori assumptions, molecules that regulate the complex phenotype of sleep.

Cheers,
Colin