Recent work suggests a role for sleep in memory and/or synaptic plasticity. There is a large difference in how much sleep people need, ranging from less than 6 to more than 9 hours. Short sleepers are found in families, as are long sleepers, which suggests a genetic basis for sleep duration. He et al. now show that a mutation in a transcriptional factor, DEC2, is associated with short sleep in humans and mice. DEC2 is a transcription factor (protein that regulates gene function) involved in cell proliferation and differentiation, response to hypoxia, and circadian rhythms. Here is their 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.