Next, the team compared the response of the genetically engineered mice and normal mice to the consequence of six hours of sleep deprivation. The engineered mice needed to compensate for their lost sleep to a much lesser extent as seen in nonREM and REM measures than their normal counterparts.
"These changes in sleep homeostasis in the mutant mice could provide an explanation for why human subjects with the mutation are able to live unaffected by shorter amounts of sleep throughout their lives," says Fu.
The next step, she says, is determining the DEC2's precise role. "We know the gene encodes a protein that is a transcriptional repressor and we know it makes the repressor's activity weaker. But we don't know if the weaker repressor is directly related to the shorter amount of sleep, because proteins can have many functions. It could be the protein functions as part of a larger transcriptional machinery, not necessarily as a repressor."
DEC2 could be involved in modulating "sleep quantity" alone, or it could be mediating both "sleep quantity" and "wakefulness-behavioral drive," according to Fu. The latter drive, she says, is critical for the procurement of food, shelter, and mates and could be more potent in individuals with this mutation.
"The mouse model also provides an opportunity to investigate whether there are other behaviors or physiological conditions associated with a short sleep syndrome," says Fu. She suspects there will be.
|Contact: Jennifer O'Brien|
University of California - San Francisco