Your browser version may not work well with NCBI's Web applications. More information here...
1: Curr Biol. 2006 Oct 24;16(20):2016-22.
Related Articles, Links
Click here to read
Comment in:
Lack of food anticipation in Per2 mutant mice.

Feillet CA, Ripperger JA, Magnone MC, Dulloo A, Albrecht U, Challet E.

Department of Neurobiology of Rhythms, Institute of Cellular and Integrative Neurosciences, University Louis Pasteur, Centre National de la Recherche Scientifique, 67084 Strasbourg, France.

Predicting time of food availability is key for survival in most animals. Under restricted feeding conditions, this prediction is manifested in anticipatory bouts of locomotor activity and body temperature. This process seems to be driven by a food-entrainable oscillator independent of the main, light-entrainable clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus . Although the SCN clockwork involves self-sustaining transcriptional and translational feedback loops based on rhythmic expression of mRNA and proteins of clock genes , the molecular mechanisms responsible for food anticipation are not well understood. Period genes Per1 and Per2 are crucial for the SCN's resetting to light . Here, we investigated the role of these genes in circadian anticipatory behavior by studying rest-activity and body-temperature rhythms of Per1 and Per2 mutant mice under restricted feeding conditions. We also monitored expression of clock genes in the SCN and peripheral tissues. Whereas wild-type and Per1 mutant mice expressed regular food-anticipatory activity, Per2 mutant mice did not show food anticipation. In peripheral tissues, however, phase shifts of clock-gene expression in response to timed food restriction were comparable in all genotypes. In conclusion, a mutation in Per2 abolishes anticipation of mealtime, without interfering with peripheral synchronization by feeding cycles.

Publication Types:
PMID: 17055980 [PubMed - indexed for MEDLINE]