Brain Versus Brawn

The clock genes that control circadian rhythms in mammals also contribute to other aspects of physiology, behavior, and health. One such clock gene, Bmal1, encodes a transcription factor whose inactivation in mice causes disturbances in circadian rhythms and alterations in activity level, body weight, and other physiological functions. By reexpressing the Bmal1 gene in selective tissues in Bmal1-deficient mice, McDearmon et al. show that the transcription factor exerts distinct tissue-specific functions. Circadian rhythmicity in the mutant mice was normalized only when Bmal1 was expressed in the brain, whereas normalization of the animals' activity level and body weight required Bmal1 expression in muscle.

Source:
Dissecting the Functions of the Mammalian Clock Protein BMAL1 by Tissue-Specific Rescue in Mice. Erin L. McDearmon et al. Science 24 November 2006: Vol. 314. no. 5803, pp. 1304 - 1308

Lack of Food Anticipation in Mutant Mice

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.

Source:

Lack of Food Anticipation in Per2 Mutant Mice. Céline A. Feillet et al. Current Biology, Vol 16, 2016-2022, 24 October 2006