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Neuron. 2007 Jun 7;54(5):831-43.

Light entrainment of the mammalian circadian clock by a PRKCA-dependent posttranslational mechanism.

Author information

1
Department of Genes and Behavior, Max Planck Institute of Biophysical Chemistry, 37077 Goettingen, Germany.

Abstract

Light is the most potent stimulus for synchronizing endogenous circadian rhythms with external time. Photic clock resetting in mammals involves cAMP-responsive element binding protein (CREB)-mediated transcriptional activation of Period clock genes in the suprachiasmatic nuclei (SCN). Here we provide evidence for an additional photic input pathway to the mammalian circadian clock based on Protein Kinase C alpha (PRKCA). We found that Prkca-deficient mice show an impairment of light-mediated clock resetting. In the SCN of wild-type mice, light exposure evokes a transient interaction between PRKCA and PERIOD 2 (PER2) proteins that affects PER2 stability and nucleocytoplasmic distribution. These posttranslational events, together with CREB-mediated transcriptional regulation, are key factors in the molecular mechanism of photic clock resetting.

PMID:
17553429
DOI:
10.1016/j.neuron.2007.04.031
[Indexed for MEDLINE]
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