Document Detail


PKCγ participates in food entrainment by regulating BMAL1.
MedLine Citation:
PMID:  23185022     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Temporally restricted feeding (RF) can phase reset the circadian clocks in numerous tissues in mammals, contributing to altered timing of behavioral and physiological rhythms. However, little is known regarding the underlying molecular mechanism. Here we demonstrate a role for the gamma isotype of protein kinase C (PKCγ) in food-mediated entrainment of behavior and the molecular clock. We found that daytime RF reduced late-night activity in wild-type mice but not mice homozygous for a null mutation of PKCγ (PKCγ(-/-)). Molecular analysis revealed that PKCγ exhibited RF-induced changes in activation patterns in the cerebral cortex and that RF failed to substantially phase shift the oscillation of clock gene transcripts in the absence of PKCγ. PKCγ exerts effects on the clock, at least in part, by stabilizing the core clock component brain and muscle aryl hydrocarbon receptor nuclear translocator like 1 (BMAL1) and reducing its ubiquitylation in a deubiquitination-dependent manner. Taken together, these results suggest that PKCγ plays a role in food entrainment by regulating BMAL1 stability.
Authors:
Luoying Zhang; Diya Abraham; Shu-Ting Lin; Henrik Oster; Gregor Eichele; Ying-Hui Fu; Louis J Ptáček
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-11-26
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  109     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-13     Completed Date:  2013-02-28     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  20679-84     Citation Subset:  IM    
Affiliation:
Department of Neurology, University of California, San Francisco, CA 94158, USA.
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MeSH Terms
Descriptor/Qualifier:
ARNTL Transcription Factors / genetics,  physiology*
Animals
Cerebral Cortex / physiology
Circadian Rhythm / genetics,  physiology*
Eating / genetics,  physiology
Feeding Behavior / physiology*
Male
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Models, Neurological
Mutation
Photoperiod
Protein Kinase C / deficiency,  genetics,  physiology*
Protein Stability
Signal Transduction
Ubiquitination
Grant Support
ID/Acronym/Agency:
GM079180/GM/NIGMS NIH HHS; HL059596/HL/NHLBI NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/ARNTL Transcription Factors; 0/Arntl protein, mouse; EC 2.7.1.-/protein kinase C gamma; EC 2.7.11.13/Protein Kinase C
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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