J. Lipid Res.
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A more recent version of this article appeared on December 1, 2006

Papers In Press, published online ahead of print September 26, 2006
J. Lipid Res., doi:10.1194/jlr.M600230-JLR200
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Submitted on May 24, 2006
Revised on September 20, 2006
Accepted on September 25, 2006

Elovl3: A model gene to dissect homeostatic links between the circadian clock and nutritional status

Ana Anzulovich, Alain Mir, Michelle Brewer, Gabriela Ferreyra, Charles Vinson, and Ruben Baler

Department of Biochemistry and Biology, National University of San Luis, San Luis, San Luis 5700

Corresponding Author: acanzu{at}unsl.edu.ar

The ELOVL3 protein is a very long chain fatty acid elongase, found in liver, skin and brown adipose tissues. Circadian expression of the Elovl3 gene in the liver is perturbed in mutant CLOCK mice but persists in mice with severe hepatic dysfunction. A reliance on an intact clock, combined with the refractoriness to liver decompensation and the finding of a robust sexually dimorphic pattern of expression, evince a particularly complex mode of transcriptional control. The Elovl3 gene upstream region was repressed by RevErba and activated by SREBP1 transcription factors. We propose that the temporal coordination of RevErba and SREBP1 activities integrates clock and nutrition signals to drive a subset of oscillatory transcripts in the liver. Proteolytic activation of SREBP1 is circadian in the liver and since the cycle of SREBP1 activation was reversed after restricting meals to the inactive phase of the day, this factor could serve as an acute sensor of nutritional state. SREBP1 regulates many known lipogenic and cholesterogenic circadian genes, hence, our results could explain how feeding can override brain-derived entraining signals in the liver. This mechanism would permit a rapid adjustment in the sequence of key aspects of the absorptive and post-absorptive phases in the liver.


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