J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M600230-JLR200 on September 26, 2006

Papers In Press, published online ahead of print December 1, 2006
J. Lipid Res., doi:10.1194/jlr.M600230-JLR200
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Journal of Lipid Research, Vol. 47, 2690-2700, December 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Elovl3: a model gene to dissect homeostatic links between the circadian clock and nutritional statusboxs

Ana Anzulovich1,*, Alain Mir{dagger}, Michelle Brewer*, Gabriela Ferreyra*, Charles Vinson{dagger} and Ruben Baler2,§

* Unit on Temporal Gene Expression, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892
{dagger} Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
§ Science Policy Branch, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD 20892

boxs The online version of this article (available at http://www.jlr.org) contains additional supplemental data.

Published, JLR Papers in Press, September 26, 2006.

1 Present address of A. Anzulovich: Laboratorio de Bioquímica Molecular, Area de Química Biológica, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, San Luis CP5700, Argentina.

2 To whom correspondence should be addressed. e-mail: balerr{at}mail.nih.gov

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 RevErb{alpha} and activated by sterol-regulatory element binding protein-1 (SREBP1) transcription factors. We propose that the temporal coordination of RevErb{alpha} 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 because 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 postabsorptive phases in the liver.

Supplementary key words fatty acid • elongase • sterol-regulatory element binding protein target genes • restricted feeding • daily rhythm • phase shift

Abbreviations: ACC, acetyl-coenzyme A carboxylase; ACS, acyl-CoA synthase; G3PAT, glycerol-3-phosphate acyltransferase; iBAT, interscapular brown adipose tissue; PPAR, peroxisome proliferator-activated receptor; SREBP, sterol-regulatory element binding protein; STAT, signal transducer and activator of transcription; VLCFA, very long-chain fatty acid; ZT, Zeitgeber time


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