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Nucleic Acids Research 2004 32(16):4742-4749; doi:10.1093/nar/gkh806
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Published online 8 September 2004

Nucleic Acids Research, Vol. 32 No. 16 © Oxford University Press 2004; all rights reserved

Functional interaction between peroxisome proliferator-activated receptors-{alpha} and Mef-2C on human carnitine palmitoyltransferase 1ß (CPT1ß) gene activation

Ángel Baldán, Joana Relat, Pedro F. Marrero and Diego Haro*

Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Barcelona, Avenue Diagonal 643, E-08028 Barcelona, Spain

* To whom correspondence should be addressed. Tel: +34 93 403 45 00; Fax: +34 93 402 45 20; Email: dharo{at}ub.edu
Present address: Ángel Baldán, Department of Medicine—Cardiology, David Geffen School of Medicine at UCLA 3230 MRL695, Los Angeles, CA 90095, USA

Received as resubmission July 21, 2004; Accepted August 17, 2004

Muscle-type carnitine palmitoyltransferase 1 (CPT1ß) is considered to be the gene that controls fatty acid mitochondrial ß-oxidation. A functional peroxisome proliferator-activated receptor (PPAR) responsive element (PPRE) and a myocite-specific (MEF2) site that binds MEF2A and MEF2C in the promoter of this gene had been previously identified. We investigated the roles of the PPRE and the MEF2 binding sites and the potential interaction between PPAR{alpha} and MEF2C regulating the CPT1ß gene promoter. Mutation analysis indicated that the MEF2 site contributed to the activation of the CPT1ß promoter by PPAR in C2C12 cells. The reporter construct containing the PPRE and the MEF2C site was synergistically activated by co-expression of PPAR, retinoid X receptor (RXR) and MEF2C in non-muscle cells. Moreover, protein-binding assays demonstrated that MEF2C and PPAR specifically bound to one another in vitro. Also for the synergistic activation of the CPT1ß gene promoter by MEF2C and PPAR{alpha}-RXR{alpha}, a precise arrangement of its binding sites was essential.


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