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PPAR α  and HNF4 α  are nuclear receptors that control gene transcription by direct binding to specific nucleotide sequences. Using transgenic mice deficient for either PPAR α  or HNF4 α , we show that the expression of the peroxisomal   3-keto-acyl-CoA thiolase B  ( Thb ) is under the dependence of these two transcription factors. Transactivation and gel shift experiments identified a novel PPAR response element within intron 3 of the  Thb  gene, by which PPAR α  but not HNF4 α  transactivates. Intriguingly, we found that HNF4 α  enhanced PPAR α /RXR α  transactivation from TB PPRE3 in a DNA-binding independent manner. Coimmunoprecipitation assays supported the hypothesis that HNF4 α  was physically interacting with RXR α . RT-PCR performed with RNA from liver-specific HNF4 α -null mice confirmed the involvement of HNF4 α  in the PPAR α -regulated induction of  Thb  by Wy14,643. Overall, we conclude that HNF4 α  enhances the PPAR α -mediated activation of  Thb  gene expression in part through interaction with the obligate PPAR α  partner, RXR α .

The Peroxisomal3-keto-acyl-CoA thiolase BGene Expression Is under the Dual Control of PPARα and HNF4α in the Liver