| First Author | Curtis AM | Year | 2004 |
| Journal | J Biol Chem | Volume | 279 |
| Issue | 8 | Pages | 7091-7 |
| PubMed ID | 14645221 | Mgi Jnum | J:207820 |
| Mgi Id | MGI:5559671 | Doi | 10.1074/jbc.M311973200 |
| Citation | Curtis AM, et al. (2004) Histone acetyltransferase-dependent chromatin remodeling and the vascular clock. J Biol Chem 279(8):7091-7 |
| abstractText | Rhythmic gene expression is central to the circadian control of physiology in mammals. Transcriptional activation of Per and Cry genes by heterodimeric bHLH-PAS proteins is a key event in the feedback loop that drives rhythmicity; however, the mechanism is not clearly understood. Here we show the transcriptional coactivators and histone acetyltransferases, p300/CBP, PCAF, and ACTR associate with the bHLH-PAS proteins, CLOCK and NPAS2, to regulate positively clock gene expression. Furthermore, Cry2 mediated repression of NPAS2:BMAL1 is overcome by overexpression of p300 in transactivation assays. Accordingly, p300 exhibits a circadian time-dependent association with NPAS2 in the vasculature, which precedes peak expression of target genes. In addition, a rhythm in core histone H3 acetylation on the mPer1 promoter in vivo correlates with the cyclical expression of their mRNAs. Temporal coactivator recruitment and HAT-dependent chromatin remodeling on the promoter of clock controlled genes in the vasculature permits the mammalian clock to orchestrate circadian gene expression. |
