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. 2006 Dec 11;27(4):1280–1295. doi: 10.1128/MCB.00882-06

FIG. 9.

FIG. 9.

Cartoon illustrating distinct pathways by which HDAC3 and HDAC4/5/7/9 repress MEF2-dependent transcription. Association with p300, CBP, and PCAF acetylates MEF2 and proximal nucleosomes (gray ovals) to activate transcription. HDAC3 cooperates with SMRT and perhaps also N-CoR to maintain MEF2 and the proximal nucleosomes in a hypoacetylated state for transcriptional repression. In addition to MEF2 and histones, HDAC3 deacetylates coactivators like PCAF, p300, and CBP. HDAC4/5/7/9 repress MEF2-dependent transcription through multiple repression domains, with the deacetylase domain perhaps deacetylating proximal nucleosomes. While it is well established that CaMKs and PKDs act through HDAC4/5/7/9 to activate MEF2 (pathway a), investigation is needed to identify kinases that may act through HDAC3 to regulate MEF2-dependent transcription (pathway b). HDAC3 is widely expressed, and HDAC4/5/7/9 display tissue-specific expression, so pathway b may be the default in most tissues. HDAC4/5/7/9 directly target MEF2, and there is no evidence indicating direct interaction of these HDACs with the coactivators PCAF and p300/CBP. The broken arrow indicates potential cross talk between the two pathways. IKK, IκB kinase; Ac, acetyl group.