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Histone Deacetylase 9 couples neuronal activity to muscle chromatin acetylation and gene expression

Abstract : Electrical activity arising from motor innervation influences skeletal muscle physiology by controlling the expression of many muscle genes, including acetylcholine receptor (AChR) subunits genes. How electrical activity is converted into a transcriptional response remains largely unknown. We show that motor innervation controls chromatin acetylation in skeletal muscle and that histone deacetylase 9 (HDAC9) is a signal-responsive transcriptional repressor, which is down-regulated upon denervation, with consequent up-regulation of chromatin acetylation and AChR expression. Forced expression of HDAC9 in denervated muscle prevents up-regulation of activity-dependent genes and chromatin acetylation by linking MEF2 and class I HDACs. Conversely, HDAC9 null mice are supersensitive to denervation-induced changes in gene expression and display chromatin hyperacetylation, and delayed perinatal downregulation of myogenin, an activator of AChR genes. These findings reveal a molecular mechanism to account for the control of chromatin acetylation by presynaptic neurons and activity-dependent regulation of skeletal muscle genes by motor innervation.
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Contributor : Laurent Schaeffer Connect in order to contact the contributor
Submitted on : Tuesday, December 11, 2007 - 2:50:29 PM
Last modification on : Friday, November 6, 2020 - 4:07:12 AM


  • HAL Id : ensl-00182187, version 1
  • PRODINRA : 251045



Alexandre Mejat, Francis Ramond, Rhonda Bassel Duby, Saadi Khochbin, Eric N Olson, et al.. Histone Deacetylase 9 couples neuronal activity to muscle chromatin acetylation and gene expression. Nature Neuroscience, Nature Publishing Group, 2005, 8 (3), pp.313-321. ⟨ensl-00182187⟩



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