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The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express  Hdac4 ,  5 , and  7  but not  Hdac9 . Here, we show that a transcription factor regulated genetic compensatory mechanism within this family of proteins, blocks negative regulators of myelination ensuring peripheral nerve developmental myelination and remyelination after injury. Thus, when  Hdac4  and  5  are knocked-out from Schwann cells in mice, a JUN-dependent mechanism induces the compensatory overexpression of  Hdac7  permitting, although with a delay, the formation of the myelin sheath. When  Hdac4 ,  5 , and  7  are simultaneously removed, the myocyte-specific enhancer-factor d (MEF2D) binds to the promoter and induces the de novo expression of  Hdac9 , and although several melanocytic lineage genes are misexpressed and Remak bundle structure is disrupted, myelination proceeds after a long delay. Thus, our data unveil a finely tuned compensatory mechanism within the class IIa  Hdac  family, coordinated by distinct transcription factors, that guarantees the ability of Schwann cells to myelinate during development and remyelinate after nerve injury.

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A genetic compensatory mechanism regulated by  Jun  and  Mef2d  modulates the expression of distinct class IIa  Hdacs  to ensure peripheral nerve myelination and repair