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Epigenetic predisposition is thought to critically contribute to adult-onset disorders, such as retinal neurodegeneration. The histone methyltransferase, enhancer of zeste homolog 2 ( Ezh2 ), is transiently expressed in the perinatal retina, particularly enriched in retinal ganglion cells (RGCs). We previously showed that embryonic deletion of  Ezh2  from retinal progenitors led to progressive photoreceptor degeneration throughout life, demonstrating a role for embryonic predisposition of  Ezh2- mediated repressive mark in maintaining the survival and function of photoreceptors in the adult. Enrichment of  Ezh2  in RGCs leads to the question if  Ezh2  also mediates gene expression and function in postnatal RGCs, and if its deficiency changes RGC susceptibility to cell death under injury or disease in the adult. To test this, we generated mice carrying targeted deletion of  Ezh2  from RGC progenitors driven by  Math5-Cre  (mKO). mKO mice showed no detectable defect in RGC development, survival, or cell homeostasis as determined by physiological analysis, live imaging, histology, and immunohistochemistry. Moreover, RGCs of  Ezh2  deficient mice revealed similar susceptibility against glaucomatous and acute optic nerve trauma-induced neurodegeneration compared to littermate floxed or wild-type control mice. In agreement with the above findings, analysis of RNA sequencing of RGCs purified from  Ezh2  deficient mice revealed few gene changes that were related to RGC development, survival and function. These results, together with our previous report, support a cell lineage-specific mechanism of  Ezh2- mediated gene repression, especially those critically involved in cellular function and homeostasis.

Ezh2 does not mediate retinal ganglion cell homeostasis or their susceptibility to injury