GSE65082
Ezh2 maintains proliferation, transcriptional integrity, and the timing of late differentiation during mouse retina development
We investigated the gene expression profile changes after Ezh2 conditional knockout in the mouse retina at E16.5. Loss of Ezh2 leads to up-regulation of PRC2 targeted genes including cell cycle regulators and multiple genes which are not normally expressed in the retina, including many Hox genes. Loss of Ezh2 resulted in a dramatic decline in progenitor proliferation by postnatal day 3, such that there is an early end to neurogenesis, and disruption of laminar organization. Although there are only minor effects on embryonic retinal development, there is accelerated differentiation of several late born cell types postnatally, including photoreceptors and Mueller glia, which become reactive by postnatal day 14. Overall design: Peripheral retina was dissected at E16.5 from Pax6alpha-Cre:Ezh2fl/+ and Pax6alpha-Cre:Ezh2fl/null mouse embryos. Total RNA was purified and RNA deep sequencing was done using 4 controls and 4 conditional knockout samples.