Loss of Ezh2 promotes a midbrain-to-forebrain identity switch by direct gene derepression and Wnt-dependent regulation

ABSTRACT: Background: Precise spatiotemporal control of gene expression is essential for the establishment of correct cell numbers and identities during brain development. This process involves epigenetic control mechanisms, such as those mediated by the polycomb group protein Ezh2 that catalyzes trimethylation of histone H3K27 (H3K27me3) and thereby represses gene expression. Results: Here we show that Ezh2 plays a crucial role in development and maintenance of the midbrain. Conditional deletion of Ezh2 in the developing midbrain resulted in decreased neural progenitor proliferation, which is associated with derepression of cell cycle inhibitors and negative regulation of Wnt/beta-catenin signaling. Of note, Ezh2 ablation also promoted ectopic expression of a forebrain transcriptional program in

ORGANISM(S): Mus musculus

SUBMITTER: Martina Zemke 

PROVIDER: E-GEOD-74538 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress