DOT1L promotes progenitor proliferation and primes neuronal layer identity in the developing cerebral cortex.

ABSTRACT: Cortical development is controlled by transcriptional programs, which are orchestrated by transcription factors. Yet, stable inheritance of spatio-temporal activity of factors influencing cell fate and localization in different layers is only partly understood. Here we find that deletion of Dot1l in the murine telencephalon leads to cortical layering defects, indicating DOT1L activity and chromatin methylation at H3K79 impact on the cell cycle, and influence transcriptional programs conferring upper layer identity in early progenitors. Specifically, DOT1L prevents premature differentiation by increasing expression of genes that regulate asymmetric cell division (Vangl2, Cenpj). Loss of DOT1L results in reduced numbers of progenitors expressing genes including SoxB1 gene family members. Los

SUBMITTER: Franz H 

PROVIDER: S-EPMC6326801 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature