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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. Loss of DOT1L also leads to altered cortical distribution of deep layer neurons that express either TBR1, CTIP2 or SOX5, and less activation of transcriptional programs that are characteristic for upper layer neurons (Satb2, Pou3f3, Cux2, SoxC family members). Data from three different mouse models suggest that DOT1L balances transcriptional programs necessary for proper neuronal composition and distribution in the six cortical layers. Furthermore, because loss of DOT1L in the pre-neurogenic phase of development impairs specifically generation of SATB2-expressing upper layer neurons, our data suggest that DOT1L primes upper layer identity in cortical progenitors.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Franz H,Villarreal A,Heidrich S,Videm P,Kilpert F,Mestres I,Calegari F,Backofen R,Manke T,Vogel T

doi

10.1093/nar/gky953

subject

Has Abstract

pub_date

2019-01-10 00:00:00

pages

168-183

issue

1

eissn

0305-1048

issn

1362-4962

pii

5133670

journal_volume

47

pub_type

杂志文章

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