E2F4 regulates transcriptional activation in mouse embryonic stem cells independently of the RB family

Jenny Hsu, Julia Arand, Andrea Chaikovsky, Nancie A. Mooney, Janos Demeter, Caileen M. Brison, Romane Oliverio, Hannes Vogel, Seth M. Rubin, Peter K. Jackson and Julien Sage ()
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Jenny Hsu: 300 Pasteur Drive, Stanford University
Julia Arand: 300 Pasteur Drive, Stanford University
Andrea Chaikovsky: 300 Pasteur Drive, Stanford University
Nancie A. Mooney: 300 Pasteur Drive, Stanford University
Janos Demeter: 300 Pasteur Drive, Stanford University
Caileen M. Brison: University of California
Romane Oliverio: 300 Pasteur Drive, Stanford University
Hannes Vogel: 300 Pasteur Drive, Stanford University
Seth M. Rubin: University of California
Peter K. Jackson: 300 Pasteur Drive, Stanford University
Julien Sage: 300 Pasteur Drive, Stanford University

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract E2F transcription factors are central regulators of cell division and cell fate decisions. E2F4 often represents the predominant E2F activity in cells. E2F4 is a transcriptional repressor implicated in cell cycle arrest and whose repressive activity depends on its interaction with members of the RB family. Here we show that E2F4 is important for the proliferation and the survival of mouse embryonic stem cells. In these cells, E2F4 acts in part as a transcriptional activator that promotes the expression of cell cycle genes. This role for E2F4 is independent of the RB family. Furthermore, E2F4 functionally interacts with chromatin regulators associated with gene activation and we observed decreased histone acetylation at the promoters of cell cycle genes and E2F targets upon loss of E2F4 in RB family-mutant cells. Taken together, our findings uncover a non-canonical role for E2F4 that provide insights into the biology of rapidly dividing cells.

Date: 2019
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DOI: 10.1038/s41467-019-10901-x

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