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Nat Commun. 2016 Mar 7;7:10869. doi: 10.1038/ncomms10869.

The acetyllysine reader BRD3R promotes human nuclear reprogramming and regulates mitosis.

Author information

1
Stem Cell Institute, Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama 35294-0024, USA.
2
Department of Genetics, Howell and Elizabeth Heflin Center for Genomic Science, University of Alabama at Birmingham, Birmingham, Alabama 35294-0024, USA.

Abstract

It is well known that both recipient cells and donor nuclei demonstrate a mitotic advantage as observed in the traditional reprogramming with somatic cell nuclear transfer (SCNT). However, it is not known whether a specific mitotic factor plays a critical role in reprogramming. Here we identify an isoform of human bromodomain-containing 3 (BRD3), BRD3R (BRD3 with Reprogramming activity), as a reprogramming factor. BRD3R positively regulates mitosis during reprogramming, upregulates a large set of mitotic genes at early stages of reprogramming, and associates with mitotic chromatin. Interestingly, a set of the mitotic genes upregulated by BRD3R constitutes a pluripotent molecular signature. The two BRD3 isoforms display differential binding to acetylated histones. Our results suggest a molecular interpretation for the mitotic advantage in reprogramming and show that mitosis may be a driving force of reprogramming.

PMID:
26947130
PMCID:
PMC4786677
DOI:
10.1038/ncomms10869
[Indexed for MEDLINE]
Free PMC Article
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