The acetyllysine reader BRD3R promotes human nuclear reprogramming and regulates mitosis

Zhicheng Shao, Ruowen Zhang, Alireza Khodadadi-Jamayran, Bo Chen, Michael R. Crowley, Muhamad A. Festok, David K. Crossman, Tim M. Townes and Kejin Hu ()
Additional contact information
Zhicheng Shao: Stem Cell Institute, University of Alabama at Birmingham
Ruowen Zhang: Stem Cell Institute, University of Alabama at Birmingham
Alireza Khodadadi-Jamayran: Stem Cell Institute, University of Alabama at Birmingham
Bo Chen: Stem Cell Institute, University of Alabama at Birmingham
Michael R. Crowley: Howell and Elizabeth Heflin Center for Genomic Science, University of Alabama at Birmingham
Muhamad A. Festok: Stem Cell Institute, University of Alabama at Birmingham
David K. Crossman: Howell and Elizabeth Heflin Center for Genomic Science, University of Alabama at Birmingham
Tim M. Townes: Stem Cell Institute, University of Alabama at Birmingham
Kejin Hu: Stem Cell Institute, University of Alabama at Birmingham

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: 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.

Date: 2016
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms10869 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10869

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms10869

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().