Ronin/Hcf-1 binds to a hyperconserved enhancer element and regulates genes involved in the growth of embryonic stem cells
Name
Dejosez-2010-Ronin_Hcf-1 binds to.pdf
Size
691.8 KB
Format
Adobe PDF
Checksum (MD5)
99a3a87009da4295a329d837fc61c1f5
Author(s)
Dejosez, M.
Frampton, Garrett M.
Whyte, W. A.
Stratton, S. A.
Barton, Michelle C.
Gunaratne, P. H.
Zwaka, T. P.
Levine, Stuart S.
Young, Richard A.
Date Issued
June 2010
Journal
Genes & Development
Publisher
Cold Spring Harbor Laboratory Press
Citation
Dejosez, M., S. S. Levine, G. M. Frampton, W. A. Whyte, S. A. Stratton, M. C. Barton, P. H. Gunaratne, R. A. Young, and T. P. Zwaka. “Ronin/Hcf-1 Binds to a Hyperconserved Enhancer Element and Regulates Genes Involved in the Growth of Embryonic Stem Cells.” Genes & Development 24, no. 14 (July 15, 2010): 1479–1484. © 2010 by Cold Spring Harbor Laboratory Press
Version
Final published version
Abstract
Self-renewing embryonic stem (ES) cells have an exceptional need for timely biomass production, yet the transcriptional control mechanisms responsible for meeting this requirement are largely unknown. We report here that Ronin (Thap11), which is essential for the self-renewal of ES cells, binds with its transcriptional coregulator, Hcf-1, to a highly conserved enhancer element that previously lacked a recognized binding factor. The subset of genes bound by Ronin/Hcf-1 function primarily in transcription initiation, mRNA splicing, and cell metabolism; genes involved in cell signaling and cell development are conspicuously underrepresented in this target gene repertoire. Although Ronin/Hcf-1 represses the expression of some target genes, its activity at promoter sites more often leads to the up-regulation of genes essential to protein biosynthesis and energy production. We propose that Ronin/Hcf-1 controls a genetic program that contributes to the unimpeded growth of ES cells.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Whitehead Institute for Biomedical Research
Terms of Use
Article is available under a Creative Commons license; see publisher’s site for details.
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1101/gad.1935210
