Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

KDM5B regulates embryonic stem cell self-renewal and represses cryptic intragenic transcription.

The EMBO journal | Apr 20, 2011

http://www.ncbi.nlm.nih.gov/pubmed/21448134

Although regulation of histone methylation is believed to contribute to embryonic stem cell (ESC) self-renewal, the mechanisms remain obscure. We show here that the histone H3 trimethyl lysine 4 (H3K4me3) demethylase, KDM5B, is a downstream Nanog target and critical for ESC self-renewal. Although KDM5B is believed to function as a promoter-bound repressor, we find that it paradoxically functions as an activator of a gene network associated with self-renewal. ChIP-Seq reveals that KDM5B is predominantly targeted to intragenic regions and that it is recruited to H3K36me3 via an interaction with the chromodomain protein MRG15. Depletion of KDM5B or MRG15 increases intragenic H3K4me3, increases cryptic intragenic transcription, and inhibits transcriptional elongation of KDM5B target genes. We propose that KDM5B activates self-renewal-associated gene expression by repressing cryptic initiation and maintaining an H3K4me3 gradient important for productive transcriptional elongation.

Pubmed ID: 21448134 RIS Download

Mesh terms: Animals | Biological Markers | Blotting, Western | Cell Cycle | Cell Proliferation | Cells, Cultured | Chromatin | Chromatin Immunoprecipitation | DNA Methylation | DNA-Binding Proteins | Embryonic Stem Cells | Gene Expression Profiling | Gene Expression Regulation | Histones | Homeodomain Proteins | Jumonji Domain-Containing Histone Demethylases | Lysine | Mice | Oligonucleotide Array Sequence Analysis | RNA, Messenger | RNA, Small Interfering | Reverse Transcriptase Polymerase Chain Reaction | Transcription, Genetic

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.