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Nucleic Acids Research 2006 34(1):286-294; doi:10.1093/nar/gkj402
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Published online 10 January 2006

© The Author 2006. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

Hypoxic stress suppresses RNA polymerase III recruitment and tRNA gene transcription in cardiomyocytes

Isabelle Ernens, Sarah J. Goodfellow, Fiona Innes, Niall S. Kenneth, Louise E. Derblay, Robert J. White and Pamela H. Scott*

Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow Glasgow G12 8QQ, UK

*To whom correspondence should be addressed. Tel: +44 141 330 3703; Fax: +44 141 330 4620; Email: p.scott{at}bio.gla.ac.uk

Received September 29, 2005. Revised December 1, 2005. Accepted December 1, 2005.

RNA polymerase (pol) III transcription decreases when primary cultures of rat neonatal cardiomyocytes are exposed to low oxygen tension. Previous studies in fibroblasts have shown that the pol III-specific transcription factor IIIB (TFIIIB) is bound and regulated by the proto-oncogene product c-Myc, the mitogen-activated protein kinase ERK and the retinoblastoma tumour suppressor protein, RB. The principal function of TFIIIB is to recruit pol III to its cognate gene template, an activity that is known to be inhibited by RB and stimulated by ERK. We demonstrate by chromatin immunoprecipitation (ChIP) that c-Myc also stimulates pol III recruitment by TFIIIB. However, hypoxic conditions cause TFIIIB dissociation from c-Myc and ERK, at the same time as increasing its interaction with RB. Consistent with this, ChIP assays indicate that the occupancy of tRNA genes by pol III is significantly reduced, whereas promoter binding by TFIIIB is undiminished. The data suggest that hypoxia can inhibit pol III transcription by altering the interactions between TFIIIB and its regulators and thus compromising its ability to recruit the polymerase. These effects are independent of cell cycle changes.

Present address: Isabelle Ernens, CRP-Santé, Laboratoire de Recherche Cardio-Vasculaire, CHL-Maternité L-1150, Luxembourg


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