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Nucleic Acids Research 2005 33(20):6635-6643; doi:10.1093/nar/gki959
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Published online 30 November 2005

© The Author 2005. 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

A haploid-specific transcriptional response to irradiation in Saccharomyces cerevisiae

G. Mercier, N. Berthault, N. Touleimat, F. Képès1, G. Fourel2, E. Gilson2 and M. Dutreix*

CNRS-UMR 2027, Institut Curie Bât. 110, Centre Universitaire, F-91405 Orsay, France 1Programme d'Épigénomique, Bât. G3 93 rue Henri Rochefort, F- 91000 Evry, France 2Laboratoire de Biologie Moléculaire de la Cellule, l'Ecole Normale Supérieure de Lyon CNRS-ENS UMR5161, 46 allée d'Italie, 69364 Lyon Cedex 07, France

*To whom correspondence should be addressed. Tel: +33 1 69 86 71 86; Fax: +33 1 69 86 94 29; Email: marie.dutreix{at}curie.u-psud.fr

Received August 31, 2005. Revised October 26, 2005. Accepted October 26, 2005.

Eukaryotic cells respond to DNA damage by arresting the cell cycle and modulating gene expression to ensure efficient DNA repair. We used global transcriptome analysis to investigate the role of ploidy and mating-type in inducing the response to damage in various Saccharomyces cerevisiae strains. We observed a response to DNA damage specific to haploid strains that seemed to be controlled by chromatin regulatory proteins. Consistent with these microarray data, we found that mating-type factors controlled the chromatin-dependent silencing of a reporter gene. Both these analyses demonstrate the existence of an irradiation-specific response in strains (haploid or diploid) with only one mating-type factor. This response depends on the activities of Hdf1 and Sir2. Overall, our results suggest the existence of a new regulation pathway dependent on mating-type factors, chromatin structure remodeling, Sir2 and Hdf1 and independent of Mec1 kinase.


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