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Originally published as Genetics Published Articles Ahead of Print on June 18, 2006.
Genetics, Vol. 173, 1951-1968, August 2006, Copyright © 2006
doi:10.1534/genetics.106.057794
The RAD6/BRE1 Histone Modification Pathway in Saccharomyces Confers Radiation Resistance Through a RAD51-Dependent Process That Is Independent of RAD18
John C. Game*,1,
Marsha S. Williamson*,
Tatiana Spicakova
and
J. Martin Brown
* Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720 and Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305
1 Corresponding author: Donner Laboratory, Room 326, Lawrence Berkeley National Laboratory, 1 Cyclotron Rd., Berkeley, CA 94720.
E-mail: jcgame{at}lbl.gov
We examine ionizing radiation (IR) sensitivity and epistasis relationships of several Saccharomyces mutants affecting post-translational modifications of histones H2B and H3. Mutants bre1
, lge1, and rtf1, defective in histone H2B lysine 123 ubiquitination, show IR sensitivity equivalent to that of the dot1 mutant that we reported on earlier, consistent with published findings that Dot1p requires H2B K123 ubiquitination to fully methylate histone H3 K79. This implicates progressive K79 methylation rather than mono-methylation in IR resistance. The set2 mutant, defective in H3 K36 methylation, shows mild IR sensitivity whereas mutants that abolish H3 K4 methylation resemble wild type. The dot1, bre1, and lge1 mutants show epistasis for IR sensitivity. The paf1 mutant, also reportedly defective in H2B K123 ubiquitination, confers no sensitivity. The rad6, rad51null, rad50, and rad9 mutations are epistatic to bre1 and dot1, but rad18 and rad5 show additivity with bre1, dot1, and each other. The bre1 rad18 double mutant resembles rad6 in sensitivity; thus the role of Rad6p in ubiquitinating H2B accounts for its extra sensitivity compared to rad18. We conclude that IR resistance conferred by BRE1 and DOT1 is mediated through homologous recombinational repair, not postreplication repair, and confirm findings of a G1 checkpoint role for the RAD6/BRE1/DOT1 pathway.
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