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Genetics, Vol. 173, 1951-1968, August 2006, Copyright © 2006
doi:10.1534/genetics.106.057794
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* 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
, 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. This article has been cited by other articles:
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S. R. Bartz, Z. Zhang, J. Burchard, M. Imakura, M. Martin, A. Palmieri, R. Needham, J. Guo, M. Gordon, N. Chung, et al. Small Interfering RNA Screens Reveal Enhanced Cisplatin Cytotoxicity in Tumor Cells Having both BRCA Network and TP53 Disruptions Mol. Cell. Biol., December 15, 2006; 26(24): 9377 - 9386. [Abstract] [Full Text] [PDF] |
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