Interaction between checkpoint genes RAD9, RAD17, RAD24, RAD53, and genes SRM5/CDC28, SRM8/NET1, and SRM12/HFI1 involved in the determination of yeast Saccharomyces cerevisiae sensitivity to ionizing radiation

Interaction between checkpoint genes RAD9, RAD17, RAD24, RAD53, and genes SRM5/CDC28, SRM8/NET1,... Analysis of radiosensitivity of double mutants in the yeast Saccharomyces cerevisiae revealed that checkpoint genes RAD9, RAD17, RAD24, and RAD53 along with genes CDC28 and NET1 belong to one epistasis group designated the RAD9 group. The use of srm mutations allowed the demonstration of a branched RAD9-dependent pathway of cell radioresistance. Mutation cdc28-srm is hypostatic to rad9Δ, rad17Δ, and rad24Δ being additive with rad53. Mutation net1-srm is hypostatic to rad9Δ and rad53 but additively enhance the effects of mutations rad17Δ and rad24Δ. Gene SRM12/HFI1 is not a member of the RAD9 group. Mutation in gene hfi1-srm manifests the additive effect on mutations rad24Δ and rad9Δ. The analyzed genes can also participate in minor mechanisms of radioresistance that are relatively independent of the above RAD9-dependent mechanism. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

Interaction between checkpoint genes RAD9, RAD17, RAD24, RAD53, and genes SRM5/CDC28, SRM8/NET1, and SRM12/HFI1 involved in the determination of yeast Saccharomyces cerevisiae sensitivity to ionizing radiation

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Publisher
SP MAIK Nauka/Interperiodica
Copyright
Copyright © 2008 by MAIK Nauka
Subject
Biomedicine; Microbial Genetics and Genomics; Animal Genetics and Genomics; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1134/S1022795408080048
Publisher site
See Article on Publisher Site

Abstract

Analysis of radiosensitivity of double mutants in the yeast Saccharomyces cerevisiae revealed that checkpoint genes RAD9, RAD17, RAD24, and RAD53 along with genes CDC28 and NET1 belong to one epistasis group designated the RAD9 group. The use of srm mutations allowed the demonstration of a branched RAD9-dependent pathway of cell radioresistance. Mutation cdc28-srm is hypostatic to rad9Δ, rad17Δ, and rad24Δ being additive with rad53. Mutation net1-srm is hypostatic to rad9Δ and rad53 but additively enhance the effects of mutations rad17Δ and rad24Δ. Gene SRM12/HFI1 is not a member of the RAD9 group. Mutation in gene hfi1-srm manifests the additive effect on mutations rad24Δ and rad9Δ. The analyzed genes can also participate in minor mechanisms of radioresistance that are relatively independent of the above RAD9-dependent mechanism.

Journal

Russian Journal of GeneticsSpringer Journals

Published: Aug 22, 2008

References

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