Difference between revisions of "YLR032W"
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| − | '''Description of YLR032W:''' | + | '''Description of YLR032W:''' DNA helicase proposed to promote replication fork regression during postreplication repair by template switching; contains RING finger domain<ref name='S000124451'>Blastyak A, et al. (2007) Yeast rad5 protein required for postreplication repair has a DNA helicase activity specific for replication fork regression. Mol Cell 28(1):167-75 {{SGDpaper|S000124451}} PMID 17936713</ref><ref name='S000071643'>Kiakos K, et al. (2002) Saccharomyces cerevisiae RAD5 influences the excision repair of DNA minor groove adducts. J Biol Chem 277(46):44576-81 {{SGDpaper|S000071643}} PMID 12226100</ref><ref name='S000069690'>Torres-Ramos CA, et al. (2002) Requirement of RAD5 and MMS2 for postreplication repair of UV-damaged DNA in Saccharomyces cerevisiae. Mol Cell Biol 22(7):2419-26 |
| − | + | {{SGDpaper|S000069690}} PMID 11884624</ref> | |
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Revision as of 06:21, 26 February 2009
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| Systematic name | YLR032W |
| Gene name | RAD5 |
| Aliases | REV2, SNM2 |
| Feature type | ORF, Verified |
| Coordinates | Chr XII:204992..208501 |
| Primary SGDID | S000004022 |
Description of YLR032W: DNA helicase proposed to promote replication fork regression during postreplication repair by template switching; contains RING finger domain[1][2][3]
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Community Commentary
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- The rad5-G535R missense mutation does not cause any growth defect or gamma-ray sensitive phenotype. However, rad5-G535R strains displayed increased sensitivity to UV light at high doses when compared to wild-type strains, and rad52 rad5-G535R double mutants were more sensitive to UV light when compared to RAD52 rad5-G535R and rad52 RAD5 single mutants. Levels of direct repeat recombination were not affected by the rad-G535R allele in rad1, rad52 or rfa1-D288Y backgrounds. The efficiency of plasmid gap repair (outline of the system: Bartsch S. et al, Mol. Cell. Biol. 2000 Feb.; 20(4): 1194-1205) was not significantly affected by the rad5-G535R allele. Also, the rad-G535R allele had no effect on the proportion of crossover and non-crossover events independent of whether the DNA donor for gap repair was of chromosomal or plasmid origin. These unpublished findings support the hypothesis that the weak DNA repair phenotype conferred by the rad5-G535R mutation is caused indirectly through interaction either with proteins of the transcription machinery or with chromatin but not by direct involvement in recombination (Stephan Bartsch and Naz Erdeniz, April 2000, unpublished).
- A rad5-G535R strain did not show detectable chronic low dose ultraviolet light (CLUV) sensitivity, whereas the ATPase-deficient rad5-K538A mutant showed a CLUV hypersensitivity similar to that observed in a rad5 deletion mutant (Hishida T. et al.,(2008) Nature Online doi: 10.1038/nature07580; Hishida T., personal communication; Stephan Bartsch, December 2008)
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References
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- ↑ Blastyak A, et al. (2007) Yeast rad5 protein required for postreplication repair has a DNA helicase activity specific for replication fork regression. Mol Cell 28(1):167-75 SGD PMID 17936713
- ↑ Kiakos K, et al. (2002) Saccharomyces cerevisiae RAD5 influences the excision repair of DNA minor groove adducts. J Biol Chem 277(46):44576-81 SGD PMID 12226100
- ↑ Torres-Ramos CA, et al. (2002) Requirement of RAD5 and MMS2 for postreplication repair of UV-damaged DNA in Saccharomyces cerevisiae. Mol Cell Biol 22(7):2419-26 SGD PMID 11884624
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References
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