Difference between revisions of "YLR032W"

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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: [http://www.yeastgenome.org/cgi-bin/reference/reference.pl?dbid=S000049982 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 These unpublished findings support the hypothesis that the weak DNA repair phenotype conferred by the ''rad-G535R'' mutation is caused indirectly through interaction either with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or with chromatin but not by direct involvement in recombination (Stephan Bartsch and Naz Erdeniz, April 2000, unpublished).
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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: [http://www.yeastgenome.org/cgi-bin/reference/reference.pl?dbid=S000049982 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 These unpublished findings support the hypothesis that the weak DNA repair phenotype conferred by the ''rad5-G535R'' mutation is caused indirectly through interaction either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 delta'' mutant ([http://www.yeastgenome.org/cgi-bin/reference/reference.pl?dbid=S000128822 Hishida T. ''et al.''],(2008) Nature Online doi: 10.1038/nature07580; Hishida T., personal communication; Stephan Bartsch, December 2008)
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* 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 ([http://www.yeastgenome.org/cgi-bin/reference/reference.pl?dbid=S000128822 Hishida T. ''et al.''],(2008) Nature Online doi: 10.1038/nature07580; Hishida T., personal communication; Stephan Bartsch, December 2008)
  
 
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Revision as of 09:01, 2 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: Single-stranded DNA-dependent ATPase, involved in postreplication repair; 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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  1. 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
  2. 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
  3. Johnson RE, et al. (1994) Yeast DNA repair protein RAD5 that promotes instability of simple repetitive sequences is a DNA-dependent ATPase. J Biol Chem 269(45):28259-62 SGD PMID 7961763

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