Difference between revisions of "YLR032W"

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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://db.yeastgenome.org/cgi-bin/locus.pl?locus=YLR032W YLR032W]  
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Systematic name''' || [http://www.yeastgenome.org/cgi-bin/locus.pl?dbid=S000004022 YLR032W]  
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''RAD5 ''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Gene name'''        ||''RAD5 ''
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
 
|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Coordinates'''
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|nowrap| Chr XII:204992..208501
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|nowrap| Chr XII:204991..208500
 
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|valign="top" nowrap bgcolor="{{SGDblue}}"| '''Primary SGDID'''          || S000004022
 
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'''Description of {{PAGENAME}}:''' Single-stranded DNA-dependent ATPase, involved in postreplication repair; contains RING finger domain<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><ref name='S000041761'>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
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'''Description of YLR032W:''' DNA helicase proposed to promote replication fork regression during postreplication repair by template switching; RING finger containing ubiquitin ligase; stimulates the synthesis of free and PCNA-bound polyubiquitin chains by Ubc13p-Mms2p<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='S000131367'>Carlile CM, et al. (2009) Synthesis of free and proliferating cell nuclear antigen-bound polyubiquitin chains by the RING E3 ubiquitin ligase Rad5. J Biol Chem 284(43):29326-34 {{SGDpaper|S000131367}} PMID 19706603</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
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{{SGDpaper|S000069690}} PMID 11884624</ref>
 
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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: [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).
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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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(''check and see also [[CommunityW303.html|detailed notes]] from Rodney Rothstein and Stephan Bartsch'')
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Specifically higher expression in carbon limited chemostat cultures versus carbon excess.
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<ref>Boer VM, et al. (2003) The genome-wide transcriptional responses of Saccharomyces cerevisiae grown on glucose in aerobic chemostat cultures limited for carbon, nitrogen, phosphorus, or sulfur.
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J Biol Chem 278(5):3265-74</ref>
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==References==
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==References==
 
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Latest revision as of 06:45, 23 January 2012

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Systematic name YLR032W
Gene name RAD5
Aliases REV2, SNM2
Feature type ORF, Verified
Coordinates Chr XII:204991..208500
Primary SGDID S000004022


Description of YLR032W: DNA helicase proposed to promote replication fork regression during postreplication repair by template switching; RING finger containing ubiquitin ligase; stimulates the synthesis of free and PCNA-bound polyubiquitin chains by Ubc13p-Mms2p[1][2][3][4]




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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)

(check and see also detailed notes from Rodney Rothstein and Stephan Bartsch)



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References

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  1. ↑ 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
  2. ↑ Carlile CM, et al. (2009) Synthesis of free and proliferating cell nuclear antigen-bound polyubiquitin chains by the RING E3 ubiquitin ligase Rad5. J Biol Chem 284(43):29326-34 SGD PMID 19706603
  3. ↑ 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
  4. ↑ 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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