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Gene Review

SRS2  -  Srs2p

Saccharomyces cerevisiae S288c

Synonyms: ATP-dependent DNA helicase SRS2, HPR5, J0913, RADH, YJL092W
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Disease relevance of HPR5


High impact information on HPR5

  • Synthetic interactions defined a DNA helicase genetic network and predicted a role for SRS2 in processing damaged replication forks but, unlike SGS1, not in rDNA replication, DNA topology or lagging strand synthesis [6].
  • Overexpressing SRS2 nearly eliminates crossovers, whereas overexpression of RAD51 in srs2Delta cells almost completely eliminates the noncrossover recombination pathway [7].
  • Srs2 and Sgs1-Top3 suppress crossovers during double-strand break repair in yeast [7].
  • We used SGS1 and SRS2, two 3'-->5' DNA helicase genes, as 'queries' to identify their redundant and unique biological functions [6].
  • Mutations in the Saccharomyces cerevisiae gene SRS2 result in the yeast's sensitivity to genotoxic agents, failure to recover or adapt from DNA damage checkpoint-mediated cell cycle arrest, slow growth, chromosome loss, and hyper-recombination [8].

Biological context of HPR5


Associations of HPR5 with chemical compounds

  • Simultaneous deletion of POL32 and SRS2 dramatically decreases cellular viability at 15 degrees C and greatly increases cellular sensitivity to hydroxyurea at the permissive temperature [11].
  • Suppressors of the methyl methanesulfonate sensitivity of Saccharomyces cerevisiae diploids lacking the Srs2 helicase turned out to contain semidominant mutations in Rad5l, a homolog of the bacterial RecA protein [12].
  • Sephacryl gel filtration of pooled fractions containing the SRS2 protein yielded purified SRS2 protein by Coomassie Blue stain of SDS-polyacrylamide gel electrophoresis gels [2].

Physical interactions of HPR5

  • Moreover, Srs2 displays a preference for interacting directly with the SUMO-modified form of PCNA, owing to a specific binding site in its carboxy-terminal tail [13].

Regulatory relationships of HPR5

  • Moreover, srs2 mutants fail to activate Rad53 properly and to slow down DNA replication in response to intra-S DNA damage [14].
  • The simplest hypothesis to account for some of the hpr1 stimulated recombination events is that a heteroduplex DNA intermediate and localized gene conversion are involved. hpr1 stimulated crossover events are independent of intrachromosomal gene conversion events stimulated by the hyper-gene conversion mutation hpr5 [15].

Other interactions of HPR5

  • Saccharomyces cerevisiae mutants lacking two of the three DNA helicases Sgs1, Srs2, and Rrm3 exhibit slow growth that is suppressed by disrupting homologous recombination [16].
  • We propose that the HPR5 gene functions in the RAD6 repair pathway [9].
  • Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51 [17].
  • Two mutants (rad52 and srs2) showed a clear increase in the NHEJ/SSA ratio due to preferential impairment of SSA, but no mutant increased the absolute frequency of NHEJ significantly above the wild-type level [18].
  • The Srs2 helicase plays an important role in creating the recombinogenic substrate(s) processed by the RAD5 and RAD18 gene products [19].
  • The F-box domain of hFBH1, which is not present in Srs2, is crucial for hFBH1 functions in substituting for Srs2 and postreplication repair factors [20].

Analytical, diagnostic and therapeutic context of HPR5


  1. The short life span of Saccharomyces cerevisiae sgs1 and srs2 mutants is a composite of normal aging processes and mitotic arrest due to defective recombination. McVey, M., Kaeberlein, M., Tissenbaum, H.A., Guarente, L. Genetics (2001) [Pubmed]
  2. Purification and characterization of the SRS2 DNA helicase of the yeast Saccharomyces cerevisiae. Rong, L., Klein, H.L. J. Biol. Chem. (1993) [Pubmed]
  3. Metabolic suppressors of trimethoprim and ultraviolet light sensitivities of Saccharomyces cerevisiae rad6 mutants. Lawrence, C.W., Christensen, R.B. J. Bacteriol. (1979) [Pubmed]
  4. The dynamics of homologous pairing during mating type interconversion in budding yeast. Houston, P.L., Broach, J.R. PLoS Genet. (2006) [Pubmed]
  5. The possible roles of the DNA helicase and C-terminal domains in RECQ5/QE: complementation study in yeast. Nakayama, M., Kawasaki, K., Matsumoto, K., Shibata, T. DNA Repair (Amst.) (2004) [Pubmed]
  6. DNA helicase gene interaction network defined using synthetic lethality analyzed by microarray. Ooi, S.L., Shoemaker, D.D., Boeke, J.D. Nat. Genet. (2003) [Pubmed]
  7. Srs2 and Sgs1-Top3 suppress crossovers during double-strand break repair in yeast. Ira, G., Malkova, A., Liberi, G., Foiani, M., Haber, J.E. Cell (2003) [Pubmed]
  8. DNA helicase Srs2 disrupts the Rad51 presynaptic filament. Krejci, L., Van Komen, S., Li, Y., Villemain, J., Reddy, M.S., Klein, H., Ellenberger, T., Sung, P. Nature (2003) [Pubmed]
  9. The hyper-gene conversion hpr5-1 mutation of Saccharomyces cerevisiae is an allele of the SRS2/RADH gene. Rong, L., Palladino, F., Aguilera, A., Klein, H.L. Genetics (1991) [Pubmed]
  10. Mrc1 is required for sister chromatid cohesion to aid in recombination repair of spontaneous damage. Xu, H., Boone, C., Klein, H.L. Mol. Cell. Biol. (2004) [Pubmed]
  11. POL32, a subunit of the Saccharomyces cerevisiae DNA polymerase delta, defines a link between DNA replication and the mutagenic bypass repair pathway. Huang, M.E., de Calignon, A., Nicolas, A., Galibert, F. Curr. Genet. (2000) [Pubmed]
  12. Semidominant mutations in the yeast Rad51 protein and their relationships with the Srs2 helicase. Chanet, R., Heude, M., Adjiri, A., Maloisel, L., Fabre, F. Mol. Cell. Biol. (1996) [Pubmed]
  13. SUMO-modified PCNA recruits Srs2 to prevent recombination during S phase. Pfander, B., Moldovan, G.L., Sacher, M., Hoege, C., Jentsch, S. Nature (2005) [Pubmed]
  14. Srs2 DNA helicase is involved in checkpoint response and its regulation requires a functional Mec1-dependent pathway and Cdk1 activity. Liberi, G., Chiolo, I., Pellicioli, A., Lopes, M., Plevani, P., Muzi-Falconi, M., Foiani, M. EMBO J. (2000) [Pubmed]
  15. Genetic and molecular analysis of recombination events in Saccharomyces cerevisiae occurring in the presence of the hyper-recombination mutation hpr1. Aguilera, A., Klein, H.L. Genetics (1989) [Pubmed]
  16. Suppression of spontaneous genome rearrangements in yeast DNA helicase mutants. Schmidt, K.H., Kolodner, R.D. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  17. Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51. Milne, G.T., Ho, T., Weaver, D.T. Genetics (1995) [Pubmed]
  18. A genomics-based screen for yeast mutants with an altered recombination/end-joining repair ratio. Wilson, T.E. Genetics (2002) [Pubmed]
  19. Genetic interactions between mutants of the 'error-prone' repair group of Saccharomyces cerevisiae and their effect on recombination and mutagenesis. Liefshitz, B., Steinlauf, R., Friedl, A., Eckardt-Schupp, F., Kupiec, M. Mutat. Res. (1998) [Pubmed]
  20. The human F-Box DNA helicase FBH1 faces Saccharomyces cerevisiae Srs2 and postreplication repair pathway roles. Chiolo, I., Saponaro, M., Baryshnikova, A., Kim, J.H., Seo, Y.S., Liberi, G. Mol. Cell. Biol. (2007) [Pubmed]
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