BAIT

SRS2

HPR5, DNA helicase SRS2, RADH1, RADH, L000000809, L000001578, YJL092W
DNA helicase and DNA-dependent ATPase; involved in DNA repair and checkpoint recovery, needed for proper timing of commitment to meiotic recombination and transition from Meiosis I to II; blocks trinucleotide repeat expansion; affects genome stability; disassembles Rad51p nucleoprotein filaments during meiotic recombination; functional homolog of human RTEL1
Saccharomyces cerevisiae (S288c)
PREY

RDH54

TID1, DNA-dependent ATPase RDH54, L000002988, L000003224, YBR073W
DNA-dependent ATPase; DNA recombination/repair translocase, supercoils DNA and promotes DNA strand opening; stimulates strand exchange by modifying dsDNA topology; involved in recombinational repair of DNA double-strand breaks (DSBs) during mitosis and meiosis; phosphorylated in Mec1p-, Rad53p-dependent way in response to one DSB; contributes to remodelling of nucleosomes; proposed to be involved in crossover interference; interacts with Dmc1p; stimulates Dmc1p and Rad51p
Saccharomyces cerevisiae (S288c)

Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Publication

Tight Regulation of Srs2 Helicase Activity Is Crucial for Proper Functioning of DNA Repair Mechanisms.

Bronstein A, Bramson S, Shemesh K, Liefshitz B, Kupiec M

Proper DNA damage repair is one of the most vital and fundamental functions of every cell. Several different repair mechanisms exist to deal with various types of DNA damage, in various stages of the cell cycle and under different conditions. Homologous recombination is one of the most important repair mechanisms in all organisms. Srs2, a regulator of homologous recombination, is ... [more]

G3 (Bethesda) Dec. 04, 2017; 8(5);1615-1626 [Pubmed: 29531123]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)
  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • deletion of RDH54 abolished the sensitization caused by pSRS2

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SRS2 RDH54
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.3315BioGRID
390684
RDH54 SRS2
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.3315BioGRID
357586
SRS2 RDH54
Phenotypic Suppression
Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Low-BioGRID
3403503

Curated By

  • BioGRID