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)

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.

Publication

A Rad51-independent pathway promotes single-strand template repair in gene editing.

Gallagher DN, Pham N, Tsai AM, Janto NV, Choi J, Ira G, Haber JE

The Rad51/RecA family of recombinases perform a critical function in typical repair of double-strand breaks (DSBs): strand invasion of a resected DSB end into a homologous double-stranded DNA (dsDNA) template sequence to initiate repair. However, repair of a DSB using single stranded DNA (ssDNA) as a template, a common method of CRISPR/Cas9-mediated gene editing, is Rad51-independent. We have analyzed the ... [more]

PLoS Genet Dec. 01, 2019; 16(10);e1008689 [Pubmed: 33057349]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: chromosome/plasmid maintenance (APO:0000143)

Additional Notes

  • deleting RDH54 suppressed srs2 mutant's defect in SSTR

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
Synthetic Rescue
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.

Low-BioGRID
2544054

Curated By

  • BioGRID