BAIT

SGS1

ATP-dependent DNA helicase SGS1, L000001877, YMR190C
RecQ family nucleolar DNA helicase; role in genome integrity maintenance; regulates chromosome synapsis and meiotic joint molecule/crossover formation; stimulates DNA catenation/decatenation activity of Top3p; potential repressor of a subset of rapamycin responsive genes; rapidly lost in response to rapamycin in Rrd1p-dependent manner; similar to human BLM and WRN proteins implicated in Bloom and Werner syndromes; forms nuclear foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

SHU2

YDR078C
Component of Shu complex (aka PCSS complex); Shu complex also includes Psy3, Csm2, Shu1, and promotes error-free DNA repair, Shu complex mediates inhibition of Srs2p function; promotes formation of Rad51p filaments
GO Process (4)
GO Function (0)
GO Component (2)
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

Shu proteins promote the formation of homologous recombination intermediates that are processed by Sgs1-Rmi1-Top3.

Mankouri HW, Ngo HP, Hickson ID

CSM2, PSY3, SHU1, and SHU2 (collectively referred to as the SHU genes) were identified in Saccharomyces cerevisiae as four genes in the same epistasis group that suppress various sgs1 and top3 mutant phenotypes when mutated. Although the SHU genes have been implicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains poorly understood. Here, we have identified ... [more]

Mol. Biol. Cell Oct. 01, 2007; 18(10);4062-73 [Pubmed: 17671161]

Throughput

  • Low Throughput

Ontology Terms

  • chromosome/plasmid maintenance (APO:0000143)

Additional Notes

  • Accumulation of abnormal DNA replication intermediates (X-molecules) in MMS-treated sgs1 cells is attenuated by mutations in the SHU (csm2, psy3, shu1, shu2) genes.
  • Mutations in the SHU genes (CSM2, PSY3, SHU1, or SHU2) suppress the HU sensitivity of sgs1 mutants.

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SGS1 SHU2
Positive Genetic
Positive Genetic

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

High0.1064BioGRID
2605048
SGS1 SHU2
Positive Genetic
Positive Genetic

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

Low0.198BioGRID
560475
SGS1 SHU2
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
1255935
SGS1 SHU2
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
547254
SGS1 SHU2
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
858435
SGS1 SHU2
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
164520

Curated By

  • BioGRID