BAIT

SWE1

WEE1, tyrosine protein kinase SWE1, L000002248, YJL187C
Protein kinase that regulates the G2/M transition; regulates the G2/M transition by inhibition of Cdc28p kinase activity; localizes to the nucleus and to the daughter side of the mother-bud neck; phosphorylates conserved tyrosine residue in N-terminus of Hsp90 in cell-cycle associated manner, thus modulating the ability of Hsp90 to chaperone a selected clientele; homolog of S. pombe Wee1p; potential Cdc28p substrate
Saccharomyces cerevisiae (S288c)
PREY

BUB1

protein kinase BUB1, L000000196, YGR188C
Protein kinase involved in the cell cycle checkpoint into anaphase; in complex with Mad1p and Bub3p, prevents progression into anaphase in presence of spindle damage; Cdc28p-mediated phosphorylation at Bub1p-T566 is important for degradation in anaphase and adaptation of checkpoint to prolonged mitotic arrest; associates with centromere DNA via Skp1p; involved in Sgo1p relocalization in response to sister kinetochore tension; paralog MAD3 arose from whole genome duplication
Saccharomyces cerevisiae (S288c)

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.

Publication

Rewiring of genetic networks in response to DNA damage.

Bandyopadhyay S, Mehta M, Kuo D, Sung MK, Chuang R, Jaehnig EJ, Bodenmiller B, Licon K, Copeland W, Shales M, Fiedler D, Dutkowski J, Guenole A, van Attikum H, Shokat KM, Kolodner RD, Huh WK, Aebersold R, Keogh MC, Krogan NJ, Ideker T

Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping, we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases, and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They ... [more]

Science Dec. 03, 2010; 330(6009);1385-9 [Pubmed: 21127252]

Quantitative Score

  • -6.305709 [SGA Score]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: colony size (APO:0000063)

Additional Notes

  • An Epistatic MiniArray Profile (E-MAP) approach was used to quantitatively score genetic interactions based on fitness defects estimated from the colony size of double versus single mutants. Genetic interactions were considered significant if they had an S score >= 2.0 for positive interactions (epistatic or suppressor interactions) and S score <= -2.5 for negative interactions (synthetic sick/lethal interactions).

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SWE1 BUB1
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-3.1279BioGRID
222045
SWE1 BUB1
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-6.1824BioGRID
323569
BUB1 SWE1
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
3017836

Curated By

  • BioGRID