BAIT
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
GO Process (5)
GO Function (2)
GO Component (4)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
PREY
ROT1
L000003404, YMR200W
Molecular chaperone involved in protein folding in ER; mutation causes defects in cell wall synthesis and lysis of autophagic bodies, suppresses tor2 mutations, and is synthetically lethal with kar2-1 and with rot2 mutations; involved in N-linked glycosylation and O-mannosylation; transmembrane helix Ser250 is essential for Rot1p to interact with other membrane components and exert its functional role, avoiding exposure of Ser H-bonding group at lipid-exposed surface
GO Process (8)
GO Function (1)
GO Component (2)
Gene Ontology Biological Process
- 'de novo' protein folding [IMP, IPI]
- budding cell apical bud growth [IGI, IMP]
- endoplasmic reticulum unfolded protein response [IGI]
- establishment or maintenance of actin cytoskeleton polarity [IMP]
- fungal-type cell wall biogenesis [IMP]
- protein N-linked glycosylation [IGI, IPI]
- protein O-linked mannosylation [IGI]
- protein folding [IGI]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
Saccharomyces cerevisiae Genetics Predicts Candidate Therapeutic Genetic Interactions at the Mammalian Replication Fork.
The concept of synthetic lethality has gained popularity as a rational guide for predicting chemotherapeutic targets based on negative genetic interactions between tumor-specific somatic mutations and a second-site target gene. One hallmark of most cancers that can be exploited by chemotherapies is chromosome instability (CIN). Because chromosome replication, maintenance, and segregation represent conserved and cell-essential processes, they can be modeled ... [more]
G3 (Bethesda) Feb. 01, 2013; 3(2);273-82 [Pubmed: 23390603]
Quantitative Score
- 0.04451561 [SGA Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Additional Notes
- SGA analysis for synthetic lethal interactions between mutations whose human orthologs are found to be mutated in cancers, and the deletion mutant collection, where the interaction probability P < 0.05
Curated By
- BioGRID