BAIT

SAC1

RSD1, phosphatidylinositol-3-phosphatase SAC1, L000001790, YKL212W
Phosphatidylinositol phosphate (PtdInsP) phosphatase; involved in hydrolysis of PtdIns[4]P in the early and medial Golgi; regulated by interaction with Vps74p; ER localized transmembrane protein which cycles through the Golgi; involved in protein trafficking and processing, secretion, and cell wall maintenance; regulates sphingolipid biosynthesis through the modulation of PtdIns(4)P metabolism
Saccharomyces cerevisiae (S288c)
PREY

PTC1

CWH47, KCS2, TPD1, type 2C protein phosphatase PTC1, L000000890, L000001523, YDL006W
Type 2C protein phosphatase (PP2C); dephosphorylates Hog1p, inactivating osmosensing MAPK cascade; involved in Fus3p activation during pheromone response; deletion affects precursor tRNA splicing, mitochondrial inheritance, and sporulation
Kinome Project (Sc)
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

Regulation of intracellular phosphatidylinositol-4-phosphate by the Sac1 lipid phosphatase.

Tahirovic S, Schorr M, Mayinger P

Phosphatidylinositol 4-phosphate (PtdIns(4)P) regulates diverse cellular processes, such as actin cytoskeletal organization, Golgi trafficking and vacuolar biogenesis. Synthesis and turnover of PtdIns(4)P is mediated by a set of specific lipid kinases and phosphatases. Here we show that the polyphosphoinositide phosphatase Sac1p has a central role in compartment-specific regulation of PtdIns(4)P. We have found that sac1Delta mutants show pleiotropic, synthetically lethal ... [more]

Traffic Feb. 01, 2005; 6(2);116-30 [Pubmed: 15634212]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SAC1 PTC1
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-11.6617BioGRID
579344

Curated By

  • BioGRID