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

MSS4

1-phosphatidylinositol-4-phosphate 5-kinase, L000001203, YDR208W
Phosphatidylinositol-4-phosphate 5-kinase; involved in actin cytoskeleton organization and cell morphogenesis; multicopy suppressor of stt4 mutation
GO Process (2)
GO Function (1)
GO Component (2)

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

A phosphatidylinositol-transfer protein and phosphatidylinositol-4-phosphate 5-kinase control Cdc42 to regulate the actin cytoskeleton and secretory pathway in yeast.

Yakir-Tamang L, Gerst JE

The actin cytoskeleton rapidly depolarizes in yeast secretory (sec) mutants at restrictive temperatures. Thus, an unknown signal conferred upon secretion is necessary for actin polarity and exocytosis. Here, we show that a phosphatidylinositol (PI) transfer protein, Sfh5, and a phosphatidylinositol-4-phosphate 5-kinase, Mss4, facilitate Cdc42 activation to concomitantly regulate both actin and protein trafficking. Defects in Mss4 function led to actin ... [more]

Mol. Biol. Cell Aug. 01, 2009; 20(15);3583-97 [Pubmed: 19477927]

Throughput

  • Low Throughput

Ontology Terms

  • inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
MSS4 SAC1
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.

High2.9673BioGRID
324463

Curated By

  • BioGRID