BAIT

SIT4

PPH1, type 2A-related serine/threonine-protein phosphatase SIT4, L000001901, YDL047W
Type 2A-related serine-threonine phosphatase; functions in the G1/S transition of the mitotic cycle; regulator of COPII coat dephosphorylation; required for ER to Golgi traffic; interacts with Hrr25p kinase; cytoplasmic and nuclear protein that modulates functions mediated by Pkc1p including cell wall and actin cytoskeleton organization; similar to human PP6
Saccharomyces cerevisiae (S288c)
PREY

PTK2

STK2, protein kinase PTK2, L000003492, YJR059W
Putative serine/threonine protein kinase; involved in regulation of ion transport across plasma membrane; enhances spermine uptake; PTK2 has a paralog, PTK1, that arose from the whole genome duplication
GO Process (5)
GO Function (1)
GO Component (3)
Saccharomyces cerevisiae (S288c)

Dosage Rescue

A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene.

Publication

Identification of multicopy suppressors of cell cycle arrest at the G1-S transition in Saccharomyces cerevisiae.

Munoz I, Simon E, Casals N, Clotet J, Arino J

Inactivation of HAL3 in the absence of SIT4 function leads to cell cycle arrest at the G(1)-S transition. To identify genes potentially involved in the control of this phase of the cell cycle, a screening for multicopy suppressors of a conditional sit4 hal3 mutant (strain JC002) has been developed. The screening yielded several genes known to perform key roles in ... [more]

Yeast Jan. 30, 2003; 20(2);157-69 [Pubmed: 12518319]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: cell cycle progression through the g1/s phase transition (APO:0000269)

Additional Notes

  • genetic complex
  • overexpression rescues the G1-S cell cycle blockage seen in a Sis2/Sit4 mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SIT4 PTK2
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.

High2.9254BioGRID
324233

Curated By

  • BioGRID