BAIT

SCH9

HRM2, KOM1, serine/threonine protein kinase SCH9, L000001810, YHR205W
AGC family protein kinase; functional ortholog of mammalian S6 kinase; phosphorylated by Tor1p and required for TORC1-mediated regulation of ribosome biogenesis, translation initiation, and entry into G0 phase; involved in transactivation of osmostress-responsive genes; regulates G1 progression, cAPK activity and nitrogen activation of the FGM pathway; integrates nutrient signals and stress signals from sphingolipids to regulate lifespan
Saccharomyces cerevisiae (S288c)
PREY

GPB2

KRH1, YAL056W
Multistep regulator of cAMP-PKA signaling; inhibits PKA downstream of Gpa2p and Cyr1p, thereby increasing cAMP dependency; inhibits Ras activity through direct interactions with Ira1p/2p; regulated by G-alpha protein Gpa2p; GPB2 has a paralog, GPB1, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)

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.

Publication

Identification and Characterization of Rapidly Accumulating sch9? Suppressor Mutations in Saccharomyces cerevisiae.

Peterson PP, Liu Z

Nutrient sensing is important for cell growth, aging, and longevity. In Saccharomyces cerevisiae, Sch9, an AGC-family protein kinase, is a major nutrient sensing kinase homologous to mammalian Akt and S6 kinase. Sch9 integrates environmental cues with cell growth by functioning downstream of TORC1 and in parallel with the Ras/PKA pathway. Mutations in SCH9 lead to reduced cell growth in dextrose ... [more]

G3 (Bethesda) Apr. 26, 2021; (); [Pubmed: 33901283]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • double gbp1/gbp2 mutants rescue the growth of an sch9 mutant
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SCH9 GPB2
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-0.161BioGRID
2130198

Curated By

  • BioGRID