BAIT

ATG17

APG17, protein kinase regulatory subunit ATG17, YLR423C
Scaffold protein responsible for phagophore assembly site organization; regulatory subunit of an autophagy-specific complex that includes Atg1p and Atg13p; stimulates Atg1p kinase activity; human ortholog RB1CC1/FIP200 interacts with p53, which inhibits autophagy in human cells
Saccharomyces cerevisiae (S288c)
PREY

TEP1

L000003922, YNL128W
PTEN homolog with no demonstrated inositol lipid phosphatase activity; plays a role in normal sporulation; homolog of human tumor suppressor gene PTEN/MMAC1/TEP1 and fission yeast ptn1
Kinome Project (Sc)
GO Process (2)
GO Function (0)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

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.

Publication

High-resolution profiling of stationary-phase survival reveals yeast longevity factors and their genetic interactions.

Garay E, Campos SE, Gonzalez de la Cruz J, Gaspar AP, Jinich A, Deluna A

Lifespan is influenced by a large number of conserved proteins and gene-regulatory pathways. Here, we introduce a strategy for systematically finding such longevity factors in Saccharomyces cerevisiae and scoring the genetic interactions (epistasis) among these factors. Specifically, we developed an automated competition-based assay for chronological lifespan, defined as stationary-phase survival of yeast populations, and used it to phenotype over 5,600 ... [more]

PLoS Genet. Feb. 01, 2014; 10(2);e1004168 [Pubmed: 24586198]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: chronological lifespan (APO:0000316)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
TEP1 ATG17
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-10.2609BioGRID
324819

Curated By

  • BioGRID