BAIT

ATG1

APG1, AUT3, CVT10, serine/threonine protein kinase ATG1, L000003955, S000028502, L000004761, YGL180W
Protein serine/threonine kinase; required for vesicle formation in autophagy and the cytoplasm-to-vacuole targeting (Cvt) pathway; structurally required for phagophore assembly site formation; during autophagy forms a complex with Atg13p and Atg17p; essential for cell cycle progression from G2/M to G1 under nitrogen starvation
Saccharomyces cerevisiae (S288c)
PREY

TVP23

YDR084C
Integral membrane protein; localized to late Golgi vesicles along with the v-SNARE Tlg2p; green fluorescent protein (GFP)-fusion protein localizes to the cytoplasm in a punctate pattern
GO Process (1)
GO Function (0)
GO Component (3)

Gene Ontology Biological Process

Saccharomyces cerevisiae (S288c)

Affinity Capture-MS

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.

Publication

ER exit sites are physical and functional core autophagosome biogenesis components.

Graef M, Friedman JR, Graham C, Babu M, Nunnari J

Autophagy is a central homeostasis and stress response pathway conserved in all eukaryotes. One hallmark of autophagy is the de novo formation of autophagosomes. These double-membrane vesicular structures form around and deliver cargo for degradation by the vacuole/lysosome. Where and how autophagosomes form are outstanding questions. Here we show, using proteomic, cytological, and functional analyses, that autophagosomes are spatially, physically, ... [more]

Mol. Biol. Cell Sep. 01, 2013; 24(18);2918-31 [Pubmed: 23904270]

Throughput

  • High Throughput

Additional Notes

  • cutoff defined by probability scores of >70% and not being detected in control samples derived from the untagged atg19 deletion mutants

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
TVP23 ATG1
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-0.2513BioGRID
2094574

Curated By

  • BioGRID