BAIT

VPS41

CVT8, FET2, SVL2, VAM2, VPL20, L000003512, L000004234, YDR080W
Subunit of the HOPS endocytic tethering complex; vacuole membrane protein that functions as a Rab GTPase effector, interacting specifically with the GTP-bound conformation of Ypt7p, facilitating tethering, docking and promoting membrane fusion events at the late endosome and vacuole; required for both membrane and protein trafficking; Yck3p-mediated phosphorylation regulates the organization of vacuolar fusion sites
Saccharomyces cerevisiae (S288c)
PREY

NSL1

MIND complex subunit NSL1, L000004652, YPL233W
Essential component of the MIND kinetochore complex; joins kinetochore subunits contacting DNA to those contacting microtubules; required for accurate chromosome segregation; complex consists of Mtw1p Including Nnf1p-Nsl1p-Dsn1p (MIND)
GO Process (1)
GO Function (0)
GO Component (3)

Gene Ontology Biological Process

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Two-hybrid

Bait protein expressed as a DNA binding domain (DBD) fusion and prey expressed as a transcriptional activation domain (TAD) fusion and interaction measured by reporter gene activation.

Publication

Efficient termination of vacuolar Rab GTPase signaling requires coordinated action by a GAP and a protein kinase.

Brett CL, Plemel RL, Lobinger BT, Vignali M, Fields S, Merz AJ

Rab guanosine triphosphatases (GTPases) are pivotal regulators of membrane identity and dynamics, but the in vivo pathways that control Rab signaling are poorly defined. Here, we show that the GTPase-activating protein Gyp7 inactivates the yeast vacuole Rab Ypt7 in vivo. To efficiently terminate Ypt7 signaling, Gyp7 requires downstream assistance from an inhibitory casein kinase I, Yck3. Yck3 mediates phosphorylation of ... [more]

J. Cell Biol. Sep. 22, 2008; 182(6);1141-51 [Pubmed: 18809726]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
NSL1 VPS41
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-0.2536BioGRID
2022803

Curated By

  • BioGRID