BAIT

GLN3

nitrogen-responsive transcriptional regulator GLN3, L000000710, YER040W
Transcriptional activator of genes regulated by nitrogen catabolite repression; localization and activity regulated by quality of nitrogen source and Ure2p
Saccharomyces cerevisiae (S288c)
PREY

PMR1

BSD1, LDB1, SSC1, Ca(2+)/Mn(2+)-transporting P-type ATPase PMR1, L000004740, L000001455, YGL167C
High affinity Ca2+/Mn2+ P-type ATPase; required for Ca2+ and Mn2+ transport into Golgi; involved in Ca2+ dependent protein sorting and processing; D53A mutant (Mn2+ transporting) is rapamycin sensitive, Q783A mutant (Ca2+ transporting) is rapamycin resistant; Mn2+ transport into Golgi lumen appears to be required for rapamycin sensitivity; mutations in human homolog ATP2C1 cause acantholytic skin condition Hailey-Hailey disease
GO Process (4)
GO Function (3)
GO Component (2)
Saccharomyces cerevisiae (S288c)

Co-localization

Interaction inferred from two proteins that co-localize in the cell by indirect immunofluorescence only when in addition, if one gene is deleted, the other protein becomes mis-localized. Also includes co-dependent association of proteins with promoter DNA in chromatin immunoprecipitation experiments.

Publication

Pmr1, a Golgi Ca2+/Mn2+-ATPase, is a regulator of the target of rapamycin (TOR) signaling pathway in yeast.

Devasahayam G, Ritz D, Helliwell SB, Burke DJ, Sturgill TW

The rapamycin.FKBP12 complex inhibits target of rapamycin (TOR) kinase in TORC1. We screened the yeast nonessential gene deletion collection to identify mutants that conferred rapamycin resistance, and we identified PMR1, encoding the Golgi Ca2+/Mn2+ -ATPase. Deleting PMR1 in two genetic backgrounds confers rapamycin resistance. Epistasis analyses show that Pmr1 functions upstream from Npr1 and Gln-3 in opposition to Lst8, a ... [more]

Proc. Natl. Acad. Sci. U.S.A. Nov. 21, 2006; 103(47);17840-5 [Pubmed: 17095607]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PMR1 GLN3
Dosage Rescue
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.

Low-BioGRID
204732
GLN3 PMR1
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-0.3311BioGRID
2107557

Curated By

  • BioGRID