BAIT

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)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

PMC1

calcium-transporting ATPase PMC1, L000001451, YGL006W
Vacuolar Ca2+ ATPase involved in depleting cytosol of Ca2+ ions; prevents growth inhibition by activation of calcineurin in the presence of elevated concentrations of calcium; similar to mammalian PMCA1a
GO Process (3)
GO Function (1)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

Publication

Rabbit sarcoplasmic reticulum Ca(2+)-ATPase replaces yeast PMC1 and PMR1 Ca(2+)-ATPases for cell viability and calcineurin-dependent regulation of calcium tolerance.

Degand I, Catty P, Talla E, Thines-Sempoux D, de Kerchove d'Exaerde A, Goffeau A, Ghislain M

SERCA1a, the fast-twitch skeletal muscle isoform of sarco(endo)plasmic reticulum Ca(2+)-ATPase, was expressed in yeast using the promoter of the plasma membrane H(+)-ATPase. In the yeast Saccharomyces cerevisiae, the Golgi PMR1 Ca(2+)-ATPase and the vacuole PMC1 Ca(2+)-ATPase function together in Ca2+ sequestration and Ca2+ tolerance. SERCA1a expression restored growth of pmc1 mutants in media containing high Ca2+ concentrations, consistent with increased ... [more]

Mol. Microbiol. Jan. 01, 1999; 31(2);545-56 [Pubmed: 10027971]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PMR1 PMC1
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-0.4385BioGRID
379450
PMC1 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-0.4385BioGRID
381427
PMC1 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-0.3265BioGRID
2113803
PMR1 PMC1
Phenotypic Enhancement
Phenotypic Enhancement

A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Low-BioGRID
344118
PMR1 PMC1
Synthetic Growth Defect
Synthetic Growth Defect

A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell.

Low-BioGRID
343786

Curated By

  • BioGRID