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

SMF1

SBS1, divalent metal ion transporter SMF1, L000001931, YOL122C
Divalent metal ion transporter; broad specificity for di-valent and tri-valent metals; post-translationally regulated by levels of metal ions; member of the Nramp family of metal transport proteins
Saccharomyces cerevisiae (S288c)

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.

Publication

The overlapping roles of manganese and Cu/Zn SOD in oxidative stress protection.

Reddi AR, Jensen LT, Naranuntarat A, Rosenfeld L, Leung E, Shah R, Culotta VC

In various organisms, high intracellular manganese provides protection against oxidative damage through unknown pathways. Herein we use a genetic approach in Saccharomyces cerevisiae to analyze factors that promote manganese as an antioxidant in cells lacking Cu/Zn superoxide dismutase (sod1 Delta). Unlike certain bacterial systems, oxygen resistance in yeast correlates with high intracellular manganese without a lowering of iron. This manganese ... [more]

Free Radic. Biol. Med. Jan. 15, 2009; 46(2);154-62 [Pubmed: 18973803]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)
  • phenotype: oxidative stress resistance (APO:0000083)

Additional Notes

  • deletion of SMF1 causes growth defects in response to manganese in a SOD1/PMR1 double mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PMR1 SMF1
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
428791
PMR1 SMF1
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-0.332BioGRID
379545
PMR1 SMF1
Phenotypic Suppression
Phenotypic Suppression

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

Low-BioGRID
3537534

Curated By

  • BioGRID