BAIT

DPM1

SED3, dolichyl-phosphate beta-D-mannosyltransferase, L000000524, YPR183W
Dolichol phosphate mannose (Dol-P-Man) synthase of the ER membrane; catalyzes the formation of Dol-P-Man from Dol-P and GDP-Man; required for glycosyl phosphatidylinositol membrane anchoring, O mannosylation, and protein glycosylation
Saccharomyces cerevisiae (S288c)
PREY

RER2

L000004874, YBR002C
Cis-prenyltransferase involved in dolichol synthesis; major enzyme of polyprenol synthesis in both the endoplasmic reticulum (ER) and in lipid droplets; participates in ER protein sorting
GO Process (3)
GO Function (2)
GO Component (2)
Saccharomyces cerevisiae (S288c)

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.

Publication

Defect in dolichol-dependent glycosylation increases sensitivity of Saccharomyces cerevisiae towards anti-fungal drugs.

Juchimiuk M, Pasikowska M, Zatorska E, Laudy AE, Smolenska-Sym G, Palamarczyk G

Two temperature-sensitive Saccharomyces cerevisiae mutants, sec59-1 and dpm1-6, impaired, respectively, in dolichol kinase (Sec59p) and dolichyl phosphate mannose (DolPMan) synthase (Dpm1p), have an aberrant cell wall structure and composition. We tested their sensitivity to four classes of antifungal drugs used in clinical practice: 5-fluorocytosine, amphotericin B, caspofungin and itraconasole. The strains were resistant to itraconazole and sensitive to the other ... [more]

Yeast Aug. 01, 2010; 27(8);637-45 [Pubmed: 20602334]

Throughput

  • Low Throughput

Ontology Terms

  • cell wall morphology (APO:0000053)
  • resistance to chemicals (APO:0000087)

Additional Notes

  • Overexpression of RER2 restores sensitivity to anti-fungal chemicals seen in a SEC59 mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RER2 DPM1
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-0.7905BioGRID
1919913

Curated By

  • BioGRID