BAIT

ATM1

ATP-binding cassette Fe/S cluster precursor transporter ATM1, L000000140, YMR301C
Mitochondrial inner membrane ATP-binding cassette (ABC) transporter; exports mitochondrially synthesized precursors of iron-sulfur (Fe/S) clusters to the cytosol
GO Process (2)
GO Function (2)
GO Component (3)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

MDL1

ATP-binding cassette permease MDL1, L000001049, YLR188W
Mitochondrial inner membrane half-type ABC transporter; mediates export of peptides generated upon proteolysis of mitochondrial proteins; plays a role in the regulation of cellular resistance to oxidative stress
GO Process (1)
GO Function (2)
GO Component (4)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

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.

Publication

MDL1 is a high copy suppressor of ATM1: evidence for a role in resistance to oxidative stress.

Chloupkova M, LeBard LS, Koeller DM

The yeast ATM1 gene is essential for normal cellular iron homeostasis. Deletion of ATM1 results in mitochondrial iron accumulation and increased sensitivity to oxidative stress and transition metal toxicity. Atm1p is an ATP-binding cassette (ABC) transporter localized to the mitochondrial inner membrane. The specific function of Atm1p has not been determined, though roles in both mitochondrial iron export and cytosolic ... [more]

J. Mol. Biol. Aug. 01, 2003; 331(1);155-65 [Pubmed: 12875842]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: metal resistance (APO:0000090)
  • phenotype: oxidative stress resistance (APO:0000083)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
ATM1 MDL1
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-0.1454BioGRID
2008141

Curated By

  • BioGRID