BAIT

APN1

DNA-(apurinic or apyrimidinic site) lyase APN1, L000000096, YKL114C
Major apurinic/apyrimidinic endonuclease; 3'-repair diesterase; involved in repair of DNA damage by oxidation and alkylating agents; also functions as a 3'-5' exonuclease to repair 7,8-dihydro-8-oxodeoxyguanosine; genetically interacts with NTG1 to maintain mitochondrial genome integrity
Saccharomyces cerevisiae (S288c)
PREY

MEC1

ESR1, RAD31, SAD3, protein kinase MEC1, L000000586, S000029404, S000007656, YBR136W
Genome integrity checkpoint protein and PI kinase superfamily member; Mec1p and Dun1p function in same pathway to regulate dNTP pools and telomere length; signal transducer required for cell cycle arrest and transcriptional responses to damaged or unreplicated DNA; facilitates replication fork progression and regulates P-body formation under replication stress; promotes interhomolog recombination by phosphorylating Hop1p; associates with shortened, dysfunctional telomeres
Kinome Project (Sc)
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

Checkpoint kinase phosphorylation in response to endogenous oxidative DNA damage in repair-deficient stationary-phase Saccharomyces cerevisiae.

Pawar V, Jingjing L, Patel N, Kaur N, Doetsch PW, Shadel GS, Zhang H, Siede W

Stationary-phase Saccharomyces cerevisiae can serve as a model for post-mitotic cells of higher eukaryotes. Phosphorylation and activation of the checkpoint kinase Rad53 was observed after more than 2 days of culture if two major pathways of oxidative DNA damage repair, base excision repair (BER) and nucleotide excision repair (NER), are inactive. The wild type showed a low degree of Rad53 ... [more]

Mech. Ageing Dev. Aug. 01, 2009; 130(8);501-8 [Pubmed: 19540258]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: protein/peptide modification (APO:0000131)

Additional Notes

  • deletion of Mec1 inhibits the rad53 phosphorylation seen in a berner mutant cell
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
APN1 MEC1
Synthetic Lethality
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.

Low-BioGRID
617499

Curated By

  • BioGRID