BAIT

APN2

ETH1, DNA-(apurinic or apyrimidinic site) lyase APN2, L000004434, YBL019W
Class II abasic (AP) endonuclease involved in repair of DNA damage; homolog of human HAP1 and E. coli exoIII
GO Process (1)
GO Function (3)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

RAD53

LSD1, MEC2, SPK1, serine/threonine/tyrosine protein kinase RAD53, L000001573, YPL153C
DNA damage response protein kinase; required for cell-cycle arrest in response to DNA damage; activated by trans autophosphorylation when interacting with hyperphosphorylated Rad9p; also interacts with ARS1 and plays a role in initiation of DNA replication; activates the downstream kinase Dun1p; differentially senses mtDNA depletion and mitochondrial ROS; required for regulation of copper genes in response to DNA-damaging agents; relocalizes to cytosol in response to hyoxia
Kinome Project (Sc)
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

Abasic sites linked to dUTP incorporation in DNA are a major cause of spontaneous mutations in absence of base excision repair and Rad17-Mec3-Ddc1 (9-1-1) DNA damage checkpoint clamp in Saccharomyces cerevisiae.

Collura A, Auffret Van Der Kemp P, Boiteux S

In Saccharomyces cerevisiae, inactivation of base excision repair (BER) AP endonucleases (Apn1p and Apn2p) results in constitutive phosphorylation of Rad53p and delay in cell cycle progression at the G2/M transition. These data led us to investigate genetic interactions between Apn1p, Apn2p and DNA damage checkpoint proteins. The results show that mec1 sml1, rad53 sml1 and rad9 is synthetic lethal with ... [more]

DNA Repair (Amst.) Mar. 01, 2012; 11(3);294-303 [Pubmed: 22226374]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • deletion of rad53/sml1 causes lethality in an apn1/apn2 mutant background
  • genetic complex

Curated By

  • BioGRID