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
Saccharomyces cerevisiae (S288c)
PREY
SML1
ribonucleotide reductase inhibiting protein SML1, L000004580, YML058W
Ribonucleotide reductase inhibitor; involved in regulating dNTP production; regulated by Mec1p and Rad53p during DNA damage and S phase; SML1 has a paralog, DIF1, that arose from the whole genome duplication
GO Process (2)
GO Function (1)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
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.
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 mec1/sml1 causes lethality in an apn1/apn2 mutant background
- deletion of rad53/sml1 causes lethality in an apn1/apn2 mutant background
- genetic complex
Related interactions
Curated By
- BioGRID