BAIT

RAD3

REM1, TFIIH/NER complex ATP-dependent 5'-3' DNA helicase subunit RAD3, L000001557, YER171W
5' to 3' DNA helicase; involved in nucleotide excision repair and transcription; subunit of RNA polII initiation factor TFIIH and of Nucleotide Excision Repair Factor 3 (NEF3); homolog of human XPD protein; mutant has aneuploidy tolerance; protein abundance increases in response to DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

POL32

REV5, DNA polymerase delta subunit POL32, L000004337, S000029416, L000001617, YJR043C
Third subunit of DNA polymerase delta; involved in chromosomal DNA replication; required for error-prone DNA synthesis in the presence of DNA damage and processivity; forms a complex with Rev3p, Rev7p and Pol31p; interacts with Hys2p, PCNA (Pol30p), and Pol1p
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

A postincision-deficient TFIIH causes replication fork breakage and uncovers alternative Rad51- or Pol32-mediated restart mechanisms.

Moriel-Carretero M, Aguilera A

Homologous recombination is a major double-strand break (DSB) repair mechanism that acts during the S and G2 phases. In contrast, nucleotide excision repair (NER) is a major pathway for the repair of DNA bulky adducts that is unrelated to replication. We show that replication can be strongly disturbed in a specific type of rad3/XPD NER mutant of TFIIH, causing replication ... [more]

Mol. Cell Mar. 12, 2010; 37(5);690-701 [Pubmed: 20227372]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • Deletion of POL32 causes synthetic lethality in a RAD3/RAD51 double mutant background
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
POL32 RAD3
Positive Genetic
Positive Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.

High4.9223BioGRID
225142

Curated By

  • BioGRID