BAIT

POL2

DUN2, DNA polymerase epsilon catalytic subunit, L000001461, YNL262W
Catalytic subunit of DNA polymerase (II) epsilon; a chromosomal DNA replication polymerase that exhibits processivity and proofreading exonuclease activity; participates in leading-strand synthesis during DNA replication; also involved in DNA synthesis during DNA repair; interacts extensively with Mrc1p
Saccharomyces cerevisiae (S288c)
PREY

RAD51

MUT5, recombinase RAD51, L000001571, YER095W
Strand exchange protein; forms a helical filament with DNA that searches for homology; involved in the recombinational repair of double-strand breaks in DNA during vegetative growth and meiosis; homolog of Dmc1p and bacterial RecA protein
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

Synthetic Growth Defect

A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell.

Publication

Topoisomerase I-mediated cleavage at unrepaired ribonucleotides generates DNA double-strand breaks.

Huang SN, Williams JS, Arana ME, Kunkel TA, Pommier Y

Ribonuclease activity of topoisomerase I (Top1) causes DNA nicks bearing 2',3'-cyclic phosphates at ribonucleotide sites. Here, we provide genetic and biochemical evidence that DNA double-strand breaks (DSBs) can be directly generated by Top1 at sites of genomic ribonucleotides. We show that RNase H2-deficient yeast cells displayed elevated frequency of Rad52 foci, inactivation of RNase H2 and RAD52 led to synthetic ... [more]

EMBO J. Feb. 01, 2017; 36(3);361-373 [Pubmed: 27932446]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • genetic complex
  • rad51/rnh201/pol2 triple mutants show increased doubling time and abnormal cell morphology

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
POL2 RAD51
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-0.1231BioGRID
2012200

Curated By

  • BioGRID