BAIT

RAD7

UV-damaged DNA-binding protein RAD7, L000001561, YJR052W
Nucleotide excision repair (NER) protein; binds damaged DNA during NER; binds DNA in an ATP-dependent manner (with Rad16p) during NER; required for repair of non-transcribed chromatin; subunit of Nucleotide Excision Repair Factor 4 (NEF4) and the Elongin-Cullin-Socs (ECS) ligase complex
Saccharomyces cerevisiae (S288c)
PREY

NOT5

CCR4-NOT core subunit NOT5, L000004651, YPR072W
Subunit of CCR4-NOT global transcriptional regulator; involved intranscription initiation and elongation and in mRNA degradation; conserved lysine in human homolog of Not5p and Not3p is mutated in cancers
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

Genome-wide analysis of factors affecting transcription elongation and DNA repair: a new role for PAF and Ccr4-not in transcription-coupled repair.

Gaillard H, Tous C, Botet J, Gonzalez-Aguilera C, Quintero MJ, Viladevall L, Garcia-Rubio ML, Rodriguez-Gil A, Marin A, Arino J, Revuelta JL, Chavez S, Aguilera A

RNA polymerases frequently deal with a number of obstacles during transcription elongation that need to be removed for transcription resumption. One important type of hindrance consists of DNA lesions, which are removed by transcription-coupled repair (TC-NER), a specific sub-pathway of nucleotide excision repair. To improve our knowledge of transcription elongation and its coupling to TC-NER, we used the yeast library ... [more]

PLoS Genet. Feb. 01, 2009; 5(2);e1000364 [Pubmed: 19197357]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)
  • phenotype: radiation resistance (APO:0000084)

Additional Notes

  • double mutants die when exposed to UV

Curated By

  • BioGRID