BAIT

RAD6

PSO8, UBC2, E2 ubiquitin-conjugating protein RAD6, L000001560, YGL058W
Ubiquitin-conjugating enzyme (E2); involved in postreplication repair as a heterodimer with Rad18p, DSBR and checkpoint control as a heterodimer with Bre1p, ubiquitin-mediated N-end rule protein degradation as a heterodimer with Ubr1p, as well as endoplasmic reticulum-associated protein degradation (ERAD) with Ubr1p in the absence of canonical ER membrane ligases
UPS Project
Saccharomyces cerevisiae (S288c)
PREY

RAD9

chromatin-binding protein RAD9, L000001562, YDR217C
DNA damage-dependent checkpoint protein; required for cell-cycle arrest in G1/S, intra-S, and G2/M, plays a role in postreplication repair (PRR) pathway; transmits checkpoint signal by activating Rad53p and Chk1p; hyperphosphorylated by Mec1p and Tel1p; multiple cyclin dependent kinase consensus sites and the C-terminal BRCT domain contribute to DNA damage checkpoint activation; Rad9p Chk1 Activating Domain (CAD) is phosphorylated at multiple sites by Cdc28p/Clb2p
Saccharomyces cerevisiae (S288c)

Phenotypic Suppression

A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Publication

Post-replication repair suppresses duplication-mediated genome instability.

Putnam CD, Hayes TK, Kolodner RD

RAD6 is known to suppress duplication-mediated gross chromosomal rearrangements (GCRs) but not single-copy sequence mediated GCRs. Here, we found that the RAD6- and RAD18-dependent post-replication repair (PRR) and the RAD5-, MMS2-, UBC13-dependent error-free PRR branch acted in concert with the replication stress checkpoint to suppress duplication-mediated GCRs formed by homologous recombination (HR). The Rad5 helicase activity, but not its RING ... [more]

PLoS Genet. May. 01, 2010; 6(5);e1000933 [Pubmed: 20463880]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: chromosome/plasmid maintenance (APO:0000143)

Additional Notes

  • deletion of rad9 suppresses the rate of GCR in a rad6 mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD6 RAD9
Synthetic Growth Defect
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.

Low-BioGRID
438054
RAD9 RAD6
Synthetic Growth Defect
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.

High-BioGRID
457442

Curated By

  • BioGRID