BAIT

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)
PREY

REV1

L000001615, YOR346W
Deoxycytidyl transferase; involved in repair of abasic sites and adducted guanines in damaged DNA by translesion synthesis (TLS); forms a complex with the subunits of DNA polymerase zeta, Rev3p and Rev7p; relocalizes from nucleus to cytoplasm upon DNA replication stress
GO Process (2)
GO Function (2)
GO Component (5)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Phenotypic Enhancement

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

Publication

The Saccharomyces cerevisiae RAD9, RAD17 and RAD24 genes are required for suppression of mutagenic post-replicative repair during chronic DNA damage.

Murakami-Sekimata A, Huang D, Piening BD, Bangur C, Paulovich AG

In Saccharomyces cerevisiae, a DNA damage checkpoint in the S-phase is responsible for delaying DNA replication in response to genotoxic stress. This pathway is partially regulated by the checkpoint proteins Rad9, Rad17 and Rad24. Here, we describe a novel hypermutable phenotype for rad9Delta, rad17Delta and rad24Delta cells in response to a chronic 0.01% dose of the DNA alkylating agent MMS. ... [more]

DNA Repair (Amst.) Jul. 01, 2010; 9(7);824-34 [Pubmed: 20472512]

Throughput

  • High Throughput|Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • Cells were exposed to 0.01 percent methyl methanesulfonate (MMS). A high-throughput dSLAM screen was followed by a low-throughput screen that compared the MMS sensitivity of each double mutant (xxx rad9) to the original single mutants (xxx).
  • Methyl methanesulfonate (CHEBI:25255 and PubChem CID: 4156)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
REV1 RAD9
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-0.1627BioGRID
2187503

Curated By

  • BioGRID