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

ELG1

RTT110, S000007438, YOR144C
Subunit of an alternative replication factor C complex; important for DNA replication and genome integrity; suppresses spontaneous DNA damage; involved in homologous recombination-mediated repair and telomere homeostasis; required for PCNA (Pol30p) unloading during DNA replication
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
ELG1 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-0.1343BioGRID
2440721
ELG1 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-3.06BioGRID
2356650
RAD9 ELG1
Phenotypic Enhancement
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.

High-BioGRID
352451
ELG1 RAD9
Phenotypic Suppression
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.

Low-BioGRID
256910
RAD9 ELG1
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
457441

Curated By

  • BioGRID