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

PIF1

TST1, DNA helicase PIF1, L000001435, YML061C
DNA helicase, potent G-quadruplex DNA binder/unwinder; possesses strand annealing activity; promotes DNA synthesis during break-induced replication; important for crossover recombination; translation from different start sites produces mitochondrial and nuclear forms; nuclear form is a catalytic inhibitor of telomerase; mitochondrial form involved in DNA repair and recombination; mutations affect Zn, Fe homeostasis; regulated by Rad53p-dependent phosphorylation in rho0 cells
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

Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiae.

Myung K, Kolodner RD

Cancer cells show increased genome rearrangements, although it is unclear what defects cause these rearrangements. Previous studies have implicated the Saccharomyces cerevisiae replication checkpoint in the suppression of spontaneous genome rearrangements. In the present study, low doses of methyl methane sulfonate that activate the intra-S checkpoint but not the G1 or G2 DNA damage checkpoints were found to cause increased ... [more]

Proc. Natl. Acad. Sci. U.S.A. Apr. 02, 2002; 99(7);4500-7 [Pubmed: 11917116]

Throughput

  • Low Throughput

Ontology Terms

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

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD9 PIF1
Dosage Growth Defect
Dosage Growth Defect

A genetic interaction is inferred when over expression or increased dosage of one gene causes a growth defect in a strain that is mutated or deleted for another gene.

Low-BioGRID
447975
PIF1 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-0.1353BioGRID
2158475

Curated By

  • BioGRID