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

STN1

L000003921, YDR082W
Telomere end-binding and capping protein; plays a key role with Pol12p in linking telomerase action with completion of lagging strand synthesis, and in a regulatory step required for telomere capping; similar to human Stn1
GO Process (2)
GO Function (1)
GO Component (1)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

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.

Publication

Yeast telomere capping protein Stn1 overrides DNA replication control through the S phase checkpoint.

Gasparyan HJ, Xu L, Petreaca RC, Rex AE, Small VY, Bhogal NS, Julius JA, Warsi TH, Bachant J, Aparicio OM, Nugent CI

Telomere integrity is maintained through end-protection proteins that block nuclease degradation and prevent telomeres from being recognized as DNA breaks. Although less well understood, end protection proteins may also play a role in facilitating telomere replication. Here, we show that overproduction (OP) of the yeast telomere capping protein Stn1 makes cells highly sensitive to the replication inhibitors hydroxyurea (HU) and ... [more]

Proc. Natl. Acad. Sci. U.S.A. Feb. 17, 2009; 106(7);2206-11 [Pubmed: 19171895]

Throughput

  • Low Throughput

Ontology Terms

  • vegetative growth (APO:0000106)

Additional Notes

  • Overexpression of STN1 in a RAD9 mutant increases sensitivity to HU

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
STN1 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
2544418
STN1 RAD9
Synthetic Lethality
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.

Low-BioGRID
256539

Curated By

  • BioGRID