BAIT

HST4

L000003043, YDR191W
Member of the Sir2 family of NAD(+)-dependent protein deacetylases; involved along with Hst3p in silencing at telomeres, cell cycle progression, radiation resistance, genomic stability and short-chain fatty acid metabolism
GO Process (3)
GO Function (1)
GO Component (2)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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)

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

The SIR2 gene family, conserved from bacteria to humans, functions in silencing, cell cycle progression, and chromosome stability.

Brachmann CB, Sherman JM, Devine SE, Cameron EE, Pillus L, Boeke JD

Genomic silencing is a fundamental mechanism of transcriptional regulation, yet little is known about conserved mechanisms of silencing. We report here the discovery of four Saccharomyces cerevisiae homologs of the SIR2 silencing gene (HSTs), as well as conservation of this gene family from bacteria to mammals. At least three HST genes can function in silencing; HST1 overexpression restores transcriptional silencing ... [more]

Genes Dev. Dec. 01, 1995; 9(23);2888-902 [Pubmed: 7498786]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)
  • phenotype: uv resistance (APO:0000085)

Additional Notes

  • Deletion of RAD9 increases UV sensitivity in a HST3/HST4 double mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD9 HST4
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-4.075BioGRID
219342
HST4 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
3582791
HST4 RAD9
Synthetic Rescue
Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Low-BioGRID
3017575
HST4 RAD9
Synthetic Rescue
Synthetic Rescue

A genetic interaction is inferred when mutations or deletions of one gene rescues the lethality or growth defect of a strain mutated or deleted for another gene.

Low-BioGRID
2396765

Curated By

  • BioGRID