BAIT

ASF1

CIA1, nucleosome assembly factor ASF1, L000000126, YJL115W
Nucleosome assembly factor; involved in chromatin assembly and disassembly, anti-silencing protein that causes derepression of silent loci when overexpressed; plays a role in regulating Ty1 transposition; relocalizes to the cytosol in response to hypoxia
Saccharomyces cerevisiae (S288c)
PREY

PTC2

type 2C protein phosphatase PTC2, L000003403, YER089C
Type 2C protein phosphatase (PP2C); dephosphorylates Hog1p to limit maximal osmostress induced kinase activity; dephosphorylates Ire1p to downregulate the unfolded protein response; dephosphorylates Cdc28p; inactivates the DNA damage checkpoint; PTC2 has a paralog, PTC3, that arose from the whole genome duplication
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

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.

Publication

Asf1 facilitates dephosphorylation of Rad53 after DNA double-strand break repair.

Tsabar M, Waterman DP, Aguilar F, Katsnelson L, Eapen VV, Memisoglu G, Haber JE

To allow for sufficient time to repair DNA double-stranded breaks (DSBs), eukaryotic cells activate the DNA damage checkpoint. In budding yeast, Rad53 (mammalian Chk2) phosphorylation parallels the persistence of the unrepaired DSB and is extinguished when repair is complete in a process termed recovery or when the cells adapt to the DNA damage checkpoint. A strain containing a slowly repaired ... [more]

Genes Dev. Dec. 15, 2015; 30(10);1211-24 [Pubmed: 27222517]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: chromosome segregation (APO:0000208)

Additional Notes

  • Figure 3
  • PTC2 overexpression rescues checkpoint arrest in asf1 mutant after double-strand breaks

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PTC2 ASF1
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-0.1465BioGRID
2108872

Curated By

  • BioGRID