BAIT

RAD53

LSD1, MEC2, SPK1, serine/threonine/tyrosine protein kinase RAD53, L000001573, YPL153C
DNA damage response protein kinase; required for cell-cycle arrest in response to DNA damage; activated by trans autophosphorylation when interacting with hyperphosphorylated Rad9p; also interacts with ARS1 and plays a role in initiation of DNA replication; activates the downstream kinase Dun1p; differentially senses mtDNA depletion and mitochondrial ROS; required for regulation of copper genes in response to DNA-damaging agents; relocalizes to cytosol in response to hyoxia
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)
PREY

SAC3

LEP1, L000001792, YDR159W
mRNA export factor; required for biogenesis of the small ribosomal subunit; component of TREX-2 complex (Sac3p-Thp1p-Sus1p-Cdc31p) involved in transcription elongation and mRNA export from the nucleus; involved in post-transcriptional tethering of active genes to the nuclear periphery and to non-nascent mRNP; similar to the human germinal center-associated nuclear protein (GANP)
Saccharomyces cerevisiae (S288c)

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.

Publication

Rad53-Mediated Regulation of Rrm3 and Pif1 DNA Helicases Contributes to Prevention of Aberrant Fork Transitions under Replication Stress.

Rossi SE, Ajazi A, Carotenuto W, Foiani M, Giannattasio M

Replication stress activates the Mec1(ATR) and Rad53 kinases. Rad53 phosphorylates nuclear pores to counteract gene gating, thus preventing aberrant transitions at forks approaching transcribed genes. Here, we show that Rrm3 and Pif1, DNA helicases assisting fork progression across pausing sites, are detrimental in rad53 mutants experiencing replication stress. Rrm3 and Pif1 ablations rescue cell lethality, chromosome fragmentation, replisome-fork dissociation, fork ... [more]

Cell Rep Oct. 06, 2015; 13(1);80-92 [Pubmed: 26411679]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)
  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • Figure 4
  • SAC3 deletion rescues HU-sensitivity of sml1 rad53 triple mutant
  • genetic complex

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD53 SAC3
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-0.144BioGRID
2021651
RAD53 SAC3
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
571707

Curated By

  • BioGRID