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
Saccharomyces cerevisiae (S288c)
PREY

RFX1

CRT1, L000004129, YLR176C
Major transcriptional repressor of DNA-damage-regulated genes; recruits repressors Tup1p and Cyc8p to their promoters; involved in DNA damage and replication checkpoint pathway; similar to a family of mammalian DNA binding RFX1-4 proteins
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

G1/S and g2/m cyclin-dependent kinase activities commit cells to death in the absence of the s-phase checkpoint.

Manfrini N, Gobbini E, Baldo V, Trovesi C, Lucchini G, Longhese MP

The Mec1 and Rad53 protein kinases are essential for budding yeast cell viability and are also required to activate the S-phase checkpoint, which supports DNA replication under stress conditions. Whether these two functions are related to each other remains to be determined, and the nature of the replication stress-dependent lethality of mec1 and rad53 mutants is still unclear. We show ... [more]

Mol. Cell. Biol. Dec. 01, 2012; 32(24);4971-85 [Pubmed: 23045388]

Throughput

  • Low Throughput

Ontology Terms

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

Additional Notes

  • expression of a crt1 null allele suppresses the extreme sensitivity to HU (CID 3657 CHEBI 44423) and MMS (CID 4156 CHEBI 25255) seen in a rad53/sml1 double mutant
  • genetic complex
  • rad53 null viability maintained by deletion of sml1

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD53 RFX1
Dosage Lethality
Dosage Lethality

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

Low-BioGRID
154010
RFX1 RAD53
Phenotypic Enhancement
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.

Low-BioGRID
2652801
RAD53 RFX1
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
160476
RAD53 RFX1
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
2652800

Curated By

  • BioGRID