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

CLB5

B-type cyclin CLB5, L000000353, YPR120C
B-type cyclin involved in DNA replication during S phase; activates Cdc28p to promote initiation of DNA synthesis; functions in formation of mitotic spindles along with Clb3p and Clb4p; most abundant during late G1 phase; CLB5 has a paralog, CLB6, that arose from the whole genome duplication
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)

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.

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

  • phenotype: inviable (APO:0000112)

Additional Notes

  • deletion of clb5 is lethal in rad53/sml1 double mutants
  • genetic complex
  • rad53 null viability maintained by deletion of sml1

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
CLB5 RAD53
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
163298
RAD53 CLB5
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.

High-BioGRID
453381

Curated By

  • BioGRID