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

MRE11

NGS1, RAD58, XRS4, MRX complex nuclease subunit, L000004732, L000001149, L000004275, YMR224C
Nuclease subunit of the MRX complex with Rad50p and Xrs2p; complex functions in repair of DNA double-strand breaks and in telomere stability; Mre11p associates with Ser/Thr-rich ORFs in premeiotic phase; nuclease activity required for MRX function; widely conserved; forms nuclear foci upon DNA replication stress
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

Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.

Gobbini E, Villa M, Gnugnoli M, Menin L, Clerici M, Longhese MP

The MRX complex together with Sae2 initiates resection of DNA double-strand breaks (DSBs) to generate single-stranded DNA (ssDNA) that triggers homologous recombination. The absence of Sae2 not only impairs DSB resection, but also causes prolonged MRX binding at the DSBs that leads to persistent Tel1- and Rad53-dependent DNA damage checkpoint activation and cell cycle arrest. Whether this enhanced checkpoint signaling ... [more]

PLoS Genet. Nov. 01, 2015; 11(11);e1005685 [Pubmed: 26584331]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: resistance to chemicals (APO:0000087)

Additional Notes

  • deletion of mre11 inhibits the suppression of DNA damage sensitivity by Rad53-H88Y and Tel1-N2021D variants in sae2 mutant cells

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD53 MRE11
Synthetic Growth Defect
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.

High-BioGRID
454858

Curated By

  • BioGRID