High impact information on RAD24

• Rad17 and Rad24 proteins may contribute directly to formation of an arrest signal by association with single-strand DNA in mitosis and meiosis [1].
• Second, mec1 and rad24 single mutants (DMC1+) appear to undergo MI before all recombination events are complete [1].
• Ddc1 association required Rad24 but not Mec1 or Rad9 [2].
• An assay that measures DNA damage processing in vivo showed that the checkpoint genes RAD17, RAD24, and MEC3 activated an exonuclease that degrades DNA [3].
• Elg1 is redundant with Rad24 in the DNA damage response and contributes to activation of the checkpoint kinase Rad53 [4].

Biological context of RAD24

• RAD24 and RFC5 are required for DNA damage checkpoint control in the budding yeast Saccharomyces cerevisiae [5].
• The rad24Delta mutation enhances the defect of rfc5-1 in the DNA replication block checkpoint, implicating RAD24 in this checkpoint [6].
• RAD24 has been identified as a gene essential for the DNA damage checkpoint in budding yeast [6].
• Furthermore, RAD9, RAD17, and RAD24 fall into two groups with respect to both sensitivity to alkylation and regulation of S phase [7].
• The idea that RAD24 overexpression induces DNA damage, perhaps by interfering with replication/repair complexes, is further supported by our observation that RAD24 overexpression increases mitotic chromosome recombination in CDC4 strains [8].

Associations of RAD24 with chemical compounds

• Repair rates of both pyrimidine-pyrimidone (6-4) photoproducts and cyclobutane pyrimidine dimers have been measured in the UV-sensitive mutants of Saccharomyces cerevisiae: rad1 to rad12 and rad14 to rad24 [9].

Physical interactions of RAD24

• A novel Rad24 checkpoint protein complex closely related to replication factor C [10].

Regulatory relationships of RAD24

• RAD24 overexpression suppresses the sensitivity of rfc5-1 cells to DNA-damaging agents and the defect in DNA damage-induced Rad53 phosphorylation [11].
• Finally, analysis of double mutants suggests a minor role for Mec1 in promoting Rad24-dependent degradation of dsDNA [12].

Other interactions of RAD24

• Consistent with this proposal, extra copies of RAD51 and RAD54 substantially suppress not only the spore inviability of the rad24 mutant, but also the gamma-ray sensitivity of the mutant [13].
• All our data are consistent with models in which RAD17, RAD24 and MEC3 are coordinately required for the activity of one or more DNA repair pathways that link DNA damage to cell cycle arrest [8].
• RFC4 and the DNA damage checkpoint gene RAD24 were found to be epistatic with respect to DNA damage sensitivity [14].
• RAD9 and RAD24 define two additive, interacting branches of the DNA damage checkpoint pathway in budding yeast normally required for Rad53 modification and activation [15].
• Both the RFC subunits and Rad24 contain a consensus sequence for nucleoside triphosphate (NTP) binding [5].

Analytical, diagnostic and therapeutic context of RAD24

• Sequence analysis revealed its extensive homology with checkpoint genes rad17 of Schizosaccharomyces pombe and RAD24 of Saccharomyces cerevisiae [16].
• We showed by northern and Southern blot analysis that dmc1(+) and rad24(+) are co-transcribed as a bicistronic mRNA of 2.8 kb with meiotic specificity, whereas rad24(+) itself is constitutively transcribed as a 1.0-kb mRNA species during meiosis [17].

References