High impact information on rad1

• Identification of a gene involved in checkpoint control as a rescue of a cdc2 mutant links the rad1-dependent DNA-damage-sensing pathway and p34cdc2 activity [1].
• The mutants define eight linkage groups, three of which consist of alleles of the rad1, rad3, and rad17 genes [2].
• Our results implicate rad1 homologs in DNA damage-induced apoptosis in animals [3].
• Mutations in three genes--mrt-2, which encodes the C. elegans homolog of the S. pombe rad1 checkpoint gene, rad-5, and him-7-block both DNA damage-induced apoptosis and cell proliferation arrest [3].
• A strain carrying a null allele of rad1 was constructed and found to have a phenotype closely similar to that of the rad1-1 mutant [4].

Biological context of rad1

• As single mutants, the rad1-S1, rad1-S2, rad1-S5, and rad1-S6 alleles have a wild-type phenotype with respect to radiation sensitivity and checkpoint functions; however, like the rad1 null allele, the rad1-S1 and rad1-S2 alleles exhibit synthetic lethality at the restrictive temperature with the cdc17-K42 or the wee1-50 mutation [5].
• Separation of phenotypes in mutant alleles of the Schizosaccharomyces pombe cell-cycle checkpoint gene rad1+ [5].
• The Schizosaccharomyces pombe rad1+ gene is involved in the G2 DNA damage cell-cycle checkpoint and in coupling mitosis to completed DNA replication [5].
• Cloning and analysis of a gene involved in DNA repair and recombination, the rad1 gene of Schizosaccharomyces pombe [4].
• We have localized the rad1 gene to NotI fragment E of the S. pombe genome [4].

Regulatory relationships of rad1

• The checkpoint controls for which rad1 is required appear to regulate G2-M progression through the activity of cdc2, here implicated in this role by the coincidence of the radiation transition point and the cdc2 execution point [6].

Other interactions of rad1

• In the present study, we have attempted to test the predictions of this model by asking whether the PCNA alignment identifies functionally important residues or explains mutant phenotypes of hus1, rad1, or rad9 alleles [7].
• Cell cycle arrest depends on the checkpoint genes rad1 and rad3 [8].
• We included rad1 and rad13 mutants in our experiments which do not affect MT switching [9].

Analytical, diagnostic and therapeutic context of rad1

• We have introduced mutations into the coding regions of rad1+ by site-directed mutagenesis [5].

References