High impact information on rad3

• Further, DSB-induced cell cycle delay and efficient HR required the DNA integrity checkpoint gene rad3(+) [1].
• Following DNA damage, rad3 is required to initiate but not maintain the Chk1 response [2].
• Irradiated cells eventually progress into S phase and arrest in early S by a rad3- and cds1-dependent mechanism, most likely the intra-S checkpoint [3].
• The rad3+ gene is also likely to play a role in DNA repair [4].
• DSB formation is restored in rad3 mutant even in the presence of hydroxyurea, although repair of DSBs does not take place or is significantly delayed, indicating that the subsequent recombination steps may be still inhibited [5].

Biological context of rad3

• Fission yeast rad3 mutant cells, which are deficient in DNA replication checkpoint function, enter, progress through, and exit mitosis even when DNA replication is blocked [6].
• The rad3 gene was mapped to NotI fragment C on chromosome II [7].
• The predicted Esr1 protein had a mosaic structure composed of homologous regions and showed amino acid sequence similarities to Schizosaccharomyces pombe rad3+ protein, which monitors completion of DNA repair synthesis, and cut1+ protein, which is required for spindle pole body (SPB) duplication [8].

Other interactions of rad3

• Further we show that a novel, epitope-tagged allele of rad4+/cut5+ acts as a dominant suppressor of the checkpoint deficiencies of rad3-, rad26- and rad17- mutants [9].
• Cell cycle arrest depends on the checkpoint genes rad1 and rad3 [10].

References