The intra-S-phase checkpoint is a signaling pathway that induces slow DNA replication in the presence of DNA damage. In humans, defects in this checkpoint pathway might account for phenotypes seen in autosomal recessive diseases including ataxia telangiectasia-like disorder and Nijmegen breakage syndrome, where MRN complex components, Mre11 and Nbs1, are mutated. Here we provide evidence that the equivalent budding yeast complex, MRX (Mre11/Rad50/Xrs2), is not required for the intra-S-phase checkpoint in response to DNA alkylation damage, but is required in the presence of double-stranded DNA breaks. These data indicate, at least in budding yeast, that alternate pathways enforce replication slowing depending on the particular DNA lesion.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Aug 2005|
Bibliographical noteFunding Information:
We thank Nick Rhind, Steve Jackson, Shosh Squires and John Petrini for helpful discussion of the data and manuscript. This work was supported in part by NIH grant 1R01CA099033-01 (DJC).
- Intra-S-phase checkpoint