Please contact OriDB if you think this paper has been mis-annotated.
Hélène Tourrière, Gwennaëlle Versini, Violeta Cordón-Preciado, Constance Alabert, Philippe Pasero
Mol. Cell (2005), 19(5):699-706PubMed | Mol. Cell
The yeast checkpoint factors Mrc1p and Tof1p travel with the replication fork and mediate the activation of the Rad53p kinase in response to a replication stress. We show here that both proteins are required for normal fork progression but play different roles at stalled forks. Tof1p is critical for the activity of the rDNA replication fork barrier (RFB) but plays a minor role in the replication checkpoint. In contrast, Mrc1p is not necessary for RFB activity but is essential to mediate the replication stress response. Interestingly, stalled forks did not collapse in mrc1Delta cells exposed to hydroxyurea (HU) as they do in rad53 mutants. However, forks failed to restart when mrc1Delta cells were released from the block. The critical role of Mrc1p in HU is therefore to promote fork recovery in a Rad53p-independent manner, presumably through the formation of a stable fork-pausing complex.
None curated.
None curated.
None curated.
None curated.
None curated.
None curated.
None curated.
The data on this page come directly from PubMed and OriDB databases, please report any errors to OriDB.
This page is new! Please let us know of any problems you experience.