Please contact OriDB if you think this paper has been mis-annotated.
Shawn J Szyjka, Christopher J Viggiani, Oscar M Aparicio
Mol. Cell (2005), 19(5):691-7PubMed | Mol. Cell
Mrc1 associates with replication forks, where it transmits replication stress signals and is required for normal replisome pausing in response to nucleotide depletion. Mrc1 also plays a poorly understood role in DNA replication, which appears distinct from its role in checkpoint signaling. Here, we demonstrate that Mrc1 functions constitutively to promote normal replication fork progression. In mrc1Delta cells, replication forks proceed slowly throughout chromatin, rather than being specifically defective in pausing and progression through loci that impede fork progression. Analysis of genetic interactions with Rrm3, a DNA helicase required to resolve paused forks, indicates that Mrc1 checkpoint signaling is dispensable for the resolution of stalled replication forks and suggests that replication forks lacking Mrc1 create DNA damage that must be repaired by Rrm3. These findings elucidate a central role for Mrc1 in normal replisome function, which is distinct from its role as a checkpoint mediator, but nevertheless critical to genome stability.
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.