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During S-phase replication forks can stall at specific genetic loci. At some loci, the stalling events depend on the replisome components  Schizosaccharomyces pombe  Swi1 ( Saccharomyces cerevisiae  Tof1) and Swi3 ( S .  cerevisiae  Csm3) as well as factors that bind DNA in a site-specific manner. Using a new genetic screen we identified Mrc1 ( S .  cerevisiae  Mrc1/ metazoan  Claspin) as a replisome component involved in replication stalling. Mrc1 is known to form a sub-complex with Swi1 and Swi3 within the replisome and is required for the intra-S phase checkpoint activation. This discovery is surprising as several studies show that  S .  cerevisiae  Mrc1 is not required for replication barrier activity. In contrast, we show that deletion of  S .  pombe mrc1  leads to an approximately three-fold reduction in barrier activity at several barriers and that Mrc1’s role in replication fork stalling is independent of its role in checkpoint activation. Instead,  S .  pombe  Mrc1 mediated fork stalling requires the presence of a functional copy of its phylogenetically conserved DNA binding domain. Interestingly, this domain is on the sequence level absent from  S .  cerevisiae  Mrc1. Our study indicates that direct interactions between the eukaryotic replisome and the DNA are important for site-specific replication stalling.

The DNA-Binding Domain of S. pombe Mrc1 (Claspin) Acts to Enhance Stalling at Replication Barriers