Mismatch repair (MMR) increases the fidelity of DNA replication by identifying 
and correcting replication errors. Processivity clamps are vital components of 
DNA replication and MMR, yet the mechanism and extent to which they participate 
in MMR remains unclear. We investigated the role of the Bacillus subtilis 
processivity clamp DnaN, and found that it serves as a platform for mismatch 
detection and coupling of repair to DNA replication. By visualizing functional 
MutS fluorescent fusions in vivo, we find that MutS forms foci independent of 
mismatch detection at sites of replication (i.e. the replisome). These MutS foci 
are directed to the replisome by DnaN clamp zones that aid mismatch detection by 
targeting the search to nascent DNA. Following mismatch detection, MutS 
disengages from the replisome, facilitating repair. We tested the functional 
importance of DnaN-mediated mismatch detection for MMR, and found that it 
accounts for 90% of repair. This high dependence on DnaN can be bypassed by 
increasing MutS concentration within the cell, indicating a secondary mode of 
detection in vivo whereby MutS directly finds mismatches without associating 
with the replisome. Overall, our results provide new insight into the mechanism 
by which DnaN couples mismatch recognition to DNA replication in living cells.