PriA and PriC recognize abandoned replication forks and direct reloading of the DnaB replicative helicase onto the lagging-strand template coated with single-stranded DNA-binding protein (SSB). Both PriA and PriC have been shown by biochemical and structural studies to physically interact with the C terminus of SSB. , these interactions trigger remodeling of the SSB on ssDNA. (R697A) and (R155A) negated the SSB remodeling reaction Plasmid-carried (R155A) did not complement ::, and (R697A) has not yet been tested for complementation. Here, we further studied the SSB-binding pockets of PriA and PriC by placing (R697A), (R697E), (Q701E), and (R155A) on the chromosome and characterizing the mutant strains. All three mutants behaved like the wild type. In a Δ strain, the mutations caused modest increases in SOS expression, cell size, and defects in nucleoid partitioning (Par). Overproduction of SSB partially suppressed these phenotypes for (R697A) and (R697E). The (R155A) mutant behaved as expected: there was no phenotype in a single mutant, and there were severe growth defects when this mutation was combined with Δ Analysis of the mutant revealed two populations of cells: those with wild-type phenotypes and those that were extremely filamentous and Par and had high SOS expression. We conclude that , (R155A) identified an essential residue and function for PriC, that PriA R697 and Q701 are important only in the absence of PriB, and that this region of the protein may have a complicated relationship with SSB. PriA and PriC recruit the replication machinery to a collapsed replication fork after it is repaired and needs to be restarted. studies suggest that the C terminus of SSB interacts with certain residues in PriA and PriC to recruit those proteins to the repaired fork, where they help remodel it for restart. Here, we placed those mutations on the chromosome and tested the effect of mutating these residues The mutation completely abolished function. The mutations had no effect by themselves. They did, however, display modest phenotypes in a -null strain. These phenotypes were partially suppressed by SSB overproduction. These studies give us further insight into the reactions needed for replication restart.