DNA replication is an essential process for cell growth. However, exposure to chemically damaging agents such as antibiotics or UV radiation can form lesions on the DNA strand, which may stall replication and ultimately lead to cell death. One way the cell prevents stalling during replication is through a DNA damage tolerance mechanism called translesion synthesis (TLS). During TLS, the replicative DNA polymerases are replaced by specialized translesion DNA polymerases that are able to continue synthesis past lesions. TLS polymerases are prone to mutagenic activity and have been found to facilitate the development of antibiotic resistance in bacteria, as well as to be upregulated in cancer in humans. Given their low fidelity, the activity of TLS polymerases in the cell must be properly regulated. Bacterial TLS has been primarily studied in the gram-negative bacterium Escherichia coli, but there appear to be considerable differences in the pathway of TLS in other species, including the model gram-positive bacterium Bacillus subtilis. To overcome the current research gap, research in our group uses in vivo single-molecule fluorescence microscopy to characterize the localization and dynamics of the TLS polymerase Pol Y1 in B. subtilis under normal conditions and upon DNA damage. This study also investigates the role of interactions with the replication processivity factor, the DnaN clamp, in Pol Y1 activity.

Characterizing translesion synthesis by Pol Y1 in Bacillus subtilis using single-molecule fluorescence microscopy

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