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. 2021 Aug 26;87(18):e00919-21. doi: 10.1128/AEM.00919-21

FIG 6.

FIG 6

Hypothetical model of ImuA function in template switching and TLS in M. xanthus. Bacteria have two pathways to rescue stalled replication forks, error-prone TLS and error-free template switching. When replication encounters a DNA damage lesion and is blocked, ssDNA is exposed as a DNA damage signal to activate the SOS response. The SOS genes, including recA1, imuA, imuB, and dnaE2, are induced. RecA protein binds to the ssDNA at the stalled replication fork to form nucleoprotein filaments and initiates the template-switching pathway. At the same time, DnaE2 approaches the stalled replication fork to initiate the TLS pathway. The combination of ImuA and RecA hinders the extension of RecA nucleoprotein filaments and the recombinase activity of RecA, thus inhibiting template switching. ImuB guides DnaE2 to assemble on the replication fork by binding to ImuA/β-clamp to start TLS. In the absence of ImuA, RecA binds to the exposed ssDNA to form a filament, which promotes error-free template switching.