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. 2023 Dec 5;48(1):fuad065. doi: 10.1093/femsre/fuad065

Figure 3.

Figure 3.

Proposed model for remodeling stalled forks in B. subtilis. (A) and (G) When a replisome encounters a lesion in the template strand, it stalls and disassembles. SsbA bound to the resulting lesion-containing gap on the template leading-strand [termed here forked-Lead (A)] or on the template lagging-strand [termed here forked-Lag (G)] inhibits RecA loading. Mediators such as RecO (or RecO–RecR, not depicted), or RadA/Sms, displace SsbA, and interact with and recruit RecA, which then binds onto the lesion-containing gap on the template strand. DisA scans the genome, searching for branched intermediates, and pauses. DisA interacts with and inhibits the ATPase of RecA, and this indirectly avoids filament growth and SOS induction. (B) and (H) RecA bound to the template strand interacts with and loads the RadA/Sms helicase on the nascent-lagging-strand, with RadA/Sms unwinding it. (C) and (I) Spontaneous remodeling (or fork remodeler-mediated) places the deleterious lesion on duplex DNA for its removal by specialized pathways. Finally, PriA, which recognizes a 3′-fork DNA, recruits other preprimosomal proteins (DnaD–DnaD–DnaI) to load the DnaC helicase for replication restart. (D) and (J). Alternatively, the RecG remodeler converts forked-Lead (A) into a HJ DNA with a nascent lagging-strand longer than the leading-strand (termed here HJ-Lag DNA) (D), or the forked-Lag (G) into a HJ DNA with a nascent leading-strand longer than the lagging-strand (termed here HJ-Lead DNA) (J). DisA bound to these HJ structures limits RecG or RuvAB mediated branch migration, and RuvAB–RecU-mediated HJ cleavage. RadA/Sms bound itself (E), or been recruited by RecA bound to HJ-Lead DNA (K), unwinds the nascent lagging-strand to yield a 3′-fork DNA. Then, PriA bound to the 3′-fork DNA substrate recruits other preprimosomal components to reinitiate DNA replication (F) and (L). (E) RecA, with the help of its accessory proteins (RecO and SsbA) or DisA may limit RadA/Sms loading at the 5′-tailed HJ-Lag DNA to facilitate that DNA synthesis occurs by the extension of the nascent leading-strand using the nascent lagging-strand as a template to bypass the deleterious lesion. (K) DisA and SsbA may regulate RadA/Sms recruitment by RecA to HJ-Lead DNA.