1. Model for activation of the SOS response in B. subtilis.
Model for activation of the SOS response in B. subtilis. (A) In this model, UV damage has created a cyclobutane pyrimidine dimer (CPD) in the leading strand template, creating a daughter strand gap after repriming and continued replication beyond the lesion. (B) SSB binds to the daughter strand gap, preserving the integrity of the DNA. (C) Recombinase mediator proteins RecF, RecO, and RecR, and possibly other accessory factors, stimulate RecA loading at the gap region as SSB is displaced from the site. (D) RecA forms a nucleoprotein filament on ssDNA. (E) The RecA-ssDNA nucleoprotein filament then interacts with LexA, activating its latent protease activity and resulting in autocleavage of LexA. Following autocleavage and inactivation of LexA, SOS gene transcription is activated, and a global transcriptional response is induced. (F) SOS-dependent changes in gene expression help B. subtilis to survive DNA damage by upregulating DNA repair proteins, preventing the bacterium from undergoing cell division, and finally increasing the regulatory products RecA and LexA to reset the system after repair is completed. (Adapted from reference 385.)‏
Justin S. Lenhart et al. Microbiol. Mol. Biol. Rev. 2012; doi: /MMBR