Fig 10.

Model for DinB(C66A) activity in vivo. In dinB⁺ cells, Pol IV MPCs form relatively early in the SOS response or may be preexisting. However, as DNA damage becomes extensive or as Pol V cognate lesions are introduced, greater amounts of active Pol V are formed. The formation of Pol V requires the sequestration and cleavage of the accessory protein UmuD, forming UmuD′ and thereby reducing the activity of Pol IV complexes by direct competition for UmuD. In dinB(C66A) cells, Pol IV complexes form more frequently, as the MPC components exhibit an increased binding affinity for one another. The sequestration of UmuD to form Pol V mutasomes is consequently limited, as full-length UmuD remains bound to DinB(C66A) and RecA. This increases the activity of Pol IV, resulting in higher fidelity in the TLS of DinB cognate lesions, increased DinB-mediated extension to enhance HR, and limited TLS by Pol V complexes.