The SOS repair system tackles severely damaged DNA, especially regions where the DNA has become single-stranded.
Error prone repair fills in dangerous gaps in the DNA at the cost of generating base changes, i.e., point mutations.
many RecA proteins. Activated RecA induces the SOS system by activating LexA, a transcriptional repressor of the SOS genes, by inducing its self-cleavage. Once cleaved, LexA no longer blocks transcription of SOS genes. The SOS proteins combat the DNA damage (Fig. 14.24).
Among the genes induced by the SOS response two are of special note. These are umuC and umuD (umu = ultraviolet mutagenesis), which encode DNA polymerase V. This polymerase lacks a proofreading subunit so it can replicate past pyrimidine dimers and missing bases (i.e. AP-sites). PolV makes mistakes when passing damaged DNA and, for example, tends to put in GA (rather than the correct AA) opposite a thymine dimer. Normal DNA polymerase (PolIII) cannot replicate past such damage because its proofreading subunit stops it from proceeding until a correct base pair has been inserted. If this is impossible due to damage, then PolIII grinds to a halt and PolV takes over. The PolV subunits, UmuC and UmuD, form a complex containing a dimer of UmuD plus one UmuC protein. However, when first made, UmuD2C does not act as a polymerase but delays normal DNA replication in order to allow time for repair. Activated RecA then induces UmuD to undergo self-cleavage to UmuD'. When a
DNA polymerase V A repair polymerase in bacteria that can replicate past pyrimidine dimers and AP-sites ds DNA
Broken new strand
Replication halts ^ at damage and re-initiates beyond damage
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