lon incompatibility associated with mutations causing SOS induction: Null uvrD alleles induce an SOS response in Escherichia coli

The uvrD gene in Escherichia call encodes a 720-amino-acid 3'-5' DNA helica se which, although nonessential for viability, is required for methyl-direc ted mismatch repair and nucleotide excision repair and furthermore is belie ved to participate in recombination and DNA replication. We have shown in t his study that null mutations in uvrD are incompatible with lan, the incomp atibility being a consequence of the chronic induction of SOS in uvrD strai ns and the resultant accumulation of the cell septation inhibitor SulA (whi ch is a normal target for degradation by Lon protease), uvrD-lon incompatib ility was suppressed by sulA, lexA3(Ind(-)), or recA (Def) mutations. Other mutations, such as priA, dan, polA, and dnaQ (mutD) mutations, which lead to persistent SOS induction, were also ion incompatible. SOS induction was not observed in uvrC and mutH (or nutS) mutants defective, respectively, in excision repair and mismatch repair, Nor was uvrD-mediated SOS induction a bolished by mutations in genes that affect mismatch repair (mutH), excision repair (uvrC), or recombination (recB and recF), These data suggest that S OS induction in uvrD mutants is not a consequence of defects in these three pathways. We propose that the UvrD helicase participates in DNA replicatio n to unwind secondary structures on the lagging strand immediately behind t he progressing replication fork, and that it is the absence of this functio n which contributes to SOS induction in uvrD strains.