Inducible Excision Repair in Escherichia coli
Excision repair of ultraviolet-irradiation (UV) damage in wild type Escherichia coli results in a bimodal distribution of repair patch sizes.1 The majority of lesions are repaired with short patches approximately 20 nucleotides in length by a pathway mediated by DNA polymeras I, while a minority are repaired with much longer patches by a recA+ -dependent pathway.2 Excision repair assayed by closure of incision breaks similarly seems to proceed via two pathways, one which is polymerase I-dependent and one which is recA+-dependent. The latter pathway additionally requires the lexAnotype and protein synthesis.3 The long patch pathway and the recA+-dependent closure of incision breaks presumably represent manifestations of a single process, having a number of features in common with the coordinately controlled group of responses to DNA damage known collectively as “SOS functions”.4 Indeed, it has recently been shown that long patch repair is UV-inducible and requires protein synthesis, unlike the constitutive short patch pathway;5 moreover, the requirement for the lexA + genotype as well as recA+ for long patch repair has been confirmed.° However, the role of the long patch pathway, its relationship to other inducible responses to damage, and its importance for cell survival have yet to be established. We have begun to address these questions through use of the tif mutations7 to induce the long patch pathway prior to DNA damage.
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