Partial suppression of the LexA phenotype by mutations (rnm) which restore ultraviolet resistance but not ultraviolet mutability to Escherichia coli B/r uvr A lexA.
In Escherichia coli, lexA mutations eliminate expression of UV-inducible functions, causing pleiotropic effects which include sensitivity to ultraviolet (UV) light and loss of UV mutability. Selection for UV resistance, after 5-bromouracil (BU) treatment of E. coli B/r uvrA lexA-102, has yielded derivatives more resistant than lexA but still refractory to UV mutagenesis. The mutation responsible for the UV-resistant UV-nonmutable phenotype (rnm) is cotransducible with malB to about the same extent as is lexA-102 and is tightly linked to lexA-102 in at least one strain. The rnm mutation may therefore be an intragenic partial suppressor of the LexA phenotype. In addition to increased UV resistance and lack of UV mutability, rnm strains show improved ability to perform postreplication repair and to control postirradiation DNA degration compared to the lexA parent. We ascribe the properties of rnm mutants to their having reacquired control of Exonuclease V activity without having reacquired UV-inducible error-prone postreplication repair. We relate our results to current interpretations of UV mutagenesis and to models of coordinate regulation of UV-inducible functions.
D004926:Escherichia coli / Q000201:enzymology / Q000528:radiation effects*; D005092:Exonucleases / Q000378:metabolism; D009154:Mutation / Q000528:radiation effects*; D010641:Phenotype; D011831:Radiation Genetics; D014466:Ultraviolet Rays
D005092:Exonucleases