Recombinant E. coli LexA protein (a.a. 1-202) [His]

Stress-induced mutagenesis is a collection of mechanisms observed in bacterial, yeast, and human cells in which adverse conditions provoke mutagenesis, often under the control of stress responses. Control Of mutagenesis by stress responses may accelerate evolution specifically when cells are maladapted to their environments, i.e., are stressed. It is therefore important to understand how stress responses increase mutagenesis. In the Escherichia coli Lac assay, stress-induced point mutagenesis requires induction Of at least two stress responses: the RpoS-controlled general/starvation stress response and the SOS DNA-damage response, both of which upregulate Mull error-prone DNA polymerase, among other genes required for Lac mutagenesis. We show that upregulation of Mull is the only, aspect of the SOS response needed for stress-induced mutagenesis. We constructed two dinB(o(c)) (operator-constitutive) Mutants. Both produce SOS-induced levels of DinB constitutively. WC find that both dinB(o(c)) alleles fully suppress the phenotype of constitutively SOS-"off" lexA(Ind(-)) mutant cells, restoring normal levels of stress-induced mutagenesis. Thus, dinB is the only SOS gene required at induced levels for stress-induced point. mutagenesis. Furthermore, although spontaneous SOS induction has been observed to occur ill only a small fraction of cells, upregulation of din B by the dinB(oc) alleles in all cells does not promote a further increase in mutagenesis, implying that SOS induction of DinB, although necessary, is insufficient to differentiate cells into a hypermutable condition.

The main problem of the modern medical microbiology is the widespread resistance of bacteria to many antibiotics used in therapy. Resistance to antibiotics is mainly developed due to mutations in the bacterial genome. One of the proposed mechanisms for the occurrence of mutations is the functioning of the inducible SOS response system, the proteins of which are synthesized in the cell affected by antibiotics. The RecA and LexA proteins encoded by the corresponding genes are regulators of the SOS response in bacteria. The effect of the recA13 and lexA1 mutations on bacterial resistance to nalidixic acid and novobiocin and on the rates of antibiotic resistance development was studied. The SOS response system was shown to play a minor role in the development of the bacterial resistance to quinolones and aminocoumarins, as well as in mutagenesis, during application of these antibiotics.