Isolation and characterization of mutants of the plasmid pKM101 deficient in their ability to enhance mutagenesis and repair

Publisher Website
Google Scholar
Abstract
A screening procedure was developed for identifying mutants of the plasmid pKM101 no longer capable of enhancing mutagenesis. The test was based on the large pKM101-mediated increase in the number of Gal+ papillae observed on colonies of Salmonella typhimurium gal mutants plated on tetrazolium-galactose plates in the presence of a mutagen. The pKM101 mutant plasmids transferred normally, were stably maintained in cells, caused normal levels of ampicillin resistance, and still imparted sensitivity to phage Ike to their hosts. The pKM101 mutants lost the ability to enhance the reversion of both point and frameshift mutations, protect the cells against killing by UV irradiation, increase the spontaneous reversion rates of point mutations, enhance plasmid-mediated reactivation of UV-irradiated phage P22, enhance Weigle reactivation. One pKM101 mutant with different properties from the others was identified by its increased spontaneous mutator effect. Plasmid pKM101 amplifies the activity of the inducible error-prone [DNA] repair systems in bacteria and this is the function of pKM101 in the Ames Salmonella tester strains used for detection of carcinogens as mutagens.

This publication has 36 references indexed in Scilit: