RecA-independent mutagenesis in Escherichia coli may be subject to glucose repression

Abstract

The frameshift mutagen 9-aminoacridine (9AA) causes DNA damage via a recA +-independet mechanism in Escherichia coli. In this this study we have exposed E. Coli cells carrying the lacZ19124 frameshift marker to 9AA in defined minimal media, washed them, and plated to score for Lac + revertants. Our results show that 9AA-induced reversion to Lac + occures in teh absence of any exogenous carbon source and when cells are plated on media which do not allow much, if any, cell replication prior to expression of ther revertant phenotype. When glycerol (1% w/v) was added to the liquid tratment medium, the number of Lac + E. Coli revertants was similar to that obtained when no carbon source was present. By contrast the addition of glucose (1% w/v) during the mutagenesis treatment caused a significant decreae in the number of revertants. Further experiments indicate that the repressing effects of glucose may be due to a reduction in cAMP concentration, since 9AA mutgenesis was abolished in a cya strain in which no adenylate cyclase is produced. These results are consistent with (butdo not prove) the notion that at least one part of the process leading to 9AA mutagenesis is subject to catabolite repression.