RESUMO
The lon(-) mutants of Escherichia coli grow apparently normally except that, after temporary periods of inhibition of deoxyribonucleic acid synthesis, septum formation is specifically inhibited. Under these conditions, long, multinucleate, nonseptate filaments result. The lon(-) mutation also creates a defect such that wild-type bacteriophage lambda fails to lysogenize lon(-) mutants efficiently and consequently forms clear plaques on a lon(-) host. Two lines of evidence suggest that this failure probably results from interference with expression of the lambdacI gene, which codes for repressor, or with repressor action:-(i) when a lon(-) mutant was infected with a lambdacII, cIII, or c Y mutant, there was an additive effect between the lon(-) mutation and the lambdac mutations upon reduction of lysogenization frequency; and (ii) lon(-) mutants permitted the growth of the lambdacro(-) mutant under conditions in which the repressor was active. The isolation of lambda mutants (lambdatp) which gained the ability to form turbid plaques on lon(-) cells is also reported.