Hydrazine and methylhydrazine as recA+-independent mutagens in Escherichia coli

The ultimate cause of both physical and chemical mutagenesis is assumed in most cases, to be some inducible error-prone repair process acting on the lesions caused by the mutagenic agent 7]. In Escherichia coli this mutagenic pathway seems to be dependent on both recA⁺ and lexA⁺ loci 10]. There are some mutagens, however, such as simple base analogs or some strong alkylating agents, such as N-methyl-N′-nitro-N′-nitrosoguanidine, that probably act by simply causing mis-pairing of bases in DNA. There is some evidence, based on work done with bacteriophages 2] or with Haemophilus influenzae 6], that hydrazine also acts by producing errors in base pairing. In this paper, further evidence is reported in support of this theory by showing that the recA lexA genotype does not affect the mutagenic properties of either hydrazine or methylhydrazine in Escherichia coli.