Repair of methyl methane sulfonate-damaged phage by Haemophilus influenzae.
Seven mutants of Haemophilus influenzae strain Rd (mmsA-) have been isolated that are more sensitive to methyl methane sulfonate (mms) than recombination-deficient (recA-) mutants. The mutations cotransformed about 25% with the strA locus while the five studied clustered tightly; they are all probably allelic. The mutants are not sensitive to ultraviolet radiation, X-rays, or nitrous acid. Mms-damaged phage HP1 plated very inefficiently on these mutants, indicating that they lack the first step in the excision repair of the lesion N3-methyladenine (m3A). Incubation of damaged phage at 30 degrees C in the absence of mms resulted in a steady decline of viability when the phage were plated on the wild mmsA+ host but an initial steep rise was seen when it was plated on an mmsA- mutant. The rise is explained by the assumption that m3A lesions hydrolyzed off the DNA giving rise to repairable apurinic sites by both the mmsA+ and mmsA- hosts. No decline in viability was observed when hydroxylamine was present in the medium. This compound is known to prevent or slow down beta-elimination. The delayed decline in viability is therefore explained by assuming that apurinic sites give rise to beta-elimination-induced single strand breaks in the phage DNA that cannot be repaired by either host. Marker rescue experiments indicated that these breaks did not interrupt injection of phage DNA.
D001435:Bacteriophages / Q000187:drug effects* / Q000235:genetics; D004260:DNA Repair; D004277:DNA, Single-Stranded / Q000235:genetics; D004279:DNA, Viral / Q000235:genetics; D006193:Haemophilus influenzae / Q000187:drug effects / Q000235:genetics*; D008741:Methyl Methanesulfonate / Q000494:pharmacology*; D008745:Methylation; D009154:Mutation
D004277:DNA, Single-Stranded; D004279:DNA, Viral; D008741:Methyl Methanesulfonate