Mutation induction in Haemophilus influenzae by ICR-191. I. Development of a detection system for frameshift mutations.
The investigation of mutagenic mechanisms in Haemophilus influenzae has been confined until now to mutagens that normally produce mainly base pair substitutions. This paper describes the development of a system suitable for detecting frameshift mutations induced by ICR-191. The system involves reversions from thymidine dependence to thymidine independence. Evidence is presented from a comparison of the responses to ICR-191 and to N-methyl-N'-nitro-N-nitrosoguanidine that the system is specific for frameshift mutations. The genetic recombination involved in transformation leads to a marked increase in "spontaneous" reversion of the frameshift mutations but not of the base substitution mutations. Presumably, this is a consequence of mispairing, with consequent change in the number of bases, during the recombination.
D000585:Aminacrine / Q000031:analogs & derivatives / Q000494:pharmacology*; D000609:Aminoacridines / Q000494:pharmacology*; D001431:Bacteriological Techniques; D005815:Genetic Code; D005821:Genetic Techniques; D006193:Haemophilus influenzae / Q000235:genetics*; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D009152:Mutagenicity Tests / Q000379:methods*; D009153:Mutagens; D009154:Mutation; D009588:Nitrogen Mustard Compounds / Q000494:pharmacology*; D014176:Protein Biosynthesis
D000609:Aminoacridines; D009153:Mutagens; D009588:Nitrogen Mustard Compounds; D008769:Methylnitronitrosoguanidine; D000585:Aminacrine; C004294:acridine half-mustard