Cytoplasmic and nuclear mutations to chloramphenicol resistance in Aspergillus nidulans.
Two chloramphenicol resistance mutations out of 123 tested in Aspergillus nidulans are inherited extranuclearly as judged by transmissibility in heterokaryons, lack of segregation at meiosis, and independent segregation from all of the eight nuclear linkage groups. They do not recombine with each other. However, experiments in collaboration with G. Turner and R.T. Rowlands show that they do recombine with cytoplasmic mutations to oligomycin resistance (Rowlands and Turner, 1973) and cold-sensitivity (Waldron and Roberts, 1973). These cytoplasmic chloramphenicol resistance mutations are stable and do not affect growth or morphology on antibiotic-free media. Nuclear mutations to chloramphenicol resistance map at a minimum of three loci. At one of these loci, most, but not all, mutations lead pleiotropically to cycloheximide hypersensitivity, and most of these, but not all, also confer pleiotropic hypersensitivity to salicylhydroxamic acid.
D001233:Aspergillus nidulans / Q000187:drug effects* / Q000254:growth & development; D002701:Chloramphenicol / Q000494:pharmacology*; D002874:Chromosome Mapping; D002876:Chromosomes, Bacterial; D003080:Cold Temperature; D004352:Drug Resistance, Microbial; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D009153:Mutagens; D009154:Mutation; D009840:Oligomycins / Q000494:pharmacology; D011815:R Factors
D009153:Mutagens; D009840:Oligomycins; D008769:Methylnitronitrosoguanidine; D002701:Chloramphenicol