title: Chloramphenicol acetylransferase-independent chloramphenicol resistance in Streptomyces coelicolor A3(2).
abstract: Streptomyces coelicolor A3(2) and S. lividans 66, which lack chloramphenicol acetyltraferase, gave rise to vhloramphenicol-sensitive (CmlS) variants spontaneously at frequencies of 0-5 to 2%. The fertility type of S. coelicolor in respect of the SCPI plasmid (SCPI+, SCPI- or NF) had no effect on chloramphenicol sensitivity or on the frequency at which CmlS variants arose. CmlS isolates spontaneously reverted to CmlR at frequencies one to three orders of magnitude lower than the frequency with which CmlS strains arose from CmlR. CmlR revertants obtained spontaneously from CmlS clones again produced CmlS isolates at the normal frequency of several per cent. Therefore, CmlS and CmlR are reversible phenotypes. In crosses between marked CmlR and CmlS S. coelicolor strains, transfer of chloramphenicol resistance into the sensitive strain apparently occurred independently of chromosomal recombination. Mapping experiments excluded the possibility that segregation of a chromosomal locus determines CmlR versus CmlS phenotype. In crosses between SCPI- strains, fertility was not significantly different in CmlR x CmlS, CmlR x CmlR and CmlS x CmlS combinations. Covalently closed circular DNA from CmlS and CmlR strains of S. coelicolor was indistinguishable in molecular weight and restriction endonuclease cleavage pattern. It is suggested that chloramphenicol resistance in S. coelicolor A3(2)  is affected by some kind of transposable genetic element that may be capable of extra-chromosomal existence.
mesh_terms: D000123:Acetyltransferases; D002701:Chloramphenicol / Q000494:pharmacology*; D002874:Chromosome Mapping; D002876:Chromosomes, Bacterial; D003433:Crosses, Genetic; D004352:Drug Resistance, Microbial; D005111:Extrachromosomal Inheritance; D013302:Streptomyces / Q000187:drug effects* / Q000201:enzymology
chemical_list: D002701:Chloramphenicol; D000123:Acetyltransferases