Abstract
Evidence is presented that genes determining the pathway of methylenomycin A synthesis are carried on the SCP1 plasmid. All 16 mutations (mmy) leading to lack of antibiotic synthesis were SCP1-linked. Phenotypic classification, by co-synthesis and other criteria, suggested that they fell into at least five classes. When the wild-type SCP1 plasmid was transferred to Streptomyces lividans or Streptomyces parvulus, material that was chromatographically and biologically indistinguishable from methylenomycin A was produced. Recombination between some pairs of mmy mutations was detected. In crosses of mmy mutants of NF (integrated SCP1 donor) strains with SCP1-, a very high frequency of chromosomal recombination occurred; thus methylenomycin production appears not to be an important cause of the ultra-fertility normally associated with NF X SCP1- crosses.
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