SUMMARY: Evidence is presented that genes determining the pathway of methylenomycin A synthesis are carried on the SCP1 plasmid. All 16 mutations () 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 or , material that was chromatographically and biologically indistinguishable from methylenomycin A was produced. Recombination between some pairs of mutations was detected. In crosses of 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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