Analysis of the biosynthetic gene cluster for the polyether antibiotic monensin in Streptomyces cinnamonensis and evidence for the role of monB and monC genes in oxidative cyclization

Molecular Microbiology
2003.0

Abstract

<jats:title>Summary</jats:title><jats:p>The analysis of a candidate biosynthetic gene cluster (97 kbp) for the polyether ionophore monensin from <jats:italic>Streptomyces cinnamonensis</jats:italic> has revealed a modular polyketide synthase composed of eight separate multienzyme subunits housing a total of 12 extension modules, and flanked by numerous other genes for which a plausible function in monensin biosynthesis can be ascribed. Deletion of essentially all these clustered genes specifically abolished monensin production, while overexpression in <jats:italic>S. cinnamonensis</jats:italic> of the putative pathway‐specific regulatory gene <jats:italic>monR</jats:italic> led to a fivefold increase in monensin production. Experimental support is presented for a recently‐proposed mechanism, for oxidative cyclization of a linear polyketide intermediate, involving four enzymes, the products of <jats:italic>monBI</jats:italic>, <jats:italic>monBII</jats:italic>, <jats:italic>monCI</jats:italic> and <jats:italic>monCII</jats:italic>. In frame deletion of either of the individual genes <jats:italic>monCII</jats:italic> (encoding a putative cyclase) or <jats:italic>monBII</jats:italic> (encoding a putative novel isomerase) specifically abolished monensin production. Also, heterologous expression of <jats:italic>monCI</jats:italic>, encoding a flavin‐linked epoxidase, in <jats:italic>S. coelicolor</jats:italic> was shown to significantly increase the ability of <jats:italic>S. coelicolor</jats:italic> to epoxidize linalool, a model substrate for the presumed linear polyketide intermediate in monensin biosynthesis.

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