PhcA and PhcR Regulate Ralsolamycin Biosynthesis Oppositely in .

Ralsolamycin, one of secondary metabolites in , is known to be involved in crosstalk between and fungi. Ralsolamycin formation is catalyzed by two-hybrid synthetases of RmyA (non-ribosomal peptide synthetase) and RmyB (polyketide synthase). A methyltransferase PhcB catalyzes formation of 3-OH MAME or 3-OH PAME, signals for the quorum sensing (QS) in , while PhcB positively modulates ralsolamycin biosynthesis. A two-component system of PhcS and PhcR can response these QS signals and activate expression. Here, we experimentally demonstrated that deletion of (Δ) substantially impaired the ralsolamycin production and expression of and in strain EP1, and failed to induce chlamydospore formation of plant fungal pathogen f. (stran FOC4). However, deletion of significantly increased ralsolamycin production and expression of and , and mutants exhibited enhanced ability to induce chlamydospore formation of FOC4. Results of the electrophoretic mobility shift assay suggested that both PhcA and PhcR bind to promoter of operon. Taken together, these results demonstrated that both PhcA and PhcR bind to promoter of operon, but regulate ralsolamycin biosynthesis in an opposite way. It could extend our knowledge on the sophisticated regulatory networks of ralsolamycin biosynthesis in .