, A Global Regulatory Gene, is Required for Pyrrolnitrin but not for Phenazine-1-carboxylic Acid Biosynthesis in G05.

In our previous study, pyrrolnitrin produced in G05 plays more critical role in suppression of mycelial growth of some fungal pathogens that cause plant diseases in agriculture. Although some regulators for pyrrolnitrin biosynthesis were identified, the pyrrolnitrin regulation pathway was not fully constructed. During our screening novel regulator candidates, we obtained a white conjugant G05W02 while transposon mutagenesis was carried out between a fusion mutant G05ΔΔ:: and S17-1 (pUT/mini-Tn5Kan). By cloning and sequencing of the transposon-flanking DNA fragment, we found that a gene in the conjugant G05W02 was disrupted with mini-Tn5Kan. In one other previous study on , however, it was reported that the deletion of the caused increased production of pyrrolnitrin and other antifungal metabolites. To confirm its regulatory function, we constructed the -knockout mutant G05Δ and G05ΔΔ::Δ. By quantifying β-galactosidase activities, we found that deletion of the decreased the operon expression dramatically. Meanwhile, by quantifying pyrrolnitrin production in the mutant G05Δ, we found that deficiency of the Vfr caused decreased pyrrolnitrin production. However, production of phenazine-1-carboxylic acid was same to that in the wild-type strain G05. Taken together, Vfr is required for pyrrolnitrin but not for phenazine-1-carboxylic acid biosynthesis in G05.