Biological control of potato late blight by Streptomyces sp. FXP04 and potential role of secondary metabolites.

• Streptomyces sp. FXP04 inhibited the mycelial growth of P. infestans in vitro. • Streptomyces sp. FXP04 reduced late blight damage on potato plants in pot trials. • Streptomyces sp. FXP04 secretes Piericidin A, a polyketide secondary metabolite. • Piericidin A inhibits the mycelial growth of P. infestans in vitro. Potato late blight, caused by the oomycete Phytophthora infestans , is a devastating disease of potato globally. Antagonistic microorganisms have been used as biological control agents to inhibit P. infestans and reduce the use of synthetic fungicides. In the present study, a bacterial isolate (FXP04) was obtained from the rhizosphere soil of potato plants and demonstrated to significantly inhibit the mycelial growth of P. infestans in vitro. In a pot experiment, application of FXP04 to potato tubers prior to planting and to the soil after planting decreased both disease incidence and the disease index of potato late blight. Analysis of the 16S rDNA sequence of FXP04 indicated that the strain belonged to the genus, Streptomyces, and thus the strain was named Streptomyces sp. FXP04. The genome of Streptomyces sp. FXP04 was sequenced to determine the presence of gene clusters encoding secondary metabolites. AntiSMASH software analysis identified 15 gene clusters responsible for the biosynthesis of secondary metabolites, including the antimicrobial compound, Piericidin A. Metabolomic analysis of the fermentation broth of Streptomyces sp. FXP04 identified the presence of Piericidin A. Additional experiments indicated that Piericidin A inhibited the mycelial growth of P. infestans. The results of our study indicate that Streptomyces sp. FXP04 represents a potential biocontrol agent that could be used to control potato late blight. Furthermore, Piericidin A may represent the antimicrobial secondary metabolite responsible for the biological control activity of Streptomyces sp. FXP04. [ABSTRACT FROM AUTHOR]