Lysobacter enzymogenes employs diverse genes for inhibiting hyphae growth and spore germination of soybean fungal pathogens.

Abstract

Lysobacter enzymogenes strain C3 (LeC3) is a potential biocontrol agent for plant diseases caused by fungi and oomycetes. Understanding the interaction between LeC3 and soybean pathogens at the molecular level could help improve its biocontrol efficacy. In this study, we obtained mutants with decreased abilities in inhibiting hyphae growth of the white mold pathogen Sclerotinia sclerotiorum. Insertion sites for 50 mutants, which no longer inhibited S. sclerotiorum hyphae growth in dual cultural assay, were determined and seven mutants were selected for further characterization. These seven mutants also completely lost their abilities in suppressing spore germination of Fusarium virguliforme, the causal agent of soybean sudden death syndrome. Furthermore, mutation of the seven genes, which encode diguanylate cyclase (Dgc), transcriptional regulators from the TetR family (TetR1 and TetR2), hemolysin III family channel protein (YqfA), type IV secretion system VirB10 protein (T4SS, VirB10), phenol hydroxylase (Ph), and phosphoadenosine phosphosulfate reductase (CysH), respectively, led to reduced production and/or secretion of four extracellular enzymes and heat stable antifungal factor (HSAF). These results suggested that these seven genes play important roles in L. enzymogenes in suppressing hyphae growth and spore germination of fungal pathogens, probably by influencing production and/or secretion of extracellular enzymes and HSAF.