Fengycin Controls the Apple Blue Disease Caused by Penicillium expansum

摘要

The fenC gene deletion mutant of Bacillus amyloliquefaciens BA-16-8 was constructed to investigate the function of fengycin in controlling apple blue mold disease. The upstream and the downstream sequences of the fenC gene were cloned through PCR by using the genome of B. amyloliquefaciens BA-16-8 as a template in accordance with the homologous recombination principle. The recombinant plasmid pMAD-Δfen was constructed by connecting the upstream and the downstream homologous regions of fenC with the spectinomycin resistance gene spc and then transformed into B. amyloliquefaciens through electroporation. The fenC knockout mutant strain BA-16-8-Δfen was subcultured continuously at 42°C and selected though blue–white colony screening, high-temperature screening, and antibiotic resistance tests. The inhibitory effect of the fengycin-deficient mutant BA-16-8-Δfen on apple blue mold disease was tested via high-performance liquid chromatography, mass spectrometry, and Penicillium expansum growth inhibition assay in vitro. Compared with the wild-type B.amyloliquefaciens BA-16-8 strain, the B. amyloliquefaciens BA-16-8-Δfen mutant lost its fengycin-synthesizing capability and showed a significantly reduced inhibitory effect against P. expansum. This study concludes that Fengycin is the key component of B. amyloliquefaciensBA-16-8 in the control of blue mold disease.