目的:从细胞层面探究B.amyloliquefaciensBA-16-8所产fengycin对Penicillium expansum的抑制机制。方法:采用扫描电镜、透射电镜、核酸染色、光谱吸收和荧光显微观察分析fengycin对P.expansum细胞膜通透性及线粒体等细胞器的影响;采用凝胶阻滞实验探讨fengycin对菌丝体核酸的作用效果。结果:Fengycin处理P.expansum的菌丝体细胞,会导致细胞表面粗糙且细胞形态发生改变,细胞膜的完整性发生了改变,细胞结构遭到破坏。PI染色及光谱吸收实验结果显示,Fengycin可破坏细胞膜的完整性并增加P.expansum细胞膜的通透性。凝胶阻滞实验结果表明fengycin可与P.expansum的DNA于体外结合。结论:Fengycin可改变P.expansum的细胞膜通透性并作用于核酸,抑制基因的表达和细胞器的合成。
Objective: In order to explore theant amyloliquefaciensBA-16-8 on P. expansum at the (SEM), transmission electron microscopy (TEM), PI -fungal mechanism of fengycin produced by B. cell level. Methods: Scanning electron microscopy nucleic acid fluorescent dye (PNCFD), fluorescence microscopy (FM) and spectral absorption was performed to investigate the effect of fengycin on the cellular morphological characteristics and structure of P. expansum mycelium. Electrophoretic mobility shift assays (EMSA) was performed toexamine the effect of fengycin on the nucleic acid of P. expansum. Results: SEM and TEM results revealed that the surface and intracellular protoplasm of P. expansum mycelium became roughand the morphological structure of the fungal cells were alteredafter with fengycin treatments, which meant fengycin could damage the cell membrane integrity and cell structure. The result of EMSA indicated that fengycin could combine with nonspecific P. expansum DNA in vitro. Conclusion: Fengycin could alter the cell membrane integrity and combined with nucleic acid such as DNA, which could inhibit gene expression and organelle synthesis.