Contribution of macrolactin in Bacillus velezensis CLA178 to the antagonistic activities against Agrobacterium tumefaciens C58

被引:1
|
作者
Lin Chen
Xinghong Wang
Yunpeng Liu
机构
[1] Chinese Academy of Forestry,Experimental Center of Forestry in North China
[2] Chinese Academy of Agricultural Sciences,Key Laboratory of Agricultural Microbial Resources Collection and Preservation, Ministry of Agriculture and Rural Affairs, Institute of Agricultural Resources and Regional Planning
[3] National Permanent Scientific Research Base for Warm Temperate Zone Forestry of Jiulong Mountain,undefined
来源
Archives of Microbiology | 2021年 / 203卷
关键词
Biocontrol; Macrolactin; Antagonistic;
D O I
暂无
中图分类号
学科分类号
摘要
Beneficial rhizobacteria can inhibit soilborne pathogens by secreting an array of polyketides, lipopeptides and dipeptides, but the effect of polyketides on crown gall disease caused by Agrobacterium tumefaciens C58 is unclear. In this study, the antagonistic compounds of the plant growth-promoting rhizobacterium Bacillus velezensis CLA178 was sorted with different organic phases, purified by high-pressure liquid chromatography, and detected by a liquid chromatography ionization-mass spectrometry system. Macrolactins were found to be the compounds with antagonistic activity against A. tumefaciens C58. When the macrolactin synthesis pathway was disrupted, the mutant △mlnA only showed slight antagonistic activity against A. tumefaciens C58. Transmission electron microscopy showed that the inhibition of C58 cell division by cell-free culture from the mutant △mlnA was weaker than that by cell-free culture from CLA178. The mutant deficient in production of macrolactin showed a weaker transcription of genes involved in attachment of C58 to plant and lower biocontrol of crown gall disease in rose than the wild-type strain CLA178. The effect of macrolactins on pathogen C58 has been also confirmed by the purified macrolactins. These results reveal that macrolactins contribute to the biocontrol activity of C58 by inhibiting cell division and downregulating the transcription of chvB and chvE.
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页码:1743 / 1752
页数:9
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