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通过转录组分析评估脂肽类丰原素对马铃薯的生物防治作用及作用机制

Biocontrol and Action Mechanism of Lipopeptides' Fengycins Against in Potato as Assessed by a Transcriptome Analysis.

作者信息

Zhang Dai, Qiang Ran, Zhou Zhijun, Pan Yang, Yu Shuiqing, Yuan Wei, Cheng Jianing, Wang Jinhui, Zhao Dongmei, Zhu Jiehua, Yang Zhihui

机构信息

College of Plant Protection, Hebei Agricultural University, Baoding, China.

Practice and Training Center, Hebei Agricultural University, Baoding, China.

出版信息

Front Microbiol. 2022 May 11;13:861113. doi: 10.3389/fmicb.2022.861113. eCollection 2022.

DOI:10.3389/fmicb.2022.861113
PMID:35633712
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9130778/
Abstract

is an airborne fungus and the primary causal agent of potato early blight worldwide. No available fungicides that are both effective and environmentally friendly are usable to control this fungus. Therefore, biological control is a potential approach for its suppression. In this study, strain ZD01's fermentation broth strongly reduced pathogenicity under greenhouse conditions. The effects of strain ZD01's secondary metabolites on were investigated. The exposure of hyphae to the supernatant resulted in swelling and swollen sacs, and the ZD01 supernatant reduced conidial germination significantly. Matrix-assisted laser desorption/ionization time of flight mass spectrometry and pure product tests revealed that fengycins were the main antifungal lipopeptide substances. To elucidate the molecular mechanism of the fengycins' biological control, RNA sequencing analyses were performed. A transcriptome analysis revealed that 304 and 522 genes in were differentially expressed after 2-h and 6-h fengycin treatments, respectively. These genes were respectively mapped to 53 and 57 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. In addition, the most enriched KEGG pathway analysis indicated that the inhibitory mechanisms of fengycins against regulated the expression of genes related to cell wall, cell membrane, transport, energy process, protein synthesis and genetic information. In particular, cell wall and cell membrane metabolism were the main processes affected by fengycin stress. Scanning and transmission electron microscope results revealed hyphal enlargement and a wide range of abnormalities in cells after exposure to fengycins. Furthermore, fengycins induced chitin synthesis in treated cells, and also caused the capture of cellular fluorescent green labeling and the release of adenosine triphosphate (ATP) from outer membranes of cells, which may enhance the fengycins ability to alter cell membrane permeability. Thus, this study increases the transcriptome data resources available and supplies a molecular framework for ZD01 inhibition of HWC-168 through various mechanisms, especially damaging cell walls and membranes. The transcriptomic insights may lead to an effective control strategy for potato early blight.

摘要

是一种空气传播的真菌,也是全球马铃薯早疫病的主要致病因子。目前没有既有效又环保的可用杀菌剂来控制这种真菌。因此,生物防治是抑制它的一种潜在方法。在本研究中,菌株ZD01的发酵液在温室条件下显著降低了致病性。研究了菌株ZD01次生代谢产物对其的影响。将病原菌菌丝暴露于上清液中会导致肿胀和囊泡肿大,并且ZD01上清液显著降低了分生孢子萌发率。基质辅助激光解吸/电离飞行时间质谱和纯产物测试表明,丰原素是主要的抗真菌脂肽物质。为阐明丰原素生物防治的分子机制,进行了RNA测序分析。转录组分析显示,在丰原素处理2小时和6小时后,病原菌中分别有304个和522个基因差异表达。这些基因分别映射到53条和57条京都基因与基因组百科全书(KEGG)途径。此外,最富集的KEGG途径分析表明,丰原素对病原菌的抑制机制调节了与细胞壁、细胞膜、转运、能量过程、蛋白质合成和遗传信息相关基因的表达。特别是,细胞壁和细胞膜代谢是受丰原素胁迫影响的主要过程。扫描和透射电子显微镜结果显示,暴露于丰原素后病原菌细胞出现菌丝肿大和广泛的异常。此外,丰原素诱导处理后细胞中几丁质合成,还导致细胞荧光绿色标记的捕获以及病原菌细胞外膜三磷酸腺苷(ATP)的释放,这可能增强了丰原素改变细胞膜通透性的能力。因此,本研究增加了可用的转录组数据资源,并为菌株ZD01通过多种机制抑制病原菌HWC - 168提供了分子框架,尤其是破坏病原菌的细胞壁和细胞膜。转录组学见解可能会带来一种有效的马铃薯早疫病防治策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/e24b8c9bde3b/fmicb-13-861113-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/70279386115b/fmicb-13-861113-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/96f2f8b0ce1c/fmicb-13-861113-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/3dbf445efb78/fmicb-13-861113-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/ccec1420c531/fmicb-13-861113-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/f10633e2a425/fmicb-13-861113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/2e16b7071c72/fmicb-13-861113-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/e24b8c9bde3b/fmicb-13-861113-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/70279386115b/fmicb-13-861113-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/a486ca559f67/fmicb-13-861113-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/96f2f8b0ce1c/fmicb-13-861113-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/3dbf445efb78/fmicb-13-861113-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/ccec1420c531/fmicb-13-861113-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/f10633e2a425/fmicb-13-861113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/2e16b7071c72/fmicb-13-861113-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a766/9130778/e24b8c9bde3b/fmicb-13-861113-g008.jpg

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