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组学揭示猕猴桃中LMY3 - 5对(病原体)防御作用的见解

Omics insights into LMY3-5 defense against in kiwifruit.

作者信息

Ren Chunguang, Liu Yu, Su Wenwen, Han Zhengcheng, Wu Di, Li Weijie

机构信息

Guizhou Institute of Mountain Resources, Guiyang, China.

Guizhou Botanical Garden, Guiyang, China.

出版信息

Front Microbiol. 2025 Aug 20;16:1633015. doi: 10.3389/fmicb.2025.1633015. eCollection 2025.

Abstract

is the main cause of soft rot in kiwifruit, significantly reducing both yield and quality. While chemical treatments are commonly used, their effectiveness is limited and they may pose environmental risks. As a result, biological control using Bacillus species has emerged as a promising alternative. In this study, we explored the antifungal mechanism of the biocontrol strain LMY3-5 against kiwifruit soft rot through integrated genomic and transcriptomic analyses. In terms of antagonistic activity: LMY3-5 exhibits strong antagonism against , the causal agent of kiwifruit soft rot, showing a 70.44% biocontrol efficacy in inoculation tests. In terms of genomic features: genome 4.03 Mb circular chromosome with 46.5% GC content. Eight antimicrobial BGCs were identified, including those for surfactin, fengycin, bacillaene, bacillibactin, and others, explaining its biocontrol potential. In terms of transcriptomic insights: during coculture with , 114 DEGs (31 upregulated, 93 downregulated) were detected. Downregulated: flagellar assembly and chemotaxis genes (suggesting reduced motility during antagonism). Upregulated: genes linked to fengycin, siderophores, and lysozyme production, critical for antifungal activity. In terms of mechanism and implications lipopeptides (e.g., fengycin) and siderophores are key in inhibiting fungal growth. Findings support LMY3-5's potential as a biocontrol agent for plant protection against . The main conclusion of this study is LMY3-5 combats via antimicrobial metabolites, with genomics and transcriptomics revealing its molecular basis for biocontrol. This strain holds promise for sustainable plant disease management. This may provide a theoretical basis for the potential application of LMY3-5 in the field of plant protection in the future.

摘要

是猕猴桃软腐病的主要病因,会显著降低产量和品质。虽然化学处理方法常用,但其效果有限且可能带来环境风险。因此,利用芽孢杆菌属进行生物防治已成为一种有前景的替代方法。在本研究中,我们通过整合基因组和转录组分析,探究了生防菌株LMY3 - 5对猕猴桃软腐病的抗真菌机制。在拮抗活性方面:LMY3 - 5对猕猴桃软腐病的病原菌表现出强烈拮抗作用,在接种试验中显示出70.44%的生防效果。在基因组特征方面:基因组为4.03 Mb的环状染色体,GC含量为46.5%。鉴定出8个抗菌生物合成基因簇,包括表面活性素、丰原素、杆菌霉素、杆菌铁载体等相关基因簇,解释了其生防潜力。在转录组见解方面:与共培养期间,检测到114个差异表达基因(31个上调,93个下调)。下调的基因:鞭毛组装和趋化性基因(表明拮抗过程中运动性降低)。上调的基因:与丰原素、铁载体和溶菌酶产生相关的基因,这些对抗真菌活性至关重要。在作用机制及意义方面:脂肽(如丰原素)和铁载体是抑制真菌生长的关键。研究结果支持LMY3 - 5作为防治植物软腐病生防菌剂的潜力。本研究的主要结论是LMY3 - 5通过抗菌代谢产物对抗软腐病,基因组学和转录组学揭示了其生防的分子基础。该菌株有望用于可持续的植物病害管理。这可能为未来LMY3 - 5在植物保护领域的潜在应用提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ff6/12405161/10c869b93e65/fmicb-16-1633015-g001.jpg

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