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一种新的关键毒力因子FoSSP71抑制植物免疫并促进草莓炭疽病菌的致病作用。

A novel key virulence factor, FoSSP71, inhibits plant immunity and promotes pathogenesis in f. sp. .

作者信息

Liu Shuang, Wu Junyu, Sun Yinhui, Xu Yun, Zhou Siyu, Luo Peiping, Wang Zhibiao, Chen Daipeng, Liang Xiaofei, Kang Zhensheng, Zheng Li

机构信息

National Key Laboratory for Tropical Crop Breeding, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Sanya, Hainan, China.

Key Laboratory of Green Prevention and Control of Tropical Plant Diseases and Pests, School of Tropical Agriculture and Forestry, Ministry of Education, Hainan University, Haikou, Hainan, China.

出版信息

Microbiol Spectr. 2025 Mar 25;13(5):e0294024. doi: 10.1128/spectrum.02940-24.

DOI:10.1128/spectrum.02940-24
PMID:40130862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12054145/
Abstract

wilt of banana ( spp.), caused by f. sp. (), poses a significant threat to the global banana industry. Particularly, tropical race 4 of exhibits high pathogenicity toward the major commercial banana cultivar Cavendish, and there are no effective control measures available. Here, we characterize a novel effector protein, FoSSP71, from , which was significantly induced during the early stages of the 4 banana interaction and could suppress BAX-triggered programmed cell death in . Transient expression of in leaves could weaken the upregulation expression of genes involved in the SA signaling pathway induced by flg22 and significantly reduce both reactive oxygen species bursts and callose accumulation. To verify the function of FoSSP71, a deletion mutant was created. The deletion mutant displayed a reduced growth rate in and a marked reduction in virulence toward bananas compared to the wild type (WT). Furthermore, the expression levels of and were significantly downregulated in bananas infected with the strain compared to bananas infected with the WT strain. These findings indicate that FoSSP71 is essential for 4 pathogenicity and plays a key virulence role during invasion. Therefore, FoSSP71 presents a potential target for future wilt control, offering a scientific foundation for breeding disease-resistant banana varieties and developing novel control measures.IMPORTANCEEffector proteins are critical virulence factors for fungi, playing essential roles during the fungal infection of plants. In this study, we identified a novel effector protein, FoSSP71, which is an important regulatory protein involved in the invasion of bananas by f. sp. race 4 (4). Understanding its regulatory mechanisms is necessary. Our research indicates that FoSSP71 is an essential virulence factor for 4, as it suppresses plant immune responses by inhibiting the accumulation of reactive oxygen species and callose. The 4 mutant lacking showed significantly reduced pathogenicity toward bananas, demonstrating that FoSSP71 is a potential target for controlling banana wilt disease. These findings provide a scientific basis for breeding banana varieties resistant to wilt disease and for developing new disease control strategies, which are crucial for the sustainable development of the global banana industry.

摘要

香蕉枯萎病(由尖孢镰刀菌古巴专化型引起)对全球香蕉产业构成重大威胁。特别是,古巴专化型热带4号生理小种对主要商业香蕉品种卡文迪什表现出高致病性,且目前没有有效的防治措施。在此,我们鉴定了一种来自尖孢镰刀菌古巴专化型热带4号生理小种的新型效应蛋白FoSSP71,它在与香蕉互作的早期阶段被显著诱导,并且能够抑制BAX触发的程序性细胞死亡。在烟草叶片中瞬时表达FoSSP71能够削弱由flg22诱导的水杨酸(SA)信号通路相关基因的上调表达,并显著降低活性氧爆发和胼胝质积累。为了验证FoSSP71的功能,构建了一个FoSSP71缺失突变体。与野生型相比,该缺失突变体在尖孢镰刀菌古巴专化型热带4号生理小种中生长速率降低,对香蕉的毒力显著下降。此外,与感染野生型菌株的香蕉相比,感染FoSSP71缺失菌株的香蕉中PAL和PR1的表达水平显著下调。这些结果表明,FoSSP71对古巴专化型热带4号生理小种的致病性至关重要,并且在其侵染过程中发挥关键的毒力作用。因此,FoSSP71是未来防治香蕉枯萎病的潜在靶点,为培育抗病香蕉品种和开发新的防治措施提供了科学依据。

重要性

效应蛋白是真菌关键的毒力因子,在真菌侵染植物过程中发挥重要作用。在本研究中,我们鉴定了一种新型效应蛋白FoSSP71,它是参与尖孢镰刀菌古巴专化型热带4号生理小种侵染香蕉的重要调控蛋白。了解其调控机制很有必要。我们的研究表明,FoSSP71是古巴专化型热带4号生理小种的必需毒力因子,因为它通过抑制活性氧和胼胝质的积累来抑制植物免疫反应。缺失FoSSP71的突变体对香蕉的致病性显著降低,表明FoSSP71是控制香蕉枯萎病的潜在靶点。这些发现为培育抗枯萎病香蕉品种和开发新的病害防治策略提供了科学依据,这对全球香蕉产业的可持续发展至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/a64841aef5e7/spectrum.02940-24.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/f8221d16096f/spectrum.02940-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/3d94c53ee428/spectrum.02940-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/aec5dc0477a4/spectrum.02940-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/1a580ebd64a6/spectrum.02940-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/5314486d125c/spectrum.02940-24.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/a64841aef5e7/spectrum.02940-24.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/f8221d16096f/spectrum.02940-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/3d94c53ee428/spectrum.02940-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/aec5dc0477a4/spectrum.02940-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/1a580ebd64a6/spectrum.02940-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/5314486d125c/spectrum.02940-24.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f722/12054145/a64841aef5e7/spectrum.02940-24.f006.jpg

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