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效应因子 FsMEP1 通过干扰甘蔗硫胺素噻唑合成酶 ScTHI2 的定位来促进毒力。

Effector FsMEP1 Contributes to Virulence by Disturbing Localization of Thiamine Thiazole Synthase ScTHI2 from Sugarcane.

机构信息

Guangxi Key Laboratory of Sugarcane Biology, Nanning 530004, China.

State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530004, China.

出版信息

Int J Mol Sci. 2024 Nov 10;25(22):12075. doi: 10.3390/ijms252212075.

DOI:10.3390/ijms252212075
PMID:39596144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11593444/
Abstract

is a significant pathogenic fungus that causes sugarcane Pokkah Boeng. Proteins secreted by pathogenic fungi can be delivered into hosts to suppress plant immunity and establish infection. However, there is still much to be discovered regarding 's secreted effectors in overcoming plant immunity. In this paper, we characterize a novel effector called FsMEP1, which is essential for the virulence of . FsMEP1 contains a conserved zinc-binding motif sequence, HEXXH, and is highly expressed during host infection. Using the -mediated transient expression system, it was confirmed that FsMEP1 could suppress Bcl-2-associated X protein (BAX)-triggered cell death, callose deposition, and ROS explosion in . Furthermore, the deletion of FsMEP1 demonstrated its requirement for contributing to the pathogenicity of in sugarcane. Further analysis revealed that FsMEP1 could interact with the sugarcane thiamine thiazole synthase ScTHI2 and disrupt its normal localization, thereby inhibiting the synthesis of thiamine and the defense responses mediated by ScTHI2. Based on these findings, we propose that ScTHI2 represents a potential molecular target for improving sugarcane resistance to Pokkah Boeng disease.

摘要

是一种重要的致病真菌,可引起甘蔗泊赫博恩病。致病真菌分泌的蛋白质可以被输送到宿主中,抑制植物免疫并建立感染。然而,对于在克服植物免疫方面的“分泌效应物”,仍有许多需要发现。在本文中,我们描述了一种名为 FsMEP1 的新型效应物,它是致病所必需的。FsMEP1 含有一个保守的锌结合基序序列 HEXXH,并且在宿主感染期间高度表达。使用介导的瞬时表达系统,证实 FsMEP1 可以抑制 Bcl-2 相关 X 蛋白 (BAX) 触发的细胞死亡、胼胝质沉积和 ROS 爆发。此外,FsMEP1 的缺失表明其对甘蔗中致病的贡献。进一步的分析表明,FsMEP1 可以与甘蔗硫胺素噻唑合酶 ScTHI2 相互作用并破坏其正常定位,从而抑制硫胺素的合成和由 ScTHI2 介导的防御反应。基于这些发现,我们提出 ScTHI2 代表了提高甘蔗对泊赫博恩病抗性的潜在分子靶标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/159d24cb92bc/ijms-25-12075-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/514aade4f890/ijms-25-12075-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/443da7bff37b/ijms-25-12075-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/c8a195cbd863/ijms-25-12075-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/159d24cb92bc/ijms-25-12075-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/dd4707325920/ijms-25-12075-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/c9d576ea7700/ijms-25-12075-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f00/11593444/514aade4f890/ijms-25-12075-g003.jpg
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