Auxilin-like protein MoSwa2 promotes effector secretion and virulence as a clathrin uncoating factor in the rice blast fungus Magnaporthe oryzae.

Auxilin-like protein MoSwa2 promotes effector secretion and virulence as a clathrin uncoating factor in the rice blast fungus Magnaporthe oryzae.
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生长素样蛋白MoSwa2作为稻瘟病菌Magnaporthe oryzae的网格蛋白脱衣因子促进效应子分泌和毒力

DOI:
10.1111/nph.17181
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发表时间:
2021-04
期刊:
The New phytologist
影响因子:
--
通讯作者:
Zhang Z
Zhang Z
中科院分区:
其他
文献类型:
--
作者:
Liu M;Hu J;Zhang A;Dai Y;Chen W;He Y;Zhang H;Zheng X;Zhang Z

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植物病原体在与宿主相互作用的过程中,利用细胞外基质(ECM)抑制宿主免疫。ECM的形成涉及一系列连续的囊泡运输事件步骤。为了了解这种囊泡运输如何影响稻瘟病菌中的ECM和毒力,我们将MoSwa 2(一种先前鉴定的肌动蛋白调节激酶MoArk 1相互作用蛋白)表征为芽殖酵母酿酒酵母的生长素样网格蛋白脱壳因子Swa 2的直系同源物。我们发现MoSwa 2通过与COPII亚基MoSec 24 - 2相互作用,作为外壳蛋白复合物II(COPII)的未包被因子发挥作用。MoSwa 2的缺失导致胞外蛋白分泌的缺陷,导致侵入性菌丝的生长受限和宿主免疫抑制的降低。此外,细胞外液(ECF)蛋白质组分析显示,MoSwa 2调节的细胞外蛋白包括许多氧化还原蛋白,如小檗碱桥酶样(BBE样)蛋白MoSef 1。我们进一步发现MoSef 1作为一种质外体毒力因子发挥作用,抑制宿主免疫反应。我们的研究揭示了COPII脱壳因子在囊泡转运中的新功能,该功能在抑制宿主免疫和M.米。
Plant pathogens exploit the extracellular matrix (ECM) to inhibit host immunity during their interactions with the host. The formation of ECM involves a series of continuous steps of vesicular transport events. To understand how such vesicle trafficking impacts ECM and virulence in the rice blast fungus Magnaporthe oryzae, we characterised MoSwa2, a previously identified actin‐regulating kinase MoArk1 interacting protein, as an orthologue of the auxilin‐like clathrin uncoating factor Swa2 of the budding yeast Saccharomyces cerevisiae. We found that MoSwa2 functions as an uncoating factor of the coat protein complex II (COPII) via an interaction with the COPII subunit MoSec24‐2. Loss of MoSwa2 led to a deficiency in the secretion of extracellular proteins, resulting in both restricted growth of invasive hyphae and reduced inhibition of host immunity. Additionally, extracellular fluid (ECF) proteome analysis revealed that MoSwa2‐regulated extracellular proteins include many redox proteins such as the berberine bridge enzyme‐like (BBE‐like) protein MoSef1. We further found that MoSef1 functions as an apoplastic virulent factor that inhibits the host immune response. Our studies revealed a novel function of a COPII uncoating factor in vesicular transport that is critical in the suppression of host immunity and pathogenicity of M. oryzae.
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