Liu Muxing, Hu Jiexiong, Zhang Ao, Dai Ying, Chen Weizhong, He Yanglan, Zhang Haifeng, Zheng Xiaobo, Zhang Zhengguang
Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, 210095, China.
The Key Laboratory of Plant Immunity, Nanjing Agricultural University, Nanjing, 210095, China.
New Phytol. 2021 Apr;230(2):720-736. doi: 10.1111/nph.17181. Epub 2021 Feb 13.
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.
植物病原体在与宿主相互作用期间利用细胞外基质（ECM）来抑制宿主免疫。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Magnaporthe oryzae中的ECM和毒力，我们将MoSwa2（一种先前鉴定的与肌动蛋白调节激酶MoArk1相互作用的蛋白）鉴定为芽殖酵母Saccharomyces cerevisiae中类auxilin网格蛋白脱衣因子Swa2的直系同源物。我们发现MoSwa2通过与COPII亚基MoSec24-2相互作用而作为II型被膜小泡蛋白复合体（COPII）的脱衣因子发挥作用。MoSwa2的缺失导致细胞外蛋白分泌不足，从而导致侵入菌丝的生长受限以及对宿主免疫的抑制作用降低。此外，细胞外液（ECF）蛋白质组分析表明，MoSwa2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MoSef1。我们进一步发现MoSef1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脱衣因子在囊泡运输中的新功能，这对于稻瘟病菌抑制宿主免疫和致病性至关重要。
