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南京农大张正光研究组发表稻瘟病菌感知水稻表面信号机制研究论文

生物耗材网:bioconsumable.com | 更新时间:2017-6-28

国际微生物学知名期刊《PLOS Pathogens》在线发表了南京农业大学植保学院张正光教授研究组和美国路易斯安娜州立大学的Ping Wang教授研究组合作的一篇研究论文,研究论文题为“MoEnd3 Regulates Appressorium Formation and Virulence through Mediating Endocytosis in Rice Blast Fungus Magnaporthe oryzae”。研究报道了稻瘟病菌识别水稻表面信号调控附着胞形成和致病力。博士生李潇为第一作者,张正光教授为通讯作者。

稻瘟病菌引起的稻瘟病是水稻上的毁灭性病害,每年给我国造成30亿公斤的粮食损失,每年给全球造成的粮食损失可养活6千万人口,威胁着全球粮食安全。该病菌识别水稻叶片表面信号后产生攻击水稻必需的武器—附着胞,但是病菌将水稻表面信号传导至胞内的分子机制仍不清楚。

稻瘟病菌细胞膜上的跨膜受体蛋白Pth11和Sho1识别水稻表面信号(如蜡质、硬度与疏水性),产生侵染水稻必需的附着胞,但是Pth11和Sho1识别表面信号后的传导机制仍不清楚。张正光研究组前期发现稻瘟病菌的肌动蛋白调控激酶MoArk1控制内吞,将细胞膜上的蛋白转运至胞内。该研究发现与MoArk1互作的蛋白MoEnd3控制内吞。Pth11和MoSho1识别表面信号后,MoEnd3介导的内吞将这两个膜蛋白运输至内涵体,进而将信号传递给MAPK激酶—Pmk1激酶级联信号途径,调控附着胞的形成和致病力。进一步研究发现激酶MoArk1对MoEnd3蛋白的第222位丝氨酸进行磷酸化修饰,负调控MoEnd3的生物学功能。同时发现MoEnd3调控无毒效应子的分子。该研究解析了稻瘟病菌通过内吞将识别寄主表面信号的膜蛋白运输至胞内,进而产生附着胞的分子机制,拓展了人们对植物病原真菌附着胞形成机制的认识,同时对防治稻瘟病新型药剂的开发具有重要参考价值。

图:稻瘟病菌MoEnd3介导细胞膜受体Pth11和Sho1的内吞调控附着胞的形成和致病力

原文链接:

MoEnd3 Regulates Appressorium Formation and Virulence through Mediating Endocytosis in RICE Blast Fungus Magnaporthe oryzae

原文摘要:

Eukaryotic cells respond to environmental stimuli when cell surface receptors are bound by environmental ligands. The binding initiates a signal transduction cascade that results in the appropriate intracellular responses. Studies have shown that endocytosis is critical for receptor internalization and signaling activation. In the rice blast fungus Magnaporthe oryzae, a non-canonical G-protein coupled receptor, Pth11, and membrane sensors MoMsb2 and MoSho1 are thought to function upstream of G-protein/cAMP signaling and the Pmk1 MAPK pathway to regulate appressorium formation and pathogenesis. However, little is known about how these receptors or sensors are internalized and transported into intracellular compartments. We found that the MoEnd3 protein is important for endocytic transport and that the ΔMoend3 mutant exhibited defects in efficient internalization of Pth11 and MoSho1. The ΔMoend3 mutant was also defective in Pmk1 phosphorylation, autophagy, appressorium formation and function. Intriguingly, restoring Pmk1 phosphorylation levels in ΔMoend3 suppressed most of these defects. Moreover, we demonstrated that MoEnd3 is subject to regulation by MoArk1 through protein phosphorylation. We also found that MoEnd3 has additional functions in facilitating the secretion of effectors, including Avr-Pia and AvrPiz-t that suppress rice immunity. Taken together, our findings suggest that MoEnd3 plays a critical role in mediating receptor endocytosis that is critical for the signal transduction-regulated development and virulence of M.oryzae.

 

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