The ARP2/3 complex, acting cooperatively with Class I formins, modulates penetration resistance in Arabidopsis against powdery mildew invasion
文献类型: 外文期刊
第一作者: Qin, Li
作者: Qin, Li;Liu, Lijiang;Wilson, Kenneth E.;Wei, Yangdou;Liu, Lijiang;Tu, Jiangying;Peng, Gary;Yang, Guogen;Wang, Sheng;Wang, Hong;Quilichini, Teagen D.;Xiang, Daoquan;Gao, Peng;Datla, Raju;Blancaflor, Elison B.
作者机构:
期刊名称:PLANT CELL ( 影响因子:11.277; 五年影响因子:12.061 )
ISSN: 1040-4651
年卷期: 2021 年 33 卷 9 期
页码:
收录情况: SCI
摘要: The actin cytoskeleton regulates an array of diverse cellular activities that support the establishment of plant-microbe interactions and plays a critical role in the execution of plant immunity. However, molecular and cellular mechanisms regulating the assembly and rearrangement of actin filaments (AFs) at plant-pathogen interaction sites remain largely elusive. Here, using live-cell imaging, we show that one of the earliest cellular responses in Arabidopsis thaliana upon powdery mildew attack is the formation of patch-like AF structures beneath fungal invasion sites. The AFs constituting actin patches undergo rapid turnover, which is regulated by the actin-related protein (ARP)2/3 complex and its activator, the WAVE/SCAR regulatory complex (W/SRC). The focal accumulation of phosphatidylinositol-4,5-bisphosphate at fungal penetration sites appears to be a crucial upstream modulator of the W/SRC-ARP2/3 pathway-mediated actin patch formation. Knockout of W/SRC-ARP2/3 pathway subunits partially compromised penetration resistance with impaired endocytic recycling of the defense-associated t-SNARE protein PEN1 and its deposition into apoplastic papillae. Simultaneously knocking out ARP3 and knocking down the Class I formin (AtFH1) abolished actin patch formation, severely impaired the deposition of cell wall appositions, and promoted powdery mildew entry into host cells. Our results demonstrate that the ARP2/3 complex and formins, two actin-nucleating systems, act cooperatively and contribute to Arabidopsis penetration resistance to fungal invasion.
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