Actin‐bundling protein fimbrin regulates pathogenicity via organizing F‐actin dynamics during appressorium development in Colletotrichum gloeosporioides

附着胞 细胞生物学 生物 肌动蛋白细胞骨架 细胞骨架 肌动蛋白 神经元肌动蛋白重塑 叶尖生长 电池极性 菌丝 植物 遗传学 细胞 花粉管 授粉 花粉
作者
Yi Zhang,Bang An,Wenfeng Wang,Bei Zhang,Chaozu He,Hongli Luo,Qiannan Wang
出处
期刊:Molecular Plant Pathology [Wiley]
卷期号:23 (10): 1472-1486 被引量:7
标识
DOI:10.1111/mpp.13242
摘要

Anthracnose caused by Colletotrichum gloeosporioides leads to serious economic loss to rubber tree yield and other tropical crops. The appressorium, a specialized dome-shaped infection structure, plays a crucial role in the pathogenesis of C. gloeosporioides. However, the mechanism of how actin cytoskeleton dynamics regulate appressorium formation and penetration remains poorly defined in C. gloeosporioides. In this study, an actin cross-linking protein fimbrin homologue (CgFim1) was identified in C. gloeosporioides, and the knockout of CgFim1 led to impairment in vegetative growth, conidiation, and pathogenicity. We then investigated the roles of CgFim1 in the dynamic organization of the actin cytoskeleton. We observed that actin patches and cables localized at the apical and subapical regions of the hyphal tip, and showed a disc-to-ring dynamic around the pore during appressorium development. CgFim1 showed a similar distribution pattern to the actin cytoskeleton. Moreover, knockout of CgFim1 affected the polarity of the actin cytoskeleton in the hyphal tip and disrupted the actin dynamics and ring structure formation in the appressorium, which prevented polar growth and appressorium development. The CgFim1 mutant also interfered with the septin structure formation. This caused defects in pore wall overlay formation, pore contraction, and the extension of the penetration peg. These results reveal the mechanism by which CgFim1 regulates the growth and pathogenicity of C. gloeosporioides by organizing the actin cytoskeleton.

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