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

Actin-bundling protein fimbrin regulates pathogenicity via organizing F-actin dynamics during appressorium development in Colletotrichum gloeosporioides.
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球孢炭疽菌附着胞发育过程中,肌动蛋白结合蛋白Fimbrin通过组织F-肌动蛋白动态调控致病性。

DOI:
10.1111/mpp.13242
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发表时间:
2022-10
影响因子:
4.9
通讯作者:
Wang, Qiannan
Wang, Qiannan
中科院分区:
农林科学1区
文献类型:
--
作者:
Zhang, Yi;An, Bang;Wang, Wenfeng;Zhang, Bei;He, Chaozu;Luo, Hongli;Wang, Qiannan

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胶孢炭疽病对橡胶树和其他热带作物造成严重的经济损失。附着胞是一种特殊的圆顶状感染结构,在胶孢炭疽菌的发病机制中起着至关重要的作用。然而,肌动蛋白细胞骨架动力学如何调节附着胞的形成和渗透的机制仍然不清楚,在C. gloeosporioides。在这项研究中,在C. gloeosporioides中鉴定了肌动蛋白交联蛋白fimplant同源物(CgFim1),CgFim1的敲除导致营养生长,分生孢子和致病性的损害。然后,我们研究了CgFim 1在肌动蛋白细胞骨架的动态组织中的作用。我们观察到,肌动蛋白补丁和电缆定位在顶端和亚顶端区域的菌丝顶端,并显示了一个盘到环的动态围绕孔在附着胞发育。CgFim 1显示出与肌动蛋白细胞骨架相似的分布模式。此外,CgFim1基因敲除影响了菌丝顶端肌动蛋白细胞骨架的极性,破坏了附着胞中肌动蛋白的动态和环状结构的形成,从而阻止了极性生长和附着胞的发育。CgFim1突变体也干扰了septin结构的形成。这导致孔壁覆盖层形成、孔收缩和渗透栓延伸中的缺陷。这些结果揭示了CgFim1通过组织肌动蛋白细胞骨架来调控胶孢炭疽菌生长和致病性的机制。 CgFim1突变体在附着胞中表现出破坏的环形F‐actin网络和septin环结构,然后影响炭疽菌孔壁覆盖物的形成,孔收缩和穿透钉的延伸。
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. CgFim1 mutant showed a disrupted toroidal F‐actin network and septin ring structure in the appressorium, which then affected pore wall overlay formation, pore contraction, and the extension of a penetration peg in Colletotrichum gloeosporioides.
基因组和转录组分析的植物致病性真菌的生活方式过渡。
DOI: 10.1038/ng.2372
发表时间: 2012-09
期刊: NATURE GENETICS
影响因子: 30.8
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DOI: 10.1046/j.1365-313x.2000.00907.x
发表时间: 2000-12-01
期刊: PLANT JOURNAL
影响因子: 7.2
作者:
Kovar, DR;Staiger, CJ;McCurdy, DW
通讯作者: McCurdy, DW
DOI: 10.1016/0147-5975(89)90036-4
发表时间: 1989-12-01
期刊: EXPERIMENTAL MYCOLOGY
影响因子: --
作者:
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通讯作者: FERRARI, MA
DOI: 10.1046/j.1464-6722.2001.00084.x
发表时间: 2001-11-01
影响因子: 4.9
作者:
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DOI: 10.1038/nmeth.1220
发表时间: 2008-07-01
期刊: NATURE METHODS
影响因子: 48
作者:
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