The mitotic exit mediated by small GTPase Tem1 is essential for the pathogenicity of Fusarium graminearum.
The mitotic exit mediated by small GTPase Tem1 is essential for the pathogenicity of Fusarium graminearum.
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DOI：
10.1371/journal.ppat.1011255
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发表时间：
2023-03
期刊：
影响因子：
6.7
通讯作者：
中科院分区：
文献类型：
--
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有丝分裂退出是细胞周期中的关键步骤，但小麦赤霉病菌有丝分裂退出网络的机制尚不清楚。F.禾谷镰刀菌感染小麦小穗并通过生长穿过每个小穗底部的轴节而定殖于整个穗头。在本研究中，我们发现一个小的GTbFgTem 1在F.禾谷镰刀菌对小麦的致病性和侵染结构的形成及侵入性菌丝在小麦小穗和胚芽鞘中的生长具有调节作用，但对植物病原菌的营养生长和分生孢子的形成作用不大。FgTem 1定位于核内周边和纺锤体极体，负调控F.禾谷早熟禾此外，FgTem 1的调控机制已通过高通量免疫共沉淀和遗传策略进行了进一步研究。septins FgCdc 10和FgCdc 11被证明与FgTem 1的显性负性形式相互作用，并且发现FgCdc 11调节FgTem 1的定位。细胞周期阻滞蛋白FgBub 2-FgBfa 1复合物被证明是FgTem 1的GTP酶激活蛋白（GAP）。FgBub 2和FgBfa 1之间存在直接的相互作用，对F.禾谷早熟禾FgBUB 2和FgBFA 1基因的缺失导致更少的周皮和未成熟的子囊形成，并显着下调了三萜烯生物合成（TRI）基因的表达。FgBUB 2/FgBFA 1基因的双缺失表明FgBUB 2和FgBFA 1在F.禾谷早熟禾总之，我们系统地证明了FgTem 1及其GAP FgBub 2-FgBfa 1复合物是F.禾谷早熟禾细胞周期由许多机制控制，确保正确的细胞分裂。细胞周期中的一个基本问题是有丝分裂的退出和进入下一个周期，但小麦赤霉病菌有丝分裂退出网络的机制仍不清楚。在这项研究中，我们确定了一个小的GTbaseFgTem 1参与有丝分裂出口在该真菌，并证明该蛋白是所需的真菌致病性和功能，在调节感染结构的形成和入侵菌丝生长的小麦小穗和小麦胚芽鞘。此外，FgTem 1的调控机制已被进一步研究。据我们所知，这项工作是最全面的丝状真菌病原体Tem 1基因解剖。我们的研究结果揭示了有丝分裂出口网络和植物病原体的致病性之间的关键联系。这些发现为设计和开发预防植物病原体感染的化学物质提供了新的分子基础。
The mitotic exit is a key step in cell cycle, but the mechanism of mitotic exit network in the wheat head blight fungus Fusarium graminearum remains unclear. F. graminearum infects wheat spikelets and colonizes the entire head by growing through the rachis node at the bottom of each spikelet. In this study, we found that a small GTPase FgTem1 plays an important role in F. graminearum pathogenicity and functions in regulating the formation of infection structures and invasive hyphal growth on wheat spikelets and wheat coleoptiles, but plays only little roles in vegetative growth and conidiation of the phytopathogen. FgTem1 localizes to both the inner nuclear periphery and the spindle pole bodies, and negatively regulates mitotic exit in F. graminearum. Furthermore, the regulatory mechanisms of FgTem1 have been further investigated by high-throughput co-immunoprecipitation and genetic strategies. The septins FgCdc10 and FgCdc11 were demonstrated to interact with the dominant negative form of FgTem1, and FgCdc11 was found to regulate the localization of FgTem1. The cell cycle arrest protein FgBub2-FgBfa1 complex was shown to act as the GTPase-activating protein (GAP) for FgTem1. We further demonstrated that a direct interaction exists between FgBub2 and FgBfa1 which crucially promotes conidiation, pathogenicity and DON production, and negatively regulates septum formation and nuclear division in F. graminearum. Deletion of FgBUB2 and FgBFA1 genes caused fewer perithecia and immature asci formations, and dramatically down-regulated trichothecene biosynthesis (TRI) gene expressions. Double deletion of FgBUB2/FgBFA1 genes showed that FgBUB2 and FgBFA1 have little functional redundancy in F. graminearum. In summary, we systemically demonstrated that FgTem1 and its GAP FgBub2-FgBfa1 complex are required for fungal development and pathogenicity in F. graminearum. Cell cycle is controlled by numerous mechanisms ensuring correct cell division. One fundamental question in the cell cycle is the mitotic exit and entry into the next cycle, but the mechanism of mitotic exit network in the wheat head blight fungus Fusarium graminearum remains unclear. In this study, we identified a small GTPase FgTem1 to be involved in mitotic exit in this fungus and demonstrated that this protein is required for the fungal pathogenicity and functions in regulating the infection structures formation and invasive hyphal growth on wheat spikelets and wheat coleoptiles. Furthermore, the regulatory mechanisms of FgTem1 have been further investigated. To the best of our knowledge, this work is the most comprehensive genetic dissection of Tem1 in filamentous fungal pathogens. Our results unveil a key link between mitotic exit network and the pathogenicity of the phytopathogen. These findings provide a novel molecular basis for the design and development of chemicals that prevent phytopathogen infection.
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