Colletotrichum higginsianum is an important fungal pathogen causing anthracnose disease of cruciferous plants. In this study, we characterized a putative orthologue of yeast SPE1 in C. higginsianum, named ChODC. Deletion mutants of ChODC were defective in hyphal and conidial development. Importantly, deletion of ChODC significantly affected appressorium-mediated penetration in C. higginsianum. However, polyamines partially restore appressorium function and virulence indicating that loss of ChODC caused significantly decreased virulence by the crosstalk between polyamines and other metabolic pathways. Subsequently, transcriptomic and metabolomic analyses demonstrated that ChODC played an important role in metabolism of various carbon and nitrogen compounds including amino acids, carbohydrates and lipids. Along with these clues, we found deletion of ChODC affected glycogen and lipid metabolism, which were important for conidial storage utilization and functional appressorium formation. Loss of ChODC affected the mTOR signalling pathway via modulation of autophagy. Interestingly, cAMP treatment restored functional appressoria to the ΔChODC mutant, and rapamycin treatment also stimulated formation of functional appressoria in the ΔChODC mutant. Overall, ChODC was associated with the polyamine biosynthesis pathway, as a mediator of cAMP and mTOR signalling pathways to regulate appressorium function. Our study provides evidence of a link between ChODC and the cAMP signalling pathway and defines a novel mechanism by which ChODC regulates infection-associated autophagy and plant infection by fungi.

中文翻译：

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真菌病原体 Colletotrichum higginsianum 的鸟氨酸脱羧酶在调节全球代谢途径和毒力中起重要作用

Colletotrichum higginsianum是引起十字花科植物炭疽病的重要真菌病原菌。在这项研究中，我们描述了酵母 SPE1 在C中的假定直系同源物。higginsianum，命名为ChODC。ChODC的缺失突变体在菌丝和分生孢子发育方面存在缺陷。重要的是，ChODC的缺失显着影响了附着胞介导的C中的渗透。希金斯_ 然而，多胺部分恢复附着胞功能和毒力，表明ChODC的损失由于多胺和其他代谢途径之间的串扰，导致毒力显着降低。随后，转录组学和代谢组学分析表明，ChODC在包括氨基酸、碳水化合物和脂质在内的各种碳和氮化合物的代谢中发挥着重要作用。除了这些线索，我们发现ChODC的缺失会影响糖原和脂质代谢，这对于分生孢子储存利用和功能性附着胞形成很重要。ChODC的缺失通过调节自噬影响了 mTOR 信号通路。有趣的是，cAMP 治疗恢复了 ΔChODC 的功能性附着体突变体和雷帕霉素处理也刺激了ΔChODC突变体中功能性附着体的形成。总体而言，ChODC与多胺生物合成途径相关，作为 cAMP 和 mTOR 信号通路调节附着胞功能的介质。我们的研究提供了 ChODC 和 cAMP 信号通路之间联系的证据，并定义了 ChODC 调节感染相关自噬和真菌感染植物的新机制。