N'Guyen Guillaume Quang, Raulo Roxane, Porquier Antoine, Iacomi Beatrice, Pelletier Sandra, Renou Jean-Pierre, Bataillé-Simoneau Nelly, Campion Claire, Hamon Bruno, Kwasiborski Anthony, Colou Justine, Benamar Abdelilah, Hudhomme Pietrick, Macherel David, Simoneau Philippe, Guillemette Thomas
UNIV Angers, Institut Agro, INRAE, IRHS, SFR 4207 QuaSaV, Angers, France.
Institut Charles Viollette - EA 7394, Université de Lille, INRA, ISA, Université d'Artois, Université du Littoral Côte d'Opale, Lille, France.
Front Plant Sci. 2021 Jan 14;11:611643. doi: 10.3389/fpls.2020.611643. eCollection 2020.
causes black spot disease in . During host infection, this necrotrophic fungus is exposed to various antimicrobial compounds, such as the phytoalexin brassinin which is produced by many cultivated species. To investigate the cellular mechanisms by which this compound causes toxicity and the corresponding fungal adaptive strategies, we first analyzed fungal transcriptional responses to short-term exposure to brassinin and then used additional functional approaches. This study supports the hypothesis that indolic phytoalexin primarily targets mitochondrial functions in fungal cells. Indeed, we notably observed that phytoalexin treatment of disrupted the mitochondrial membrane potential and resulted in a significant and rapid decrease in the oxygen consumption rates. Secondary effects, such as Reactive oxygen species production, changes in lipid and endoplasmic reticulum homeostasis were then found to be induced. Consequently, the fungus has to adapt its metabolism to protect itself against the toxic effects of these molecules, especially the activation of high osmolarity glycerol and cell wall integrity signaling pathways and by induction of the unfolded protein response.
在[具体宿主]中引发黑斑病。在宿主感染期间,这种坏死营养型真菌会接触到各种抗菌化合物,例如许多栽培[植物]物种产生的植物抗毒素油菜素内酯。为了研究这种化合物产生毒性的细胞机制以及相应的真菌适应性策略,我们首先分析了真菌对短期接触油菜素内酯的转录反应,然后采用了其他功能研究方法。这项研究支持了吲哚类植物抗毒素主要靶向真菌细胞中线粒体功能的假说。确实,我们显著观察到用植物抗毒素处理[具体真菌]会破坏线粒体膜电位,并导致耗氧率显著且迅速下降。随后发现会诱导产生诸如活性氧生成、脂质和内质网稳态变化等次级效应。因此,真菌必须调整其代谢以保护自身免受这些分子的毒性影响,特别是通过激活高渗甘油和细胞壁完整性信号通路以及诱导未折叠蛋白反应。