Department of Plant Pathology and Crop Physiology, Louisiana State University Agricultural Center, Baton Rouge, LA, USA.
Plant Signal Behav. 2024 Dec 31;19(1):2350869. doi: 10.1080/15592324.2024.2350869. Epub 2024 May 9.
Fungal pathogens deliver effector proteins into living plant cells to suppress plant immunity and control plant processes that are needed for infection. During plant infection, the devastating rice blast fungus, , forms the specialized biotrophic interfacial complex (BIC), which is essential for effector translocation. Cytoplasmic effectors are first focally secreted into BICs, and subsequently packaged into dynamic membranous effector compartments (MECs), then translocated via clathrin-mediated endocytosis (CME) into the host cytoplasm. This study demonstrates that clathrin-heavy chain inhibitors endosidin-9 (ES9) and endosidin-9-17 (ES9-17) blocked the internalization of the fluorescently labeled effectors Bas1 and Pwl2 in rice cells, leading to swollen BICs lacking MECs. In contrast, ES9-17 treatment had no impact on the localization pattern of the apoplastic effector Bas4. This study provides further evidence that cytoplasmic effector translocation occurs by CME in BICs, suggesting a potential role for effectors in co-opting plant endocytosis.
真菌病原体将效应蛋白输送到活植物细胞中，以抑制植物免疫并控制感染所需的植物过程。在植物感染过程中，破坏性的稻瘟病菌会形成专门的生物营养界面复合物（BIC），这对于效应子的易位是必不可少的。细胞质效应子首先被聚焦分泌到 BIC 中，然后被包装到动态膜效应子隔室（MEC）中，然后通过网格蛋白介导的内吞作用（CME）易位到宿主细胞质中。本研究表明，网格蛋白重链抑制剂 endosidin-9（ES9）和 endosidin-9-17（ES9-17）阻断了荧光标记效应子 Bas1 和 Pwl2 在水稻细胞中的内化，导致缺乏 MEC 的肿胀 BIC。相比之下，ES9-17 处理对质外体效应子 Bas4 的定位模式没有影响。本研究进一步证明细胞质效应子的易位是通过 BIC 中的 CME 发生的，这表明效应子在植物内吞作用中可能具有潜在作用。
