Quime Berlaine G, Ryder Lauren S, Talbot Nicholas J
The Sainsbury Laboratory, University of East Anglia, Norwich, UK.
J Microsc. 2025 Mar;297(3):274-288. doi: 10.1111/jmi.13382. Epub 2025 Jan 11.
Magnaporthe oryzae is the causal agent of rice blast, one of the most serious diseases affecting rice cultivation around the world. During plant infection, M. oryzae forms a specialised infection structure called an appressorium. The appressorium forms in response to the hydrophobic leaf surface and relies on multiple signalling pathways, including a MAP kinase phosphorelay and cAMP-dependent signalling, integrated with cell cycle control and autophagic cell death of the conidium. Together, these pathways regulate appressorium morphogenesis.The appressorium generates enormous turgor, applied as mechanical force to breach the rice cuticle. Re-polarisation of the appressorium requires a turgor-dependent sensor kinase which senses when a critical threshold of turgor has been reached to initiate septin-dependent re-polarisation of the appressorium and plant infection. Invasive growth then requires differential expression and secretion of a large repertoire of effector proteins secreted by distinct secretory pathways depending on their destination, which is also governed by codon usage and tRNA thiolation. Cytoplasmic effectors require an unconventional Golgi-independent secretory pathway and evidence suggests that clathrin-mediated endocytosis is necessary for their delivery into plant cells. The blast fungus then develops a transpressorium, a specific invasion structure used to move from cell-to-cell using pit field sites containing plasmodesmata, to facilitate its spread in plant tissue. This is controlled by the same MAP kinase signalling pathway as appressorium development and requires septin-dependent hyphal constriction. Recent progress in understanding the mechanisms of rice infection by this devastating pathogen using live cell imaging procedures are presented.
稻瘟病菌是稻瘟病的病原体，稻瘟病是影响全球水稻种植的最严重病害之一。在侵染植物过程中，稻瘟病菌形成一种特殊的侵染结构，称为附着胞。附着胞的形成是对叶片疏水表面的响应，并依赖于多种信号通路，包括丝裂原活化蛋白激酶磷酸化信号转导和环磷酸腺苷（cAMP）依赖性信号转导，这些信号通路与分生孢子的细胞周期调控和自噬性细胞死亡整合在一起。这些信号通路共同调节附着胞的形态发生。附着胞产生巨大的膨压，作为机械力来突破水稻角质层。附着胞的重新极化需要一种依赖膨压的传感器激酶，该激酶能感知何时达到临界膨压阈值，从而启动附着胞和植物侵染所依赖的隔膜蛋白依赖性重新极化。然后，侵入性生长需要根据效应蛋白的不同目的地，通过不同的分泌途径差异表达和分泌大量效应蛋白，这也受密码子使用和tRNA硫醇化的调控。细胞质效应蛋白需要一种非常规的不依赖高尔基体的分泌途径，有证据表明网格蛋白介导的内吞作用对于它们进入植物细胞是必要的。接着，稻瘟病菌会形成一种跨壁附着胞，这是一种特殊的侵染结构，用于通过含有胞间连丝的纹孔场位点在细胞间移动，以促进其在植物组织中的传播。这一过程由与附着胞发育相同的丝裂原活化蛋白激酶信号通路控制，并且需要隔膜蛋白依赖性菌丝收缩。本文介绍了利用活细胞成像技术在了解这种毁灭性病原体侵染水稻机制方面的最新进展。
