Magnaporthe oryzae is the causal agent of rice blast disease, the most widespread and serious disease of cultivated rice. Live cell imaging and quantitative 4D image analysis have provided new insight into the mechanisms by which the fungus infects host cells and spreads rapidly in plant tissue. In this video review article, we apply live cell imaging approaches to understanding the cell and developmental biology of rice blast disease. To gain entry to host plants, M. oryzae develops a specialised infection structure called an appressorium, a unicellular dome-shaped cell which generates enormous turgor, translated into mechanical force to rupture the leaf cuticle. Appressorium development is induced by perception of the hydrophobic leaf surface and nutrient deprivation. Cargo-independent autophagy in the three-celled conidium, controlled by cell cycle regulation, is essential for appressorium morphogenesis. Appressorium maturation involves turgor generation and melanin pigment deposition in the appressorial cell wall. Once a threshold of turgor has been reached, this triggers re-polarisation which requires regulated generation of reactive oxygen species, to facilitate septin GTPase-dependent cytoskeletal re-organisation and re-polarisation of the appressorium to form a narrow, rigid penetration peg. Infection of host tissue requires a further morphogenetic transition to a pseudohyphal-type of growth within colonised rice cells. At the same time the fungus secretes an arsenal of effector proteins to suppress plant immunity. Many effectors are secreted into host cells directly, which involves a specific secretory pathway and a specialised structure called the biotrophic interfacial complex. Cell-to-cell spread of the fungus then requires development of a specialised structure, the transpressorium, that is used to traverse pit field sites, allowing the fungus to maintain host cell membrane integrity as new living plant cells are invaded. Thereafter, the fungus rapidly moves through plant tissue and host cells begin to die, as the fungus switches to necrotrophic growth and disease symptoms develop. These morphogenetic transitions are reviewed in the context of live cell imaging studies.

Magnaporthe oryzae是稻瘟病的病原体，稻瘟病是栽培稻中最普遍和最严重的病害。活细胞成像和定量 4D 图像分析为真菌感染宿主细胞并在植物组织中快速传播的机制提供了新的见解。在这篇视频评论文章中，我们应用活细胞成像方法来了解稻瘟病的细胞和发育生物学。为了进入寄主植物，M. oryzae发展出一种称为贴壁的特殊感染结构，这是一种单细胞圆顶状细胞，可产生巨大的膨胀，转化为机械力以破裂叶表皮。附着胞发育是由对疏水叶表面的感知和营养缺乏引起的。由细胞周期调节控制的三细胞分生孢子中的货物独立自噬对于附着胞形态发生至关重要。附着胞成熟涉及膨压产生和附着胞壁中的黑色素沉积。一旦达到膨胀阈值，这将触发重新极化，这需要活性氧的调节生成，以促进 septin GTPase 依赖性细胞骨架重组和贴壁的重新极化，以形成狭窄、刚性的穿透钉。宿主组织的感染需要在定植的水稻细胞内进一步形态发生转变为假菌丝类型的生长。同时，真菌会分泌一系列效应蛋白来抑制植物免疫。许多效应子直接分泌到宿主细胞中，这涉及特定的分泌途径和称为生物营养界面复合物的特殊结构。然后，真菌的细胞间传播需要开发一种特殊的结构，即反式加压层，用于穿越坑场现场，使真菌在新的活植物细胞被侵入时保持宿主细胞膜的完整性。此后，真菌迅速穿过植物组织，宿主细胞开始死亡，因为真菌转变为坏死性生长和疾病症状的发展。