Cellular adhesion mediates many important plant–microbe interactions. In the devastating blast fungus Magnaporthe oryzae¹, powerful glycoprotein-rich mucilage adhesives² cement melanized and pressurized dome-shaped infection cells—appressoria—to host rice leaf surfaces. Enormous internal turgor pressure is directed onto a penetration peg emerging from the unmelanized, thin-walled pore at the appressorial base^1,2,3,4, forcing it through the leaf cuticle where it elongates invasive hyphae in underlying epidermal cells⁵. Mucilage sealing around the appressorial pore facilitates turgor build-up², but the molecular underpinnings of mucilage secretion and appressorial adhesion are unknown. Here, we discovered an unanticipated and sole role for spermine in facilitating mucilage production by mitigating endoplasmic reticulum (ER) stress in the developing appressorium. Mutant strains lacking the spermine synthase-encoding gene SPS1 progressed through all stages of appressorial development, including penetration peg formation, but cuticle penetration was unsuccessful due to reduced appressorial adhesion, which led to solute leakage. Mechanistically, spermine neutralized off-target oxygen free radicals produced by NADPH oxidase-1 (Nox1)^3,6 that otherwise elicited ER stress and the unfolded protein response, thereby critically reducing mucilage secretion. Our study reveals that spermine metabolism via redox buffering of the ER underpins appressorial adhesion and rice cell invasion and provides insights into a process that is fundamental to host plant infection.

细胞粘附介导许多重要的植物-微生物相互作用。在毁灭性的稻瘟病菌Magnaporthe oryzae ^{1 中}，强大的富含糖蛋白的粘液粘合剂^{2 将}黑色化和加压的圆顶状感染细胞（附着胞）粘合到宿主水稻叶片表面。巨大的内部膨胀压力被引导到从附着基^1,2,3,4处未黑化的薄壁孔中出现的渗透钉，迫使它穿过叶表皮，在那里它拉长了表皮细胞^{5 中的}侵入性菌丝。附着孔周围的粘液密封有利于膨胀²，但粘液分泌和贴壁粘附的分子基础尚不清楚。在这里，我们发现了精胺通过减轻发育中的附着体中的内质网 (ER) 应激来促进粘液产生的意外和唯一作用。缺乏精胺合酶编码基因SPS1 的突变株经历了附着发育的所有阶段，包括渗透栓形成，但由于附着减少，角质层穿透不成功，导致溶质渗漏。从机制上讲，精胺中和了 NADPH 氧化酶-1 (Nox1) ^3,6产生的脱靶氧自由基否则会引起内质网应激和未折叠蛋白反应，从而严重减少粘液分泌。我们的研究表明，通过内质网氧化还原缓冲作用的精胺代谢支持贴壁粘附和水稻细胞侵袭，并提供了对宿主植物感染的基本过程的见解。