Laboratory of Phytopathology, Wageningen University, Droevendaalsesteeg 1, 6708 PB Wageningen, Netherlands.
Science. 2010 Aug 20;329(5994):953-5. doi: 10.1126/science.1190859.
Multicellular organisms activate immunity upon recognition of pathogen-associated molecular patterns (PAMPs). Chitin is the major component of fungal cell walls, and chitin oligosaccharides act as PAMPs in plant and mammalian cells. Microbial pathogens deliver effector proteins to suppress PAMP-triggered host immunity and to establish infection. Here, we show that the LysM domain-containing effector protein Ecp6 of the fungal plant pathogen Cladosporium fulvum mediates virulence through perturbation of chitin-triggered host immunity. During infection, Ecp6 sequesters chitin oligosaccharides that are released from the cell walls of invading hyphae to prevent elicitation of host immunity. This may represent a common strategy of host immune suppression by fungal pathogens, because LysM effectors are widely conserved in the fungal kingdom.
多细胞生物通过识别病原体相关分子模式（PAMPs）来激活免疫。几丁质是真菌细胞壁的主要成分，几丁寡糖在植物和哺乳动物细胞中作为 PAMPs 发挥作用。微生物病原体输送效应蛋白来抑制 PAMP 触发的宿主免疫并建立感染。在这里，我们表明真菌植物病原体炭疽菌的富含亮氨酸重复序列（LysM）结构域的效应蛋白 Ecp6 通过干扰几丁质触发的宿主免疫来介导毒力。在感染过程中，Ecp6 隔离从入侵菌丝细胞壁释放的几丁寡糖，以防止宿主免疫的诱导。这可能代表真菌病原体抑制宿主免疫的一种常见策略，因为 LysM 效应物在真菌界广泛保守。
