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首页> 外文期刊>Trends in Plant Science >Effector-triggered defence against apoplastic fungal pathogens
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Effector-triggered defence against apoplastic fungal pathogens

机译：效应物触发的针对质外性真菌病原体的防御

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摘要

R gene-mediated host resistance against apoplastic fungal pathogens is not adequately explained by the terms pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) or effector-triggered immunity (ETI). Therefore, it is proposed that this type of resistance is termed 'effector-triggered defence' (ETD). Unlike PTI and ETI, ETD is mediated by R genes encoding cell surface-localised receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1. In contrast to this extracellular recognition, ETI is initiated by intracellular detection of pathogen effectors. ETI is usually associated with fast, hypersensitive host cell death, whereas ETD often triggers host cell death only after an elapsed period of endophytic pathogen growth. In this opinion, we focus on ETD responses against foliar fungal pathogens of crops
机译：R基因介导的宿主对质外性真菌病原体的抗性没有通过术语病原体相关分子模式（PAMP）触发的免疫（PTI）或效应子触发的免疫（ETI）进行充分解释。因此，建议将这种类型的抵抗力称为“效应触发防御”（ETD）。与PTI和ETI不同，ETD由R基因介导，该R基因编码与受体样激酶SOBIR1结合的细胞表面定位受体样蛋白（RLP）。与这种细胞外识别相反，ETI通过病原体效应子的细胞内检测来启动。 ETI通常与快速，高度敏感的宿主细胞死亡相关，而ETD通常仅在经过内生病原体生长一段时间后才触发宿主细胞死亡。根据这种观点，我们将重点放在针对农作物叶片真菌病原体的ETD响应上。

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