Department of Plant-Microbe Interactions, Max Planck Institute for Plant Breeding Research, Carl-von-Linné-weg 10, 50829 Cologne, Germany.
Department of Biological Sciences, University of North Texas; 1511 West Sycamore, Denton, TX 76201, U.S.A.
Mol Plant Microbe Interact. 2020 Feb;33(2):328-335. doi: 10.1094/MPMI-08-19-0245-R. Epub 2019 Dec 27.
Plants have evolved mechanisms to protect themselves against pathogenic microbes and insect pests. In , the immune regulator PAD4 functions with its cognate partner EDS1 to limit pathogen growth. PAD4, independently of EDS1, reduces infestation by green peach aphid (GPA). How PAD4 regulates these defense outputs is unclear. By expressing the N-terminal PAD4 lipase-like domain (PAD4) without its C-terminal EDS1-PAD4 (EP) domain, we interrogated PAD4 functions in plant defense. Here, we show that transgenic expression of PAD4 in is sufficient for limiting GPA infestation but not for conferring basal and effector-triggered pathogen immunity. This suggests that the C-terminal PAD4 EP domain is necessary for EDS1-dependent immune functions but is dispensable for aphid resistance. Moreover, PAD4 is not sufficient to interact with EDS1, indicating the PAD4-EP domain is required for stable heterodimerization. These data provide molecular evidence that PAD4 has domain-specific functions.
植物已经进化出多种机制来保护自己免受病原微生物和昆虫的侵害。在植物中,免疫调节剂 PAD4 与其同源伴侣 EDS1 一起限制病原体的生长。PAD4 可独立于 EDS1 减少绿桃蚜(GPA)的侵害。然而,PAD4 如何调节这些防御输出尚不清楚。通过表达没有 C 端 EDS1-PAD4(EP)结构域的 N 端 PAD4 脂肪酶样结构域(PAD4),我们研究了 PAD4 在植物防御中的功能。结果表明,在 中过表达 PAD4 足以限制 GPA 的侵害,但不能赋予基础和效应物触发的病原体免疫。这表明 C 端 PAD4 EP 结构域对于 EDS1 依赖的免疫功能是必需的,但对于蚜虫抗性是可有可无的。此外,PAD4 不足以与 EDS1 相互作用,表明 PAD4-EP 结构域对于稳定的异二聚化是必需的。这些数据为 PAD4 具有特定功能的结构域提供了分子证据。