Autophagy promotes jasmonate-mediated defense against nematodes.xlsx

Autophagy, as an intracellular degradation system, plays a critical role in plant immunity. However, the involvement of autophagy in the plant immune system and its function in plant nematode resistance are largely unknown. Here, we show that root-knot nematode (RKN; <em>Meloidogyne incognita</em>) infection induced autophagy in tomato (<em>Solanum lycopersicum</em>) and different <em>atg </em>mutants exhibited high sensitivity to RKNs. The jasmonate (JA) signaling negative regulators jasmonate-associated MYC2-like 1 (JAM1), JAM2 and JAM3 interacted with ATG8s via an ATG8-interacting motif (AIM), and JAM1 was degraded by autophagy during RKN infection. JAM1 impaired the formation of a transcriptional activation complex between ethylene response factor 1 (ERF1) and mediator 25 (MED25), and interfered with transcriptional regulation of JA mediated defense-related genes by ERF1. Furthermore, ERF1 acted in positive and regulated autophagy activity via transcriptionally activating <em>ATG</em> expression in response to RKN infection. Therefore, autophagy promotes JA mediated defense against RKNs via forming a positive feedback circuit in the degradation of JAMs and transcriptional activation by ERF1.细胞自噬（Autophagy）作为一种细胞内降解系统，在植物免疫过程中发挥关键作用。然而，目前学界对于细胞自噬在植物免疫系统中的参与机制，及其在植物抗线虫过程中的功能尚不清楚。本研究发现，根结线虫（root-knot nematode, RKN; 南方根结线虫<em>Meloidogyne incognita</em>）侵染可诱导番茄（<em>Solanum lycopersicum</em>）发生细胞自噬，且不同<em>atg</em>突变体对RKN均表现出显著的高敏感性。茉莉酸（jasmonate, JA）信号通路负调控因子茉莉酸相关MYC2类蛋白1（JAM1）、JAM2及JAM3可通过ATG8相互作用基序（ATG8-interacting motif, AIM）与ATG8家族蛋白相互作用；且在RKN侵染过程中，JAM1可通过细胞自噬途径被降解。JAM1可阻碍乙烯响应因子1（ethylene response factor 1, ERF1）与中介体25（mediator 25, MED25）之间转录激活复合物的组装，并干扰ERF1介导的茉莉酸防御相关基因的转录调控。此外，ERF1发挥正向调控作用，可通过转录激活<em>ATG</em>基因的表达以响应RKN侵染，进而调控细胞自噬活性。综上，细胞自噬可通过在JAMs降解过程中形成正反馈环路，并经由ERF1介导转录激活，从而促进茉莉酸介导的植物抗RKN免疫防御。