An activated form of NB-ARC protein RLS1 functions with cysteine-rich receptor-like protein RMC to trigger cell death in rice.
An activated form of NB-ARC protein RLS1 functions with cysteine-rich receptor-like protein RMC to trigger cell death in rice.
复制标题
NB-ARC 蛋白 RLS1 的激活形式与富含半胱氨酸的受体样蛋白 RMC 共同作用，引发水稻细胞死亡
DOI：
10.1016/j.xplc.2022.100459
复制
发表时间：
2023-03-13
影响因子：
10.5
通讯作者：
Tang, Jiuyou
中科院分区：
文献类型：
--
作者：
Wang, Yiqin;Teng, Zhenfeng;Li, Hua;Wang, Wei;Xu, Fan;Sun, Kai;Chu, Jinfang;Qian, Yangwen;Loake, Gary J.;Chu, Chengcai;Tang, Jiuyou
关键词：
含有NB-ARC（由Apaf-1、R蛋白和ed-4共享的核苷酸结合接头）结构域的抗性(R)蛋白识别病原体后的一个关键事件是伴随活性氧和一氧化氮积累的超敏反应（HR）型细胞死亡。然而，支撑这一进程的整体机制仍然相对不透明。在这里，我们发现NB-ARC蛋白RLS1（快速叶片衰老1）的功能获得突变触发水稻高度依赖光的hr样细胞死亡。rls1介导的防御反应在很大程度上独立于水杨酸积累、NPR1（致病相关基因1非表达者）活性和RAR1 （Mla12抗性1所需）功能。对RLS1激活抑制因子的筛选发现，RMC（根蜿蜒卷曲）对RLS1激活的防御反应至关重要。RMC编码一种富含半胱氨酸的受体样分泌蛋白（CRRSP），并作为rls1结合伙伴发挥作用。有趣的是，它们的共表达导致亚细胞定位模式的改变，足以引发细胞死亡，并伴有抗氧化酶APX1活性的降低。总之，我们的研究结果揭示了一个NB-ARC-CRRSP信号模块，可以调节水稻的氧化状态、细胞死亡过程和相关的免疫反应。水稻突变体noe2的NB-ARC蛋白RLS1的功能获得突变导致自发氧化爆发和细胞死亡。noe2中的激活防御反应在很大程度上独立于水杨酸、NPR1或RAR1，但由于富含半胱氨酸的受体样分泌蛋白RMC的功能丧失而受到抑制。RMC与活化的RLS1相互作用，促进其在质膜上聚集，并与ROS/RNS水平形成正反馈回路，放大免疫应答。
A key event that follows pathogen recognition by a resistance (R) protein containing an NB-ARC (nucleotide-binding adaptor shared by Apaf-1, R proteins, and Ced-4) domain is hypersensitive response (HR)-type cell death accompanied by accumulation of reactive oxygen species and nitric oxide. However, the integral mechanisms that underlie this process remain relatively opaque. Here, we show that a gain-of-function mutation in the NB-ARC protein RLS1 (Rapid Leaf Senescence 1) triggers high-light-dependent HR-like cell death in rice. The RLS1-mediated defense response is largely independent of salicylic acid accumulation, NPR1 (Nonexpressor of Pathogenesis-Related Gene 1) activity, and RAR1 (Required for Mla12 Resistance 1) function. A screen for suppressors of RLS1 activation identified RMC (Root Meander Curling) as essential for the RLS1-activated defense response. RMC encodes a cysteine-rich receptor-like secreted protein (CRRSP) and functions as an RLS1-binding partner. Intriguingly, their co-expression resulted in a change in the pattern of subcellular localization and was sufficient to trigger cell death accompanied by a decrease in the activity of the antioxidant enzyme APX1. Collectively, our findings reveal an NB-ARC–CRRSP signaling module that modulates oxidative state, the cell death process, and associated immunity responses in rice. A gain-of-function mutation in the NB-ARC protein RLS1 of the rice mutant noe2 leads to spontaneous oxidative burst and cell death. The activated defense response in noe2 is largely independent of salicylic acid, NPR1, or RAR1, but it is suppressed by loss of function of the cysteine-rich receptor-like secreted protein RMC. RMC interacts with activated RLS1 and facilitates their aggregation in the plasma membrane, then forms a positive feedback loop with ROS/RNS levels to amplify immune responses.
登录
查看更多内容
影响因子：
64.8
作者：
Delledonne, M;Xia, YJ;Lamb, C
通讯作者：
Lamb, C
影响因子：
5.1
作者：
Chen, KG;Du, LQ;Chen, ZX
通讯作者：
Chen, ZX
影响因子：
4.5
作者：
Chern M;Xu Q;Bart RS;Bai W;Ruan D;Sze-To WH;Canlas PE;Jain R;Chen X;Ronald PC
通讯作者：
Ronald PC
影响因子：
7.2
作者：
Acharya, Biswa R.;Raina, Surabhi;Raina, Ramesh
通讯作者：
Raina, Ramesh
影响因子：
9.5
作者：
Elmore JM;Lin ZJ;Coaker G
通讯作者：
Coaker G