Key Laboratory of Bio-resource and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610064, China.
Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi 830046, China.
Plant Cell. 2022 Feb 3;34(2):927-944. doi: 10.1093/plcell/koab292.
High soil salinity negatively affects plant growth and development, leading to a severe decrease in crop production worldwide. Here, we report that a secreted peptide, PAMP-INDUCED SECRETED PEPTIDE 3 (PIP3), plays an essential role in plant salt tolerance through RECEPTOR-LIKE KINASE 7 (RLK7) in Arabidopsis (Arabidopsis thaliana). The gene encoding the PIP3 precursor, prePIP3, was significantly induced by salt stress. Plants overexpressing prePIP3 exhibited enhanced salt tolerance, whereas a prePIP3 knockout mutant had a salt-sensitive phenotype. PIP3 physically interacted with RLK7, a leucine-rich repeat RLK, and salt stress enhanced PIP3-RLK7 complex formation. Functional analyses revealed that PIP3-mediated salt tolerance is dependent on RLK7. Exogenous application of synthetic PIP3 peptide activated RLK7, and salt treatment significantly induced RLK7 phosphorylation in a PIP3-dependent manner. Notably, MITOGEN-ACTIVATED PROTEIN KINASE3 (MPK3) and MPK6 were downstream of the PIP3-RLK7 module in salt response signaling. Activation of MPK3/6 was attenuated in pip3 or rlk7 mutants under saline conditions. Therefore, MPK3/6 might amplify salt stress response signaling in plants for salt tolerance. Collectively, our work characterized a novel ligand-receptor signaling cascade that modulates plant salt tolerance in Arabidopsis. This study contributes to our understanding of how plants respond to salt stress.
高土壤盐度会对植物的生长和发育产生负面影响,导致全球作物产量严重下降。在这里,我们报告说,一种分泌肽,PAMP-INDUCED SECRETED PEPTIDE 3(PIP3),通过拟南芥(Arabidopsis thaliana)中的受体样激酶 7(RLK7)在植物耐盐性中发挥重要作用。编码 PIP3 前体的基因 prePIP3 被盐胁迫显著诱导。过表达 prePIP3 的植物表现出增强的耐盐性,而 prePIP3 敲除突变体表现出盐敏感表型。PIP3 与富含亮氨酸重复的 RLK RLK7 物理相互作用,盐胁迫增强了 PIP3-RLK7 复合物的形成。功能分析表明,PIP3 介导的耐盐性依赖于 RLK7。外源性施用合成 PIP3 肽激活了 RLK7,盐处理以 PIP3 依赖的方式显著诱导 RLK7 磷酸化。值得注意的是,丝裂原激活蛋白激酶 3(MPK3)和 MPK6 是盐响应信号转导中 PIP3-RLK7 模块的下游。在盐胁迫条件下,pip3 或 rlk7 突变体中 MPK3/6 的激活减弱。因此,MPK3/6 可能在植物中放大盐胁迫反应信号以提高耐盐性。总之,我们的工作描述了一个新的配体-受体信号级联,调节拟南芥的植物耐盐性。这项研究有助于我们了解植物如何应对盐胁迫。