文献类型：期刊文献

英文题名：Rice Oscipk17-Oscbl2/3 Module Contributes to Na+ Exclusion and Plant Salt Tolerance in Transgenic Arabidopsis

作者：Qin, Xin[1]; Zhang, Xiaohua[1]; Ma, Chenyujie[1]; Hu, Yibo[1]; Liu, Yuan[1]; Hu, Yunfei[1]; Wang, Dan[1]; Lv, Xiaodong[1]; Wang, Chao[2]; Shou, Jianxin[2]; Li, Bo[1]

机构：[1] Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, 730000, China; [2] College of Life Sciences, Shaoxing University, Shaoxing, 312000, China

年份：2023

外文期刊名：SSRN

收录：EI(收录号：20230121904)

语种：英文

外文关键词：Bismuth compounds - Crops - Plants (botany) - Polymerase chain reaction - Sodium compounds

外文摘要：Soil salinity is detrimental to plant growth and therefore a major threat to crop productivity. Plants employ various physiological and molecular mechanisms to resist salt stress. Identification of genes and regulatory mechanisms underlying plant salt tolerance holds the key to breeding salt tolerant crops. CIPK-CBL pathways are involved in environmental stresses via Ca2+ signals and regulate ion transport for adaptations. In this study, we showed that over-expression of OsCIPK17 in Arabidopsis increased primary root elongation under salt stress, which was in a Ca2+ dependent manner. quantitative real-time PCR (RT-qPCR) showed that, under salt stress, OsCIPK17 was significantly induced and its protein shifted from the cytosol to the tonoplast. Using both Y2H and BiFC, OsCBL2 and OsCBL3 were shown to interact with OsCIPK17. Both OsCBLs are salt-inducible, and their proteins are located at the tonoplast. Over-expressing of OsCBL2 and OsCBL3 individually in Arabidopsis both enhanced primary root elongation under salt stress. Transgenic Arabidopsis individually over-expressing OsCIPK17, OsCBL2 and OsCBL3 all leads to larger biomass and less Na+ accumulation under salt stress, suggesting that OsCIPK17- OsCBL2/3 module is responsible for the Na+ compartmentation in the vacuole, a major component of Na+ exclusion and plant salt tolerance. ? 2023, The Authors. All rights reserved.