Li Peng-Cheng, Huang Jin-Guang, Yu Shao-Wei, Li Yuan-Yuan, Sun Peng, Wu Chang-Ai, Zheng Cheng-Chao
State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, Shandong 271018, PR China.
Bio-Tech Research Center, Shandong Academy of Agricultural Sciences, Shandong Provincial Key Laboratory of Crop Genetic Improvement, Ecology and Physiology, Jinan, Shandong, PR China.
Sci Rep. 2016 Jul 22;6:30163. doi: 10.1038/srep30163.
The chloroplast-localized proteins play roles in plant salt stress response, but their mechanisms remain largely unknown. In this study, we screened a yellow leaf mutant, yl1-1, whose shoots exhibited hypersensitivity to salt stress. We mapped YL1 to AT3G57180, which encodes a YqeH-type GTPase. YL1, as a chloroplast stroma-localized protein, could be markedly reduced by high salinity. Upon exposure to high salinity, seedling shoots of yl1-1 and yl1-2 accumulated significantly higher levels of Na(+) than wild type. Expression analysis of factors involved in plant salt stress response showed that the expression of ABI4 was increased and HKT1 was evidently suppressed in mutant shoots compared with the wild type under normal growth conditions. Moreover, salinity effects on ABI4 and HKT1 were clearly weakened in the mutant shoots, suggesting that the loss of YL1 function impairs ABI4 and HKT1 expression. Notably, the shoots of yl1-2 abi4 double mutant exhibited stronger resistance to salt stress and accumulated less Na(+) levels after salt treatment compared with the yl1-2 single mutant, suggesting the salt-sensitive phenotype of yl1-2 seedlings could be rescued via loss of ABI4 function. These results reveal that YL1 is involved in the salt stress response of seedling shoots through ABI4.
叶绿体定位蛋白在植物盐胁迫响应中发挥作用,但其机制仍 largely 未知。在本研究中,我们筛选到一个黄叶突变体 yl1-1,其地上部分对盐胁迫表现出超敏反应。我们将 YL1 定位到 AT3G57180,它编码一种 YqeH 型 GTP 酶。YL1 作为一种叶绿体基质定位蛋白,在高盐度下会显著减少。在高盐处理下,yl1-1 和 yl1-2 的幼苗地上部分积累的 Na(+) 水平明显高于野生型。对参与植物盐胁迫响应的因子的表达分析表明,在正常生长条件下,与野生型相比,突变体地上部分中 ABI4 的表达增加,HKT1 的表达明显受到抑制。此外,盐度对突变体地上部分中 ABI4 和 HKT1 的影响明显减弱,这表明 YL1 功能的丧失损害了 ABI4 和 HKT1 的表达。值得注意的是,与 yl1-2 单突变体相比,yl1-2 abi4 双突变体的地上部分在盐处理后对盐胁迫表现出更强的抗性,并且积累的 Na(+) 水平更低,这表明 yl1-2 幼苗的盐敏感表型可以通过 ABI4 功能的丧失得到挽救。这些结果表明 YL1 通过 ABI4 参与幼苗地上部分的盐胁迫响应。