Hu Da-Gang, Sun Cui-Hui, Sun Mei-Hong, Hao Yu-Jin
State Key Laboratory of Crop Biology, National Research Center for Apple Engineering and Technology, College of Horticulture Science and Engineering, Shandong Agricultural University, Tai-an, 271018, Shandong, China.
Plant Cell Rep. 2016 Mar;35(3):705-18. doi: 10.1007/s00299-015-1914-6. Epub 2015 Dec 19.
Salt-induced phosphorylation of MdVHA-B1 protein was mediated by MdSOS2L1 protein kinase, and thereby increasing malate content in apple. Salinity is an important environmental factor that influences malate accumulation in apple. However, the molecular mechanism by which salinity regulates this process is poorly understood. In this work, we found that MdSOS2L1, a novel AtSOS2-LIKE protein kinase, interacts with V-ATPase subunit MdVHA-B1. Furthermore, MdSOS2L1 directly phosphorylates MdVHA-B1 at Ser(396) site to modulate malate accumulation in response to salt stress. Meanwhile, a series of transgenic analyses in apple calli showed that the MdSOS2L1-MdVHAB1 pathway was involved in the regulation of malate accumulation. Finally, a viral vector-based transformation approach demonstrated that the MdSOS2L1-MdVHAB1 pathway also modulated malate accumulation in apple fruits with or without salt stress. Collectively, our findings provide a new insight into the mechanism by which MdSOS2L1 phosphorylates MdVHA-B1 to modulate malate accumulation in response to salinity in apple.
盐诱导的MdVHA - B1蛋白磷酸化由MdSOS2L1蛋白激酶介导,从而增加苹果中的苹果酸含量。盐度是影响苹果中苹果酸积累的重要环境因素。然而,盐度调节这一过程的分子机制尚不清楚。在这项研究中,我们发现一种新型的类AtSOS2蛋白激酶MdSOS2L1与V - ATPase亚基MdVHA - B1相互作用。此外,MdSOS2L1直接在Ser(396)位点磷酸化MdVHA - B1,以响应盐胁迫调节苹果酸积累。同时,在苹果愈伤组织中的一系列转基因分析表明,MdSOS2L1 - MdVHAB1途径参与了苹果酸积累的调控。最后,基于病毒载体的转化方法表明,MdSOS2L1 - MdVHAB1途径在有或没有盐胁迫的情况下也调节苹果果实中的苹果酸积累。总的来说,我们的研究结果为MdSOS2L1磷酸化MdVHA - B1以响应苹果盐度调节苹果酸积累的机制提供了新的见解。