College of Life Sciences and Oceanography, Longhua Innovation Institute for Biotechnology, Shenzhen University, Shenzhen, China.
Department of Biology, Duke University, Durham, NC, USA.
Nature. 2019 Aug;572(7769):341-346. doi: 10.1038/s41586-019-1449-z. Epub 2019 Jul 31.
Salinity is detrimental to plant growth, crop production and food security worldwide. Excess salt triggers increases in cytosolic Ca concentration, which activate Ca-binding proteins and upregulate the Na/H antiporter in order to remove Na. Salt-induced increases in Ca have long been thought to be involved in the detection of salt stress, but the molecular components of the sensing machinery remain unknown. Here, using Ca-imaging-based forward genetic screens, we isolated the Arabidopsis thaliana mutant monocation-induced [Ca increases 1 (moca1), and identified MOCA1 as a glucuronosyltransferase for glycosyl inositol phosphorylceramide (GIPC) sphingolipids in the plasma membrane. MOCA1 is required for salt-induced depolarization of the cell-surface potential, Ca spikes and waves, Na/H antiporter activation, and regulation of growth. Na binds to GIPCs to gate Ca influx channels. This salt-sensing mechanism might imply that plasma-membrane lipids are involved in adaption to various environmental salt levels, and could be used to improve salt resistance in crops.
盐度对全球植物生长、作物产量和粮食安全都有不利影响。过量的盐会触发细胞质 Ca 浓度的增加，从而激活 Ca 结合蛋白，并上调 Na/H 反向转运体以去除 Na。长期以来，盐诱导的 Ca 增加被认为参与了盐胁迫的检测，但感应机制的分子成分仍然未知。在这里，我们使用基于 Ca 成像的正向遗传筛选，分离出拟南芥突变体单阳离子诱导的 [Ca 增加 1 (moca1)，并鉴定 MOCA1 为质膜中糖基肌醇磷酸神经酰胺 (GIPC) 鞘脂的葡萄糖醛酸基转移酶。MOCA1 是盐诱导的细胞膜电位去极化、Ca 峰和波、Na/H 反向转运体激活以及生长调节所必需的。Na 结合到 GIPCs 上以门控 Ca 流入通道。这种盐感应机制可能意味着质膜脂质参与了对各种环境盐度的适应，并且可以用于提高作物的耐盐性。
