Phosphorylation-Mediated Dynamics of Nitrate Transceptor NRT1.1 Regulate Auxin Flux and Nitrate Signaling in Lateral Root Growth

Phosphorylation-Mediated Dynamics of Nitrate Transceptor NRT1.1 Regulate Auxin Flux and Nitrate Signaling in Lateral Root Growth
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硝酸盐受体 NRT1.1 磷酸化介导的动力学调节侧根生长中的生长素通量和硝酸盐信号传导

DOI:
10.1104/pp.19.00346
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发表时间:
2019
期刊:
影响因子:
7.4
通讯作者:
Lin Jinxing
Lin Jinxing
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang Xi;Cui Yaning;Yu Meng;Su Bodan;Gong Wei;Baluska Frantisek;Komis George;Samaj Jozef;Shan Xiaoyi;Lin Jinxing

文献摘要

相似文献

双亲和硝酸盐受体硝酸盐TRANSPORTER1.1 (NRT1.1)具有两种运输和信号传导模式,受Thr-101 (T101)磷酸化调控。NRT1.1通过调节硝酸盐依赖的基部生长素输出和硝酸盐介导的信号转导来调节侧根(LR)的发育。本研究利用拟南芥(Arabidopsis thaliana) NRT1.1 t101dphosphomimetic和NRT1.1 t101anon磷酸化突变体,发现NRT1.1的磷酸化状态在LR发育过程中对NRT1.1的功能起着关键作用。单粒子跟踪显示,磷酸化影响NRT1.1的时空动态。在低硝酸盐条件下,NRT1.1T101Dform表现出快速的横向迁移和膜分配,促进了生长素的通量。相比之下,不可磷酸化的nrt1.1 t101在高硝酸盐条件下通过网格蛋白介导的内吞作用和微结构域介导的内吞作用途径诱导质膜(PM)的低横向迁移率和低寡聚。这些行为通过抑制nrt1.1控制的PM上的生长素运输和刺激来自内体的Ca2+-拟南芥硝酸盐调节1信号传导来促进LR的发育。
The dual-affinity nitrate transceptor NITRATE TRANSPORTER1.1 (NRT1.1) has two modes of transport and signaling, governed by Thr-101 (T101) phosphorylation. NRT1.1 regulates lateral root (LR) development by modulating nitrate-dependent basipetal auxin export and nitrate-mediated signal transduction. Here, using the Arabidopsis (Arabidopsis thaliana) NRT1.1T101Dphosphomimetic and NRT1.1T101Anonphosphorylatable mutants, we found that the phosphorylation state of NRT1.1 plays a key role in NRT1.1 function during LR development. Single-particle tracking revealed that phosphorylation affected NRT1.1 spatiotemporal dynamics. The phosphomimetic NRT1.1T101Dform showed fast lateral mobility and membrane partitioning that facilitated auxin flux under low-nitrate conditions. By contrast, nonphosphorylatable NRT1.1T101Ashowed low lateral mobility and oligomerized at the plasma membrane (PM), where it induced endocytosis via the clathrin-mediated endocytosis and microdomain-mediated endocytosis pathways under high-nitrate conditions. These behaviors promoted LR development by suppressing NRT1.1-controlled auxin transport on the PM and stimulating Ca2+-ARABIDOPSIS NITRATE REGULATED1 signaling from the endosome.