Ca2+-dependent TaCCD1 cooperates with TaSAUR215 to enhance plasma membrane H plus -ATPase activity and alkali stress tolerance by inhibiting PP2C-mediated dephosphorylation of TaHA2 in wheat
Ca2+-dependent TaCCD1 cooperates with TaSAUR215 to enhance plasma membrane H plus -ATPase activity and alkali stress tolerance by inhibiting PP2C-mediated dephosphorylation of TaHA2 in wheat
复制标题
Ca2依赖的TaCCD1与TaSAUR215配合通过抑制PP2C介导的TaHA2去磷酸化来增强小麦质膜H -ATP酶活性和碱胁迫耐受性
DOI：
10.1016/j.molp.2023.01.010
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发表时间：
2023-03-06
期刊：
影响因子：
27.5
通讯作者：
Liu, Shuwei
中科院分区：
文献类型：
--
作者：
Cui, Minghan;Li, Yanping;Liu, Shuwei
碱胁迫是许多盐碱地地区作物生产的主要制约因素。然而，小麦对碱胁迫的反应机制却知之甚少。在这项研究中，我们确定了一个钙离子结合蛋白，从小麦，TaCCD 1，这是至关重要的调节质膜（PM）H+-ATP酶介导的碱胁迫反应。小麦品种陕荣4号（SR 4）的质膜H+-ATPase活性与其耐碱性密切相关。我们发现两种D进化枝型2C蛋白磷酸酶TaPP2C.D1和TaPP2C.D8（TaPP2C.D1/8）通过使TaHA 2的倒数第二个苏氨酸残基（Thr 926）去磷酸化从而抑制PM H+-ATP酶活性来负调节碱胁迫耐受性。碱胁迫诱导SR 4中TaCCD 1的表达，并且TaCCD 1与TaSAUR 215（一种早期生长素响应蛋白）相互作用。这些反应都依赖于碱胁迫引发的钙信号。TaCCD 1增强了TaSAUR 215对TaPP 2C.D1/8活性的抑制作用，从而提高了PM H+-ATPase TaHA 2的活性和小麦的碱胁迫耐受性。功能和遗传分析验证了这些基因在响应碱胁迫中的作用，表明TaPP2C.D1/8在TaSAUR 215和TaCCD 1下游发挥功能。本研究揭示了Ca 2+依赖的TaCCD 1与TaSAUR 215协同作用，通过抑制TaPP2C.D1/8介导的质膜H+-ATP酶TaHA 2的去磷酸化，增强质膜H +-ATP酶活性，从而提高小麦对碱胁迫的耐受性。
Alkali stress is a major constraint for crop production in many regions of saline-alkali land. However, little is known about the mechanisms through which wheat responds to alkali stress. In this study, we identified a calcium ion-binding protein from wheat, TaCCD1, which is critical for regulating the plasma membrane (PM) H+-ATPase-mediated alkali stress response. PM H+-ATPase activity is closely related to alkali tolerance in the wheat variety Shanrong 4 (SR4). We found that two D-clade type 2C protein phosphatases, TaPP2C.D1 and TaPP2C.D8 (TaPP2C.D1/8), negatively modulate alkali stress tolerance by dephosphorylating the penultimate threonine residue (Thr926) of TaHA2 and thereby inhibiting PM H+-ATPase activity. Alkali stress induces the expression of TaCCD1 in SR4, and TaCCD1 interacts with TaSAUR215, an early auxin-responsive protein. These responses are both dependent on calcium signaling triggered by alkali stress. TaCCD1 enhances the inhibitory effect of TaSAUR215 on TaPP2C.D1/8 activity, thereby promoting the activity of the PM H+-ATPase TaHA2 and alkali stress tolerance in wheat. Functional and genetic analyses verified the effects of these genes in response to alkali stress, indicating that TaPP2C.D1/8 function downstream of TaSAUR215 and TaCCD1. Collectively, this study uncovers a new signaling pathway that regulates wheat responses to alkali stress, in which Ca2+-dependent TaCCD1 cooperates with TaSAUR215 to enhance PM H+-ATPase activity and alkali stress tolerance by inhibiting TaPP2C.D1/8-mediated dephosphorylation of PM H+-ATPase TaHA2 in wheat.