首页> 外文OA文献 >Abscisic Acid Activation of Plasma Membrane Ca2+ Channels in Guard Cells Requires Cytosolic NAD(P)H and Is Differentially Disrupted Upstream and Downstream of Reactive Oxygen Species Production in abi1-1 and abi2-1 Protein Phosphatase 2C Mutants
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Abscisic Acid Activation of Plasma Membrane Ca2+ Channels in Guard Cells Requires Cytosolic NAD(P)H and Is Differentially Disrupted Upstream and Downstream of Reactive Oxygen Species Production in abi1-1 and abi2-1 Protein Phosphatase 2C Mutants

机译:保护细胞中血浆膜Ca2 +通道的脱落酸活化需要细胞源NAD(P)H,并且在ABI1-1和ABI2-1蛋白磷酸酶2C突变体中差异地破坏反应性氧物种生产的上游和下游

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摘要

The hormone abscisic acid (ABA) regulates stress responses and developmental processes in plants. Calcium-permeable channels activated by reactive oxygen species (ROS) have been shown recently to function in the ABA signaling network in Arabidopsis guard cells. Here, we report that ABA activation of these ICa Ca2+ channels requires the presence of NAD(P)H in the cytosol. The protein phosphatase 2C (PP2C) mutant abi1-1 disrupted ABA activation of ICa channels. Moreover, in abi1-1, ABA did not induce ROS production. Consistent with these findings, in abi1-1, H2O2 activation of ICa channels and H2O2-induced stomatal closing were not disrupted, suggesting that abi1-1 impairs ABA signaling between ABA reception and ROS production. The abi2-1 mutation, which lies in a distinct PP2C gene, also disrupted ABA activation of ICa. However, in contrast to abi1-1, abi2-1 impaired both H2O2 activation of ICa and H2O2-induced stomatal closing. Furthermore, ABA elicited ROS production in abi2-1. These data suggest a model with the following sequence of events in early ABA signal transduction: ABA, abi1-1, NAD(P)H-dependent ROS production, abi2-1, ICa Ca2+ channel activation followed by stomatal closing.
机译:激素脱落酸(ABA)调节植物中的应力响应和发育过程。最近已经示出了通过反应性氧物质(ROS)激活的钙可渗透的通道在Arabidopsis保护细胞中的ABA信号网络中起作用。在这里,我们报告说,这些ICA CA2 +通道的ABA激活需要在细胞溶胶中存在NAD(P)H.蛋白质磷酸酶2C(PP2C)突变体ABI1-1破坏了ICA通道的ABA活化。此外,在Abi1-1中,ABA没有诱导ROS生产。与这些发现一致的是,在abi1-1,钙电流通道和过氧化氢诱导气孔关闭的H 2 O 2活化并没有破坏,这表明abi1-1也妨碍ABA信号ABA接收和ROS产生之间。位于不同PP2C基因的ABI2-1突变,也破坏了ICA的ABA活化。然而,与ABI1-1相比,ABI2-1损害了ICA和H2O2诱导的气孔闭合的H2O2活化。此外,ABA在ABI2-1引发了ROS生产。这些数据表明ABA信号转导序列具有以下事件序列的模型:ABA,ABI1-1,NAD(P)H依赖性ROS生产,ABI2-1,ICA CA2 +通道激活,然后进行气孔闭合。

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