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基于 TMK1 的生长素信号通过磷酸化 ABI1/2 调节脱落酸反应。

TMK1-based auxin signaling regulates abscisic acid responses via phosphorylating ABI1/2 in .

机构信息

Shanghai Center for Plant Stress Biology, Center for Excellence in Molecular Plant Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201602, People's Republic of China.

FAFU-UCR Joint Center, Horticulture and Metabolic Biology Center, Haixia Institute of Science and Technology, Fujian Agriculture and Forestry University, Fuzhou 350002, People's Republic of China.

出版信息

Proc Natl Acad Sci U S A. 2021 Jun 15;118(24). doi: 10.1073/pnas.2102544118.

Abstract

Differential concentrations of phytohormone trigger distinct outputs, which provides a mechanism for the plasticity of plant development and an adaptation strategy among plants to changing environments. However, the underlying mechanisms of the differential responses remain unclear. Here we report that a high concentration of auxin, distinct from the effect of low auxin concentration, enhances abscisic acid (ABA) responses in , which partially relies on TRANS-MEMBERANE KINASE 1 (TMK1), a key regulator in auxin signaling. We show that high auxin and TMK1 play essential and positive roles in ABA signaling through regulating ABA INSENSITIVE 1 and 2 (ABI1/2), two negative regulators of the ABA pathway. TMK1 inhibits the phosphatase activity of ABI2 by direct phosphorylation of threonine 321 (T321), a conserved phosphorylation site in ABI2 proteins, whose phosphorylation status is important for both auxin and ABA responses. This TMK1-dependent auxin signaling in the regulation of ABA responses provides a possible mechanism underlying the high auxin responses in plants and an alternative mechanism involved in the coordination between auxin and ABA signaling.

摘要

不同浓度的植物激素会触发不同的反应,这为植物发育的可塑性和植物适应环境变化的策略提供了一种机制。然而,不同反应的潜在机制仍不清楚。在这里,我们报告说,高浓度的生长素(不同于低浓度生长素的作用)增强了对脱落酸(ABA)的反应,这部分依赖于跨膜激酶 1(TMK1),它是生长素信号转导中的一个关键调节剂。我们表明,高生长素和 TMK1 通过调节 ABA 不敏感 1 和 2(ABI1/2),在 ABA 信号通路中发挥着重要的积极作用,ABI1/2 是 ABA 途径的两个负调节剂。TMK1 通过直接磷酸化 ABI2 上的苏氨酸 321(T321)抑制 ABI2 的磷酸酶活性,T321 是 ABI2 蛋白中一个保守的磷酸化位点,其磷酸化状态对生长素和 ABA 反应都很重要。这种 TMK1 依赖的生长素信号在调节 ABA 反应中提供了一种可能的机制,解释了植物中高生长素反应的原因,并为生长素和 ABA 信号之间的协调提供了一种替代机制。

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