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不同来源的活性氧和水杨酸分别调控拟南芥中CO介导的气孔运动增强

ROS of Distinct Sources and Salicylic Acid Separate Elevated CO-Mediated Stomatal Movements in Arabidopsis.

作者信息

He Jingjing, Zhang Ruo-Xi, Kim Dae Sung, Sun Peng, Liu Honggang, Liu Zhongming, Hetherington Alistair M, Liang Yun-Kuan

机构信息

State Key Laboratory of Hybrid Rice, Department of Plant Science, College of Life Sciences, Wuhan University, Wuhan, China.

School of Biological Sciences, Life Sciences Building, University of Bristol, Bristol, United Kingdom.

出版信息

Front Plant Sci. 2020 May 8;11:542. doi: 10.3389/fpls.2020.00542. eCollection 2020.

Abstract

Elevated CO (eCO) often reduces leaf stomatal aperture and density thus impacts plant physiology and productivity. We have previously demonstrated that the Arabidopsis BIG protein distinguishes between the processes of eCO-induced stomatal closure and eCO-inhibited stomatal opening. However, the mechanistic basis of this action is not fully understood. Here we show that eCO-elicited reactive oxygen species (ROS) production in mutants was compromised in stomatal closure induction but not in stomatal opening inhibition. Pharmacological and genetic studies show that ROS generated by both NADPH oxidases and cell wall peroxidases contribute to eCO-induced stomatal closure, whereas inhibition of light-induced stomatal opening by eCO may rely on the ROS derived from NADPH oxidases but not from cell wall peroxidases. As with JA and ABA, SA is required for eCO-induced ROS generation and stomatal closure. In contrast, none of these three signals has a significant role in eCO-inhibited stomatal opening, unveiling the distinct roles of plant hormonal signaling pathways in the induction of stomatal closure and the inhibition of stomatal opening by eCO. In conclusion, this study adds SA to a list of plant hormones that together with ROS from distinct sources distinguish two branches of eCO-mediated stomatal movements.

摘要

高浓度二氧化碳(eCO)通常会降低叶片气孔孔径和密度,从而影响植物生理和生产力。我们之前已经证明,拟南芥BIG蛋白能够区分eCO诱导气孔关闭和eCO抑制气孔开放的过程。然而,这种作用的机制基础尚未完全了解。在这里,我们表明,eCO诱导的突变体中活性氧(ROS)产生在气孔关闭诱导过程中受损,但在气孔开放抑制过程中未受损。药理学和遗传学研究表明,NADPH氧化酶和细胞壁过氧化物酶产生的ROS都有助于eCO诱导的气孔关闭,而eCO对光诱导气孔开放的抑制可能依赖于NADPH氧化酶产生的ROS,而非细胞壁过氧化物酶产生的ROS。与茉莉酸(JA)和脱落酸(ABA)一样,水杨酸(SA)是eCO诱导ROS产生和气孔关闭所必需的。相比之下,这三种信号在eCO抑制气孔开放过程中均无显著作用,揭示了植物激素信号通路在eCO诱导气孔关闭和抑制气孔开放过程中的不同作用。总之,本研究将SA添加到了一系列植物激素中,这些激素与来自不同来源的ROS一起区分了eCO介导的气孔运动的两个分支。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e65/7225777/66eb52dff48d/fpls-11-00542-g001.jpg

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