scholarly journals Deficient Glutathione in Guard Cells Facilitates Abscisic Acid-Induced Stomatal Closure but Does Not Affect Light-Induced Stomatal Opening

2008 ◽  
Vol 72 (10) ◽  
pp. 2795-2798 ◽  
Author(s):  
Md. Sarwar JAHAN ◽  
Ken’ichi OGAWA ◽  
Yoshimasa NAKAMURA ◽  
Yasuaki SHIMOISHI ◽  
Izumi C. MORI ◽  
...  
Keyword(s):  
Abscisic Acid ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stomatal Opening

scholarly journals The AtMYB60 transcription factor regulates stomatal opening by modulating oxylipin synthesis in guard cells

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Fabio Simeoni ◽  
Aleksandra Skirycz ◽  
Laura Simoni ◽  
Giulia Castorina ◽  
Leonardo Perez de Souza ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Abscisic Acid ◽  
Jasmonic Acid ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Gas Exchanges ◽  
Positive Regulator ◽  
Stomatal Regulation ◽  
Negative Modulator

AbstractStomata are epidermal pores formed by pairs of specialized guard cells, which regulate gas exchanges between the plant and the atmosphere. Modulation of transcription has emerged as an important level of regulation of stomatal activity. The AtMYB60 transcription factor was previously identified as a positive regulator of stomatal opening, although the details of its function remain unknown. Here, we propose a role for AtMYB60 as a negative modulator of oxylipins synthesis in stomata. The atmyb60-1 mutant shows reduced stomatal opening and accumulates increased levels of 12-oxo-phytodienoic acid (12-OPDA), jasmonic acid (JA) and jasmonoyl-l-isoleucine (JA-Ile) in guard cells. We provide evidence that 12-OPDA triggers stomatal closure independently of JA and cooperatively with abscisic acid (ABA) in atmyb60-1. Our study highlights the relevance of oxylipins metabolism in stomatal regulation and indicates AtMYB60 as transcriptional integrator of ABA and oxylipins responses in guard cells.

scholarly journals Arabidopsis NPF4.6 and NPF5.1 Control Leaf Stomatal Aperture by Regulating Abscisic Acid Transport

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 885
Author(s):  
Takafumi Shimizu ◽  
Yuri Kanno ◽  
Hiromi Suzuki ◽  
Shunsuke Watanabe ◽  
Mitsunori Seo
Keyword(s):  
Abscisic Acid ◽  
Plant Hormone ◽  
Leaf Surface ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Cell Types ◽  
Acid Transport ◽  
Wild Type ◽  
Vascular Tissues ◽  
Abscisic Acid Transport

The plant hormone abscisic acid (ABA) is actively synthesized in vascular tissues and transported to guard cells to promote stomatal closure. Although several transmembrane ABA transporters have been identified, how the movement of ABA within plants is regulated is not fully understood. In this study, we determined that Arabidopsis NPF4.6, previously identified as an ABA transporter expressed in vascular tissues, is also present in guard cells and positively regulates stomatal closure in leaves. We also found that mutants defective in NPF5.1 had a higher leaf surface temperature compared to the wild type. Additionally, NPF5.1 mediated cellular ABA uptake when expressed in a heterologous yeast system. Promoter activities of NPF5.1 were detected in several leaf cell types. Taken together, these observations indicate that NPF5.1 negatively regulates stomatal closure by regulating the amount of ABA that can be transported from vascular tissues to guard cells.

scholarly journals Abscisic acid-independent stomatal CO2 signal transduction pathway and convergence of CO2 and ABA signaling downstream of OST1 kinase

2018 ◽  
Vol 115 (42) ◽  
pp. E9971-E9980 ◽  
Author(s):  
Po-Kai Hsu ◽  
Yohei Takahashi ◽  
Shintaro Munemasa ◽  
Ebe Merilo ◽  
Kristiina Laanemets ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Protein Kinase ◽  
Stomatal Closure ◽  
Signal Transduction Pathway ◽  
Guard Cells ◽  
Aba Signaling ◽  
Time Resolved ◽  
Aba Receptor ◽  
Biochemical Analyses

Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO2]. CO2 elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO2/ABA interaction remain unclear. Two models have been considered: (i) CO2 elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (ii) CO2 signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants nced3/nced5 and aba2-1 remain responsive to CO2 elevation. Rapid CO2-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO2 elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO2 activates guard cell S-type anion channels in nced3/nced5 and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO2 does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO2 signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO2. These findings provide insights into the interaction between CO2/ABA signal transduction in light of the continuing rise in atmospheric [CO2].

scholarly journals Autophagy controls reactive oxygen species homeostasis in guard cells that is essential for stomatal opening

2019 ◽  
Vol 116 (38) ◽  
pp. 19187-19192 ◽  
Author(s):  
Shota Yamauchi ◽  
Shoji Mano ◽  
Kazusato Oikawa ◽  
Kazumi Hikino ◽  
Kosuke M. Teshima ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stomatal Closure ◽  
Reactive Oxygen ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Glycolate Oxidase ◽  
Oxygen Species ◽  
Ros Accumulation ◽  
Intracellular Ros ◽  
Ros Scavenger

Reactive oxygen species (ROS) function as key signaling molecules to inhibit stomatal opening and promote stomatal closure in response to diverse environmental stresses. However, how guard cells maintain basal intracellular ROS levels is not yet known. This study aimed to determine the role of autophagy in the maintenance of basal ROS levels in guard cells. We isolated the Arabidopsis autophagy-related 2 (atg2) mutant, which is impaired in stomatal opening in response to light and low CO2 concentrations. Disruption of other autophagy genes, including ATG5, ATG7, ATG10, and ATG12, also caused similar stomatal defects. The atg mutants constitutively accumulated high levels of ROS in guard cells, and antioxidants such as ascorbate and glutathione rescued ROS accumulation and stomatal opening. Furthermore, the atg mutations increased the number and aggregation of peroxisomes in guard cells, and these peroxisomes exhibited reduced activity of the ROS scavenger catalase and elevated hydrogen peroxide (H2O2) as visualized using the peroxisome-targeted H2O2 sensor HyPer. Moreover, such ROS accumulation decreased by the application of 2-hydroxy-3-butynoate, an inhibitor of peroxisomal H2O2-producing glycolate oxidase. Our results showed that autophagy controls guard cell ROS homeostasis by eliminating oxidized peroxisomes, thereby allowing stomatal opening.

scholarly journals Transcriptional Regulation of Protein Phosphatase 2C Genes to Modulate Abscisic Acid Signaling

2020 ◽  
Vol 21 (24) ◽  
pp. 9517
Author(s):  
Choonkyun Jung ◽  
Nguyen Hoai Nguyen ◽  
Jong-Joo Cheong
Keyword(s):  
Abscisic Acid ◽  
Osmotic Stress ◽  
Gene Transcription ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stress Conditions ◽  
Physical Interaction ◽  
Aba Signaling ◽  
Negative Feedback Regulation ◽  
Pp2c Gene

The plant hormone abscisic acid (ABA) triggers cellular tolerance responses to osmotic stress caused by drought and salinity. ABA controls the turgor pressure of guard cells in the plant epidermis, leading to stomatal closure to minimize water loss. However, stomatal apertures open to uptake CO2 for photosynthesis even under stress conditions. ABA modulates its signaling pathway via negative feedback regulation to maintain plant homeostasis. In the nuclei of guard cells, the clade A type 2C protein phosphatases (PP2Cs) counteract SnRK2 kinases by physical interaction, and thereby inhibit activation of the transcription factors that mediate ABA-responsive gene expression. Under osmotic stress conditions, PP2Cs bind to soluble ABA receptors to capture ABA and release active SnRK2s. Thus, PP2Cs function as a switch at the center of the ABA signaling network. ABA induces the expression of genes encoding repressors or activators of PP2C gene transcription. These regulators mediate the conversion of PP2C chromatins from a repressive to an active state for gene transcription. The stress-induced chromatin remodeling states of ABA-responsive genes could be memorized and transmitted to plant progeny; i.e., transgenerational epigenetic inheritance. This review focuses on the mechanism by which PP2C gene transcription modulates ABA signaling.

Ethylene inhibits darkness-induced stomatal closure by scavenging nitric oxide in guard cells of Vicia faba

2011 ◽  
Vol 38 (10) ◽  
pp. 767 ◽  
Author(s):  
Xi-Gui Song ◽  
Xiao-Ping She ◽  
Juan Wang ◽  
Yi-Chao Sun
Keyword(s):  
Nitric Oxide ◽  
Vicia Faba ◽  
Plant Hormone ◽  
No Reduction ◽  
Enzyme Commission ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Physiological Data ◽  
Oxide Synthase

The plant hormone ethylene regulates many aspects of plant growth and development. Despite the well-known relationship between ethylene and stress signalling, the involvement of ethylene in regulating stomatal movement is not completely explored. Here, the role and association between nitric oxide (NO) reduction and the inhibition of darkness-induced stomatal closure by ethylene was studied. Physiological data are provided that both ethylene-releasing compound 2-chloroethylene phosphonic acid (ethephon, ETH) and 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor of ethylene, reduced the levels of NO in Vicia faba L. guard cells, and then induced stomatal opening in darkness. In addition, ACC and ETH not only reduced NO levels in guard cells caused by exogenous NO (derived from sodium nitroprusside, SNP) in light, but also abolished NO that had been generated during a dark period and promoted stomatal opening. Interestingly, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) and hemoglobin (Hb), NO scavenger and the potent scavenger of NO/carbon monoxide (CO), respectively, also reduced NO levels by SNP and darkness. However, the above-mentioned effects of ACC and ETH were dissimilar to that of nitric oxide synthase (enzyme commission 1.14.13.39) inhibitor NG-nitro-L-Arg-methyl ester (L-NAME), which could neither reduce NO levels by SNP nor abolish NO that had been generated in the dark. Thus, it is concluded that ethylene reduces the levels of NO in V. faba guard cells via a pattern of NO scavenging, then induces stomatal opening in the dark.

scholarly journals Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure

2019 ◽  
Vol 224 (1) ◽  
pp. 177-187 ◽  
Author(s):  
Shouguang Huang ◽  
Rainer Waadt ◽  
Maris Nuhkat ◽  
Hannes Kollist ◽  
Rainer Hedrich ◽  
...  
Keyword(s):  
Abscisic Acid ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Calcium Signals

Stomatal opening: the role of abscisic acid

1971 ◽  
Vol 49 (4) ◽  
pp. 583-585 ◽  
Author(s):  
Roger F. Horton
Keyword(s):  
Abscisic Acid ◽  
Gibberellic Acid ◽  
Vicia Faba ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Water Potentials ◽  
Intact Leaves

Abscisic acid inhibits stomatal opening in isolated abaxial epidermal strips of Vicia faba. Kinetin, benzyladenine, and gibberellic acid, which can enhance stomatal apertures in intact leaves, are ineffective on isolated epidermal strips. Abscisic acid appears to act directly on the guard cells, rather than by influencing water potentials throughout the leaf.

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