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

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 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.

scholarly journals Abscisic Acid-Induced Stomatal Closure: An Important Component of Plant Defense Against Abiotic and Biotic Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Pulimamidi Bharath ◽  
Shashibhushan Gahir ◽  
Agepati S. Raghavendra
Keyword(s):  
Abscisic Acid ◽  
Plant Defense ◽  
Biotic Stress ◽  
Stomatal Closure ◽  
Compatible Solutes ◽  
Guard Cells ◽  
Model Systems ◽  
Stress Factors ◽  
Abiotic And Biotic Stress ◽  
Reactive Carbonyl Species

Abscisic acid (ABA) is a stress hormone that accumulates under different abiotic and biotic stresses. A typical effect of ABA on leaves is to reduce transpirational water loss by closing stomata and parallelly defend against microbes by restricting their entry through stomatal pores. ABA can also promote the accumulation of polyamines, sphingolipids, and even proline. Stomatal closure by compounds other than ABA also helps plant defense against both abiotic and biotic stress factors. Further, ABA can interact with other hormones, such as methyl jasmonate (MJ) and salicylic acid (SA). Such cross-talk can be an additional factor in plant adaptations against environmental stresses and microbial pathogens. The present review highlights the recent progress in understanding ABA’s multifaceted role under stress conditions, particularly stomatal closure. We point out the importance of reactive oxygen species (ROS), reactive carbonyl species (RCS), nitric oxide (NO), and Ca2+ in guard cells as key signaling components during the ABA-mediated short-term plant defense reactions. The rise in ROS, RCS, NO, and intracellular Ca2+ triggered by ABA can promote additional events involved in long-term adaptive measures, including gene expression, accumulation of compatible solutes to protect the cell, hypersensitive response (HR), and programmed cell death (PCD). Several pathogens can counteract and try to reopen stomata. Similarly, pathogens attempt to trigger PCD of host tissue to their benefit. Yet, ABA-induced effects independent of stomatal closure can delay the pathogen spread and infection within leaves. Stomatal closure and other ABA influences can be among the early steps of defense and a crucial component of plants’ innate immunity response. Stomatal guard cells are quite sensitive to environmental stress and are considered good model systems for signal transduction studies. Further research on the ABA-induced stomatal closure mechanism can help us design strategies for plant/crop adaptations to stress.

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 Novel regulation of transpiration by sugar signals within guard cells

2012 ◽  
Author(s):  
David Granot ◽  
Sarah M. Assmann
Keyword(s):  
Abscisic Acid ◽  
Signaling Pathway ◽  
Water Loss ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Feedback Mechanism ◽  
Limiting Factor ◽  
Aba Signaling ◽  
Sugar Sensing ◽  
New Discovery

Water is the major limiting factor in agriculture and stomata, composed of two guard cells and the pore they circumscribe, are the chief gates controlling plants’ water loss. The prevailing century old paradigm was that sugars act as an osmoticum in guard cells, contributing to the opening of the stomata. In contrast, we discovered that sugars close stomata and the closure is mediated by the sugar-sensing enzyme hexokinase (HXK) that triggers the abscisic acid (ABA)-signaling pathway within the guard cells. This new discovery suggests a sugar-sensing mechanism within guard cells that controls stomatal closure, and supports the existence of a stomatal feedback mechanism that coordinates photosynthesis with transpiration.

Inhibition of abscisic acid-induced stomatal closure by ethylene is related to the change of hydrogen peroxide levels in guard cells in broad bean

2011 ◽  
Vol 59 (8) ◽  
pp. 781 ◽  
Author(s):  
XiGui Song ◽  
XiaoPing She ◽  
Juan Wang
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Abscisic Acid ◽  
Nadph Oxidase ◽  
Broad Bean ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Diphenylene Iodonium ◽  
Scavenging Enzymes ◽  
Exogenous H2o2

We analysed the role and relationship between hydrogen peroxide (H2O2) reduction and the inhibition of abscisic acid (ABA)-induced stomatal closure by ethylene. Like ascorbic acid (ASA), the most important reducing substrate for H2O2 removal, catalase, one of the H2O2 scavenging enzymes and diphenylene iodonium, an inhibitor of the H2O2-generating enzyme NADPH oxidase, both ethylene-releasing compound 2-chloroethylene phosphonic acid (ethephon, ETH) and 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor of ethylene, were found to inhibit stomatal closure by ABA and to reduce H2O2 levels by ABA in guard cells, indicating that ethylene-caused inhibition of ABA-induced stomatal closure involves reduction of H2O2 levels in guard cells. Additionally, similar to ASA and catalase, ACC/ETH not only suppressed H2O2-induced stomatal closure and H2O2 levels in guard cells treated with exogenous H2O2 in light, but also reopened the stomata which had been closed by ABA and reduced H2O2 levels that had been generated by ABA. The abovementioned effects of ACC and ETH were dissimilar to that of diphenylene iodonium, an inhibitor of the H2O2-generating enzyme NADPH oxidase, which not only had incapability to reduce H2O2 levels by exogenous H2O2 but also could not abolish H2O2 that had been generated by ABA. So we suggest that ethylene probably induces H2O2 removal and reduces H2O2 levels in Vicia faba guard cells, and finally inhibits stomatal closure induced by ABA.

scholarly journals Calcium specificity signaling mechanisms in abscisic acid signal transduction in Arabidopsis guard cells

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Benjamin Brandt ◽  
Shintaro Munemasa ◽  
Cun Wang ◽  
Desiree Nguyen ◽  
Taiming Yong ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Stomatal Closure ◽  
Guard Cells ◽  
In Planta ◽  
Signaling Specificity ◽  
Downstream Signaling ◽  
Calcium Dependent ◽  
Quadruple Mutant ◽  
Dependent Protein

A central question is how specificity in cellular responses to the eukaryotic second messenger Ca2+ is achieved. Plant guard cells, that form stomatal pores for gas exchange, provide a powerful system for in depth investigation of Ca2+-signaling specificity in plants. In intact guard cells, abscisic acid (ABA) enhances (primes) the Ca2+-sensitivity of downstream signaling events that result in activation of S-type anion channels during stomatal closure, providing a specificity mechanism in Ca2+-signaling. However, the underlying genetic and biochemical mechanisms remain unknown. Here we show impairment of ABA signal transduction in stomata of calcium-dependent protein kinase quadruple mutant plants. Interestingly, protein phosphatase 2Cs prevent non-specific Ca2+-signaling. Moreover, we demonstrate an unexpected interdependence of the Ca2+-dependent and Ca2+-independent ABA-signaling branches and the in planta requirement of simultaneous phosphorylation at two key phosphorylation sites in SLAC1. We identify novel mechanisms ensuring specificity and robustness within stomatal Ca2+-signaling on a cellular, genetic, and biochemical level.

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