Ethylene inhibits abscisic acid-induced stomatal closure inVicia fabavia reducing nitric oxide levels in guard cells

The phytohormone abscisic acid (ABA) plays important roles in plant development and adaptation to environmental stress. ABA induces the production of nitric oxide (NO) in guard cells, but how NO regulates ABA signaling is not understood. Here, we show that NO negatively regulates ABA signaling in guard cells by inhibiting open stomata 1 (OST1)/sucrose nonfermenting 1 (SNF1)-related protein kinase 2.6 (SnRK2.6) through S-nitrosylation. We found that SnRK2.6 is S-nitrosylated at cysteine 137, a residue adjacent to the kinase catalytic site. Dysfunction in the S-nitrosoglutathione (GSNO) reductase (GSNOR) gene in the gsnor1-3 mutant causes NO overaccumulation in guard cells, constitutive S-nitrosylation of SnRK2.6, and impairment of ABA-induced stomatal closure. Introduction of the Cys137 to Ser mutated SnRK2.6 into the gsnor1-3/ost1-3 double-mutant partially suppressed the effect of gsnor1-3 on ABA-induced stomatal closure. A cysteine residue corresponding to Cys137 of SnRK2.6 is present in several yeast and human protein kinases and can be S-nitrosylated, suggesting that the S-nitrosylation may be an evolutionarily conserved mechanism for protein kinase regulation.

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NADK2 positively modulates abscisic acid-induced stomatal closure by affecting accumulation of H 2 O 2 , Ca 2+ and nitric oxide in Arabidopsis guard cells

Plant Science ◽

10.1016/j.plantsci.2017.06.003 ◽

2017 ◽

Vol 262 ◽

pp. 81-90 ◽

Cited By ~ 20

Author(s):

Lirong Sun ◽

Yaping Li ◽

Wenwen Miao ◽

Tingting Piao ◽

Yang Hao ◽

...

Keyword(s):

Nitric Oxide ◽

Abscisic Acid ◽

Stomatal Closure ◽

Guard Cells

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

Genes ◽

10.3390/genes12060885 ◽

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.

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Cytosolic alkalization-mediated H2O2 and NO production are involved in darkness-induced stomatal closure in Vicia faba

Canadian Journal of Plant Science ◽

10.4141/cjps2012-040 ◽

2013 ◽

Vol 93 (1) ◽

pp. 119-130 ◽

Cited By ~ 9

Author(s):

Yinli Ma ◽

Xiaoping She ◽

Shushen Yang

Keyword(s):

Nitric Oxide ◽

Vicia Faba ◽

Butyric Acid ◽

Stomatal Closure ◽

Guard Cells ◽

Weak Acid ◽

No Production ◽

Tetraacetic Acid ◽

Acetoxymethyl Ester ◽

Cytosolic Ph

Ma, Y., She, X. and Yang, S. 2013. Cytosolic alkalization-mediated H 2 O 2 and NO production are involved in darkness-induced stomatal closure in Vicia faba. Can. J. Plant Sci. 93: 119–130. Darkness raised cytosolic pH, hydrogen peroxide (H2O2) and nitric oxide (NO) levels in guard cells while inducing Vicia faba stomatal closure. These darkness effects were prevented by weak acid butyric acid, H2O2 modulators ascorbic acid (ASA), catalase (CAT), diphenyleneiodonium (DPI) and NO modulators 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), NG-nitro-L-arg-methyl ester (L-NAME) respectively. The data suggest that cytosolic alkalization, H2O2 and NO all participate in darkness-induced stomatal closure. During darkness treatment, pH rise became noticeable at 10 min and peaked at 25 min, while H2O2 and NO production increased significantly at 20 min and reached their maximums at 40 min. The H2O2 and NO levels were increased by methylamine in light and decreased by butyric acid in darkness. The results show that cytosolic alkalization induces H2O2 and NO production. ASA, CAT and DPI suppressed NO production by methylamine, c-PTIO and L-NAME prevented H2O2 generation by methylamine. Calcium chelator 1,2-bis (2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM) and 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) restricted darkness-induced alkalization, H2O2 and NO production and stomatal closure. We suggest that cytosolic alkalization is necessary for H2O2 and NO production during darkness-induced stomatal closure. H2O2 mediates NO synthesis by alkalization, and vice versa. Calcium may act upstream of cytosolic alkalization, H2O2 and NO production, besides its known action downstream of H2O2 and NO.

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1809204115 ◽

2018 ◽

Vol 115 (42) ◽

pp. E9971-E9980 ◽

Cited By ~ 28

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].

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Nitric oxide in guard cells as an important secondary messenger during stomatal closure

Frontiers in Plant Science ◽

10.3389/fpls.2013.00425 ◽

2013 ◽

Vol 4 ◽

Cited By ~ 57

Author(s):

Gunja Gayatri ◽

Srinivas Agurla ◽

Agepati S. Raghavendra

Keyword(s):

Nitric Oxide ◽

Stomatal Closure ◽

Guard Cells ◽

Secondary Messenger

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

International Journal of Molecular Sciences ◽

10.3390/ijms21249517 ◽

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.

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