scholarly journals Say “NO” to ABA signaling in guard cells by S-nitrosylation of OST1

2015 ◽  
Vol 58 (3) ◽  
pp. 313-314 ◽  
Author(s):  
ZhaoBo Lang ◽  
JianRu Zuo
Keyword(s):  
Guard Cells ◽  
Aba Signaling

scholarly journals Under salt stress guard cells rewire ion transport and abscisic acid (ABA) signaling

2021 ◽  
Author(s):  
Sohail M. Karimi ◽  
Matthias Freund ◽  
Brittney M. Wager ◽  
Michael Knoblauch ◽  
Jörg Fromm ◽  
...  
Keyword(s):  
Abscisic Acid ◽  
Salt Stress ◽  
Ion Transport ◽  
Guard Cells ◽  
Aba Signaling

Early ABA Signaling Events in Guard Cells

2005 ◽  
Vol 24 (4) ◽  
pp. 296-307 ◽  
Author(s):  
Zhen-Ming Pei ◽  
Kazuyuki Kuchitsu
Keyword(s):  
Guard Cells ◽  
Aba Signaling ◽  
Signaling Events

ABA signaling in stomatal guard cells: lessons from Commelina and Vicia

2011 ◽  
Vol 124 (4) ◽  
pp. 477-487 ◽  
Author(s):  
Izumi C. Mori ◽  
Yoshiyuki Murata
Keyword(s):  
Guard Cells ◽  
Aba Signaling ◽  
Stomatal Guard Cells

scholarly journals MAP kinases MPK9 and MPK12 are preferentially expressed in guard cells and positively regulate ROS-mediated ABA signaling

2009 ◽  
Vol 106 (48) ◽  
pp. 20520-20525 ◽  
Author(s):  
F. Jammes ◽  
C. Song ◽  
D. Shin ◽  
S. Munemasa ◽  
K. Takeda ◽  
...  
Keyword(s):  
Map Kinases ◽  
Guard Cells ◽  
Aba Signaling

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 RAP2.3 negatively regulates nitric oxide biosynthesis and related responses through a rheostat-like mechanism in Arabidopsis

2020 ◽  
Vol 71 (10) ◽  
pp. 3157-3171 ◽  
Author(s):  
José León ◽  
Álvaro Costa-Broseta ◽  
Mari Cruz Castillo
Keyword(s):  
Nitric Oxide ◽  
Root Elongation ◽  
Guard Cells ◽  
No Production ◽  
Aba Signaling ◽  
Inhibition Of Growth ◽  
Genome Wide ◽  
Molecular Rheostat ◽  
No Signaling

Abstract Nitric oxide (NO) is sensed through a mechanism involving the degradation of group-VII ERF transcription factors (ERFVIIs) that is mediated by the N-degron pathway. However, the mechanisms regulating NO homeostasis and downstream responses remain mostly unknown. To explore the role of ERFVIIs in regulating NO production and signaling, genome-wide transcriptome analyses were performed on single and multiple erfvii mutants of Arabidopsis following exposure to NO. Transgenic plants overexpressing degradable or non-degradable versions of RAP2.3, one of the five ERFVIIs, were also examined. Enhanced RAP2.3 expression attenuated the changes in the transcriptome upon exposure to NO, and thereby acted as a brake for NO-triggered responses that included the activation of jasmonate and ABA signaling. The expression of non-degradable RAP2.3 attenuated NO biosynthesis in shoots but not in roots, and released the NO-triggered inhibition of hypocotyl and root elongation. In the guard cells of stomata, the control of NO accumulation depended on PRT6-triggered degradation of RAP2.3 more than on RAP2.3 levels. RAP2.3 therefore seemed to work as a molecular rheostat controlling NO homeostasis and signaling. Its function as a brake for NO signaling was released upon NO-triggered PRT6-mediated degradation, thus allowing the inhibition of growth, and the potentiation of jasmonate- and ABA-related signaling.

scholarly journals Reactive Carbonyl Species Mediate ABA Signaling in Guard Cells

2016 ◽  
Vol 57 (12) ◽  
pp. 2552-2563 ◽  
Author(s):  
Md. Moshiul Islam ◽  
Wenxiu Ye ◽  
Daiki Matsushima ◽  
Shintaro Munemasa ◽  
Eiji Okuma ◽  
...  
Keyword(s):  
Guard Cells ◽  
Aba Signaling ◽  
Reactive Carbonyl Species ◽  
Carbonyl Species ◽  
Reactive Carbonyl

scholarly journals ABA Signaling in Guard Cells Entails a Dynamic Protein–Protein Interaction Relay from the PYL-RCAR Family Receptors to Ion Channels

2013 ◽  
Vol 6 (2) ◽  
pp. 528-538 ◽  
Author(s):  
Sung Chul Lee ◽  
Chae Woo Lim ◽  
Wenzhi Lan ◽  
Kai He ◽  
Sheng Luan
Keyword(s):  
Ion Channels ◽  
Protein Interaction ◽  
Guard Cells ◽  
Aba Signaling ◽  
Protein Protein Interaction
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