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

AbstractSeed germination is the crucial physiological process regulated by both environmental and endogenous phytohormones. ABA negatively regulates seed germination, post-germination growth and floral transition, however, the cross talk between multiple regulatory pathways are still unclear. Here, we show that ABA activates two MAP kinases, AtMPK3/AtMPK6 and selectively regulates the transcript of AtMPK3 through ABI5, a master regulator of ABA signaling. As a feedback loop, AtMPK3 interacts and phosphorylates ABI5 at the serine-314 position. ABI5 phosphorylation by MAP kinases positively regulates ABI5 nuclear localization and negatively regulates its dimerization. Subcellular localization of ABI5 phospho-null protein further suggests the role of phosphorylation in regulation of its cytoplasmic stability and its nuclear dimerization. Overexpression of phosphor-null ABI5 in abi5-8 mutant restored the ABA sensitivity during seed germination and delayed the floral transition as compared to phospho-mimic ABI5. Additionally, overexpression of constitutive phosphorylated ABI5 in abi5-8 mutants suggest that phosphorylation makes ABI5 partially inactive. Furthermore, phospho-null ABI5 plants showed drought sensitive phenotype whereas, mpk3, mkk4, mkk5, abi5-8 and phosphor-mimic plants showed drought tolerant phenotype. Our findings present a new insight between MAP kinase cascade and ABA signaling which collectively regulates the ABA response through ABI5 phosphorylation.

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Faculty Opinions recommendation of A protein kinase-phosphatase pair interacts with an ion channel to regulate ABA signaling in plant guard cells.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1570959.1061058 ◽

2010 ◽

Author(s):

Hervé Sentenac

Keyword(s):

Protein Kinase ◽

Ion Channel ◽

Guard Cells ◽

Aba Signaling

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

Journal of Experimental Botany ◽

10.1093/jxb/eraa069 ◽

2020 ◽

Vol 71 (10) ◽

pp. 3157-3171 ◽

Cited By ~ 2

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.

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