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Constitutive activation of a plasma membrane H(+)-ATPase prevents abscisic acid-mediated stomatal closure.

ABSTRACT: Light activates proton (H(+))-ATPases in guard cells, to drive hyperpolarization of the plasma membrane to initiate stomatal opening, allowing diffusion of ambient CO(2) to photosynthetic tissues. Light to darkness transition, high CO(2) levels and the stress hormone abscisic acid (ABA) promote stomatal closing. The overall H(+)-ATPase activity is diminished by ABA treatments, but the significance of this phenomenon in relationship to stomatal closure is still debated. We report two dominant mutations in the OPEN STOMATA2 (OST2) locus of Arabidopsis that completely abolish stomatal response to ABA, but importantly, to a much lesser extent the responses to CO(2) and darkness. The OST2 gene encodes the major plasma membrane H(+)-ATPase AHA1, and both mutations cause constitutive activity of this pump, leading to necrotic lesions. H(+)-ATPases have been traditionally assumed to be general endpoints of all signaling pathways affecting membrane polarization and transport. Our results provide evidence that AHA1 is a distinct component of an ABA-directed signaling pathway, and that dynamic downregulation of this pump during drought is an essential step in membrane depolarization to initiate stomatal closure.

SUBMITTER: Merlot S

PROVIDER: S-EPMC1914098 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Guard cell photosynthesis is crucial in abscisic acid-induced stomatal closure.

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| S-EPMC6589527 | biostudies-literature

Inactivation of AtRac1 by abscisic acid is essential for stomatal closure.

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| S-EPMC6630932 | biostudies-literature

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| S-EPMC3602010 | biostudies-literature

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

Project description:During drought, abscisic acid (ABA) induces closure of stomata via a signaling pathway that involves the calcium (Ca2+ )-independent protein kinase OST1, as well as Ca2+ -dependent protein kinases. However, the interconnection between OST1 and Ca2+ signaling in ABA-induced stomatal closure has not been fully resolved. ABA-induced Ca2+ signals were monitored in intact Arabidopsis leaves, which express the ratiometric Ca2+ reporter R-GECO1-mTurquoise and the Ca2+ -dependent activation of S-type anion channels was recorded with intracellular double-barreled microelectrodes. ABA triggered Ca2+ signals that occurred during the initiation period, as well as in the acceleration phase of stomatal closure. However, a subset of stomata closed in the absence of Ca2+ signals. On average, stomata closed faster if Ca2+ signals were elicited during the ABA response. Loss of OST1 prevented ABA-induced stomatal closure and repressed Ca2+ signals, whereas elevation of the cytosolic Ca2+ concentration caused a rapid activation of SLAC1 and SLAH3 anion channels. Our data show that the majority of Ca2+ signals are evoked during the acceleration phase of stomatal closure, which is initiated by OST1. These Ca2+ signals are likely to activate Ca2+ -dependent protein kinases, which enhance the activity of S-type anion channels and boost stomatal closure.

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Boolean Calcium Signalling Model Predicts Calcium Role in Acceleration and Stability of Abscisic Acid-Mediated Stomatal Closure.

Project description:Inconsistent hypotheses have proposed Ca2+ as either being essential or irrelevant and redundant in ABA induced stomatal closure. This study integrates all available information from literature to define ABA signalling pathway and presents it in a systems view for clearer understanding of the role of Ca2+ in stomatal closure. Importantly, it incorporates into an Asynchronous Boolean model time delays sourced from an extensive literature search. The model predicted the timing of ABA events and mutant behaviour close to biology. It revealed biologically reported timing for Ca2+ activation and Ca2+ dynamics consistent with biology. It also predicts that Ca2+ elevation is not essential in stomatal closure but it can accelerate closure, consistent with previous findings, but our model further explains that acting as a mediator, Ca2+ accelerates stomatal closure by enhancing plasma membrane slowly activating anion channel SLAC1 and actin rearrangement. It shows statistical significance of Ca2+ induced acceleration of closure and that of Ca2+ induced acceleration of SLAC1 activation. Further, the model demonstrates that Ca2+ enhances resilience of closure to perturbation of important elements; especially, ROS pathway, as did previous ABA model, and even to the ABA signal disruption. It goes further to elucidate the mechanisms by which Ca2+ engenders stomatal closure in these perturbations.

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A mathematical model of the interaction of abscisic acid, ethylene and methyl jasmonate on stomatal closure in plants.

Project description:Stomatal closure is affected by various stimuli such as light, atmospheric carbon dioxide concentration, humidity and phytohormones. Our research focuses on phytohormones, specifically: abscisic acid (ABA), ethylene (ET) and methyl jasmonate (MeJA) that are responsible for the regulation of several plant processes, especially in guard cell signalling. While several studies show that these three phytohormones cause stomatal closure in plants, only two studies are notable for establishing a mathematical model of guard cell signalling involving phytohormones. Those two studies employed Boolean modelling and mechanistic ordinary differential equations modelling. In this study, we propose a new mathematical model of guard cell transduction network for stomatal closure using continuous logical modelling framework. Results showed how the different components of the network function. Furthermore, the model verified the role of antioxidants in the closure mechanism, and the diminished closure level of stomata with combined ABA-ET stimulus. The analysis was extended to ABA-ET-MeJA crosstalk.

| S-EPMC5300265 | biostudies-literature

A chloroplast retrograde signal, 3'-phosphoadenosine 5'-phosphate, acts as a secondary messenger in abscisic acid signaling in stomatal closure and germination.

Project description:Organelle-nuclear retrograde signaling regulates gene expression, but its roles in specialized cells and integration with hormonal signaling remain enigmatic. Here we show that the SAL1-PAP (3'-phosphoadenosine 5'- phosphate) retrograde pathway interacts with abscisic acid (ABA) signaling to regulate stomatal closure and seed germination in Arabidopsis. Genetically or exogenously manipulating PAP bypasses the canonical signaling components ABA Insensitive 1 (ABI1) and Open Stomata 1 (OST1); priming an alternative pathway that restores ABA-responsive gene expression, ROS bursts, ion channel function, stomatal closure and drought tolerance in ost1-2. PAP also inhibits wild type and abi1-1 seed germination by enhancing ABA sensitivity. PAP-XRN signaling interacts with ABA, ROS and Ca2+; up-regulating multiple ABA signaling components, including lowly-expressed Calcium Dependent Protein Kinases (CDPKs) capable of activating the anion channel SLAC1. Thus, PAP exhibits many secondary messenger attributes and exemplifies how retrograde signals can have broader roles in hormone signaling, allowing chloroplasts to fine-tune physiological responses.

| S-EPMC5406205 | biostudies-literature

Two Clade A Phosphatase 2Cs Expressed in Guard Cells Physically Interact With Abscisic Acid Signaling Components to Induce Stomatal Closure in Rice.

Project description:BackgroundThe core ABA signaling components functioning in stomatal closure/opening, namely ABA receptors, phosphatases, SnRK2s and SLAC1, are well characterized in Arabidopsis, but their functions in guard cells of rice have not been extensively studied.ResultsIn this study, we confirmed that OsSLAC1, the rice homolog of AtSLAC1, is specifically expressed in rice guard cells. Among the rice SAPKs, SAPK10 was specifically expressed in guard cells. In addition, SAPK10 phosphorylated OsSLAC1 in vitro and transgenic rice overexpressing SAPK10 or OsSLAC1 showed significantly less water loss than control. Thus, those might be major positive signaling components to close stomata in rice. We identified that only OsPP2C50 and OsPP2C53 among 9 OsPP2CAs might be related with stomatal closure/opening signaling based on guard cell specific expression and subcellular localization. Transgenic rice overexpressing OsPP2C50 and OsPP2C53 showed significantly higher water loss than control. We also characterized the interaction networks between OsPP2C50 and OsPP2C53, SAPK10 and OsSLAC1 and found two interaction pathways among those signaling components: a hierarchical interaction pathway that consisted of OsPP2C50 and OsPP2C53, SAPK10 and OsSLAC1; and a branched interaction pathway wherein OsPP2C50 and OsPP2C53 interacted directly with OsSLAC1.ConclusionOsPP2C50 and OsPP2C53 is major negative regulators of ABA signaling regarding stomata closing in rice. Those can regulate the OsSLAC1 directly or indirectly thorough SAPK10.

| S-EPMC6536566 | biostudies-literature

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