Cytosolic malate and oxaloacetate activate S‐type anion channels in <i>Arabidopsis</i> guard cells

Wang, Cun; Zhang, Jingbo; Wu, Juyou; Brodsky, Dennis E.; Schroeder, Julian I.

doi:10.1111/nph.15292

Cited by 11 publications

(11 citation statements)

References 73 publications

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“…An alternative explanation takes into account the observation that malate is a signaling molecule or gate modifier that modulates K + channel activities in the plasma membrane. This finding is consistent with reports that malate shifts the voltage gate of anion channels toward more negative membrane potentials (Hedrich and Marten, 1993;Meyer et al, 2010), and that malateregulated channel activities depend on both resting and elevated cytosolic Ca 2+ concentrations (Wang et al, 2018). For example, malate activation of the vacuolar Cl À inward rectifying channel ALMT9 is due to a malate-dependent increase in channel opening (De Angeli et al, 2013;Baetz et al, 2016).…”

Section: Discussionsupporting

confidence: 91%

“…Most significantly, treatment with exogenous malate increased the K + channel current and turgor pressure of guard cells, and compromised the bzu1 stomatal phenotype. These results indicate that BZU1/ACN1 is involved, at least in part, in the induced metabolism of acetate, which leads to the production of malate, the most important osmoactive molecule in the osmoregulation of guard cells (Fernie and Martinoia, 2009;De Angeli et al, 2013) and a signaling component responsible for shifting the voltage gate of an ion channel toward more negative membrane potentials (Hedrich and Marten, 1993;Meyer et al, 2010;Wang et al, 2018).…”

Section: Discussionmentioning

confidence: 91%

“…Malate contributes to the regulation of stomatal movement both as a major osmotic species (Asai et al, 2000) and as a signaling molecule (Keller et al, 1989;Wang et al, 2018). However, its contribution has been described most often in terms of the parallel correlation between the degree of stomatal aperture and malate level in guard cells (Allaway, 1973;Pearson, 1973).…”

Section: Discussionmentioning

confidence: 99%

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Modulation of Guard Cell Turgor and Drought Tolerance by a Peroxisomal Acetate–Malate Shunt

et al. 2018

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In plants, stomatal movements are tightly controlled by changes in cellular turgor pressure. Carbohydrates produced by glycolysis and the tricarboxylic acid cycle play an important role in regulating turgor pressure. Here, we describe an Arabidopsis mutant, bzu1, isolated in a screen for elevated leaf temperature in response to drought stress, which displays smaller stomatal pores and higher drought resistance than wild-type plants. BZU1 encodes a known acetyl-coenzyme A synthetase, ACN1, which acts in the first step of a metabolic pathway converting acetate to malate in peroxisomes. We showed that BZU1/ACN1-mediated acetate-to-malate conversion provides a shunt that plays an important role in osmoregulation of stomatal turgor. We found that the smaller stomatal pores in the bzu1 mutant are a consequence of reduced accumulation of malate, which acts as an osmoticum and/or a signaling molecule in the control of turgor pressure within guard cells, and these results provided new genetic evidence for malate-regulated stomatal movement. Collectively, our results indicate that a peroxisomal BZU1/ACN1-mediated acetate-malate shunt regulates drought resistance by controlling the turgor pressure of guard cells in Arabidopsis.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Modulation of Guard Cell Turgor and Drought Tolerance by a Peroxisomal Acetate–Malate Shunt

et al. 2018

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“…2). In the PM, SLAC1 (Wang & Blatt, 2011; Wang et al ., 2018) and ALMT12 (Meyer et al ., 2010) channels are also regulated by malate (Fig. 2).…”

Section: Ion Flux Coordination Under the Control Of Ionic Conditions mentioning

confidence: 99%

Connecting vacuolar and plasma membrane transport networks

Cubero-Font

Angeli

2020

New Phytologist

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The coordinated control of ion transport across the two major membranes of differentiated plant cells, the plasma and the vacuolar membranes, is fundamental in cell physiology. The stomata responses to the fluctuating environmental conditions are an illustrative example. Indeed, they rely on the coordination of ion fluxes between the different cell compartments. The cytosolic environment, which is an interface between intracellular compartments, and the activity of the ion transporters localised in the different membranes influence one each other. Here we analyse the molecular mechanisms connecting and modulating the transport processes at both the plasma and the vacuolar membranes of guard cells.

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“…The Arabidopsis ecotype Columbia-0 (Col-0) was used as wildtype (WT) plants in this study. The following mutants have been described previously: max1-1, max2-1, max2-2, max3-9, and max4-1 (Stirnberg et al, 2002;Umehara et al, 2008), d14-5 (Yao et al, 2016), cpk4-1 and cpk11-2 (Zhu et al, 2007), cpk8 (Zou et al, 2015), cpk10 (Zou et al, 2010), cpk23 (Ma and Wu, 2007), cpk33-1, cpk33-2, 35S::CPK33 and 35S::CPK33 K102R (Li C.L et al, 2016), cpk3 cpk5 cpk6 cpk11 (Guzel Deger et al, 2015), and cpk5 cpk6 cpk11 cpk23 (Wang et al, 2018).…”

Section: Plant Growth Conditions and Mutants Isolationmentioning

confidence: 99%

The Calcium-Dependent Protein Kinase CPK33 Mediates Strigolactone-Induced Stomatal Closure in Arabidopsis thaliana

Wang¹,

Lv²,

Han³

et al. 2019

Front. Plant Sci.

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Strigolactones (SLs) are known to mediate plant acclimation to environmental stress. We recently reported that SLs acted as prominent regulators in promotion of stomatal closure. However, the detailed mechanism by which SLs induce stomatal closure requires further investigation. Here we studied the essential role of the calcium (Ca 2+) signal mediating by the calcium-dependent protein kinase (CPK) in SL-induced stomatal closure. SL-induced stomatal closure was strongly inhibited by a Ca 2+ chelator and Ca 2+ channel blockers, indicating that Ca 2+ functions in SL promotion of stomatal closure. Through examining a collection of cpk mutants, we identified CPK33, potentially acting as a Ca 2+ transducer, which is implicated in guard cell SL signaling. SL-and Ca 2+-induced stomatal closure were impaired in cpk33 mutants. CPK33 kinase activity is essential for SL induction of stomatal closure as SL-induced stomatal closure is blocked in the dead kinase mutant of CPK33. The cpk33 mutant is impaired in H 2 O 2-induced stomatal closure, but not in SLmediated H 2 O 2 production. Our study thus uncovers an important player CPK33 which functions as an essential Ca 2+ signals mediator in Arabidopsis guard cell SL signaling.

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Cytosolic malate and oxaloacetate activate S‐type anion channels in Arabidopsis guard cells

Cited by 11 publications

References 73 publications

Modulation of Guard Cell Turgor and Drought Tolerance by a Peroxisomal Acetate–Malate Shunt

Modulation of Guard Cell Turgor and Drought Tolerance by a Peroxisomal Acetate–Malate Shunt

Connecting vacuolar and plasma membrane transport networks

The Calcium-Dependent Protein Kinase CPK33 Mediates Strigolactone-Induced Stomatal Closure in Arabidopsis thaliana

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