CO2 signaling in guard cells: calcium sensitivity response modulation, a Ca2+-independent phase, and CO2 insensitivity of the gca2 mutant

Leaf stomata close in response to high carbon dioxide levels and open at low C0₂. CO₂ concentrations in leaves are altered by daily dark/light cycles, as well as the continuing rise in atmospheric CO₂. Relative to abscisic acid and blue light signaling, little is known about the molecular, cellular,...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2006-05, Vol.103 (19), p.7506-7511
Main Authors: Young, J.J, Mehta, S, Israelsson, M, Godoski, J, Grill, E, Schroeder, J.I
Format: Article
Language:English
Subjects:
Arabidopsis thaliana
Biological Sciences
Botany
Calcium
Carbon dioxide
chemical concentration
Guard cells
Imaging
Leaves
mutants
Mutation
phenotype
Plant cells
Plants
Sensors
Signal transduction
Stomata
Stomatal movement
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Summary:Leaf stomata close in response to high carbon dioxide levels and open at low C0₂. CO₂ concentrations in leaves are altered by daily dark/light cycles, as well as the continuing rise in atmospheric CO₂. Relative to abscisic acid and blue light signaling, little is known about the molecular, cellular, and genetic mechanisms of CO₂ signaling in guard cells. Interestingly, we report that repetitive Ca²⁺ transients were observed during the stomatal opening stimulus, low [C0₂]. Furthermore, low/high [C0₂] transitions modulated the cytosolic $Ca^{2+}$ transient pattern in Arabidopsis guard cells (Landsberg erecta). Inhibition of cytosolic $Ca^{2+}$ transients, achieved by loading guard cells with the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid and not adding external Ca²⁺, attenuated both high C0₂-induced stomatal closing and low CO₂-induced stomatal opening, and also revealed a Ca²⁺independent phase of the CO₂ response. Furthermore, the mutant, growth controlled by abscisic acid (gca2) shows impairment in [C0₂] modulation of the cytosolic $Ca^{2+}$ transient rate and strong impairment in high C0₂-induced stomatal closing. Our findings provide insights into guard cell CO₂ signaling mechanisms, reveal Ca²⁺-independent events, and demonstrate that calcium elevations can participate in opposed signaling events during stomatal opening and closing. A model is proposed in which CO₂ concentrations prime $Ca^{2+}$ sensors, which could mediate specificity in $Ca^2+$ signaling.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0602225103