Guard Cell Signaling
Yan Wu
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TL;DR: This chapter explores various signaling pathways in guard cells, including ABA, CO2, light, innate immunity, and extracellular Ca2+ sensing, providing an in-depth understanding of their roles in plant stomatal regulation and potential applications.
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Abstract: This chapter contains sections titled: Introduction ABA-mediated guard cell signaling CO2 signaling in guard cells Light signaling in guard cells Innate immunity in guard cells Extracellular Ca2+ sensing in guard cells Conclusions and prospects Acknowledgments References
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References
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TL;DR: Stomatal morphology, distribution and behaviour respond to a spectrum of signals, from intracellular signalling to global climatic change, which results from a web of control systems reminiscent of a ‘scale-free’ network, whose untangling requires integrated approaches beyond those currently used.
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Calcium channels activated by hydrogen peroxide mediate abscisic acid signalling in guard cells
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TL;DR: Activation of Ca2+-permeable channels in the plasma membrane of Arabidopsis guard cells by hydrogen peroxide indicates that ABA-induced H2O2 production and the H 2O 2-activated Ca2-activated channels are important mechanisms for A BA-induced stomatal closing.
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Plant Stomata Function in Innate Immunity against Bacterial Invasion
TL;DR: Examination of stomatal guard cells of Arabidopsis provides evidence that supports a model in which stomata, as part of an integral innate immune system, act as a barrier against bacterial infection.
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The segment polarity network is a robust developmental module.
TL;DR: It is suggested, using computer simulations, that the Drosophila segment polarity genes constitute a module, and that this module is resistant to variations in the kinetic constants that govern its behaviour.
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Arabidopsis OST1 Protein Kinase Mediates the Regulation of Stomatal Aperture by Abscisic Acid and Acts Upstream of Reactive Oxygen Species Production
TL;DR: Results suggest that OST1 acts in the interval between ABA perception and ROS production, and the relative positions of ost1 and the other ABA-insensitive mutations in the ABA signaling network (abi1-1, abi2-1 and gca2) are discussed.
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