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Non-autonomous stomatal control by pavement cell turgor via the K+ channel subunit AtKC1

Abstract : Abstract Stomata optimize land plants’ photosynthetic requirements and limit water vapor loss. So far, all of the molecular and electrical components identified as regulating stomatal aperture are produced and operate directly within the guard cells. However, a completely autonomous function of guard cells is inconsistent with anatomical and biophysical observations hinting at mechanical contributions of epidermal origins. Here, K+ assays, membrane potential measurements, microindentation and plasmolysis experiments provide evidence that disruption of the Arabidopsis thaliana K+ channel subunit gene AtKC1 reduces pavement cell turgor, due to decreased K+ accumulation, without affecting guard cell turgor. This results in an impaired back-pressure of pavement cells onto guard cells, leading to larger stomatal apertures. Poorly rectifying membrane conductances to K+ were consistently observed in pavement cells. This plasmalemma property is likely to play an essential role in K+ shuttling within the epidermis. Functional complementation reveals that restoration of the wild-type stomatal functioning requires the expression of the transgenic AtKC1 at least in the pavement cells and trichomes. Altogether, the data suggest that AtKC1 activity contributes to the building of the back-pressure that pavement cells exert onto guard cells by tuning K+ distribution throughout the leaf epidermis.
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https://hal.inrae.fr/hal-03579607
Contributor : Chantal Baracco Connect in order to contact the contributor
Submitted on : Friday, February 18, 2022 - 10:48:39 AM
Last modification on : Saturday, May 21, 2022 - 3:41:18 AM
Long-term archiving on: : Thursday, May 19, 2022 - 6:35:58 PM

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Manuel Nieves-Cordones, Farrukh Azeem, Yuchen Long, Martin Boeglin, Geoffrey Duby, et al.. Non-autonomous stomatal control by pavement cell turgor via the K+ channel subunit AtKC1. The Plant cell, American Society of Plant Biologists (ASPB), In press, 34 (5), pp.2019-2037. ⟨10.1093/plcell/koac038⟩. ⟨hal-03579607⟩

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