Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-46766
Plant J May 1, 2013; 74 (3): 372-82.

Open stomata 1 (OST1) kinase controls R-type anion channel QUAC1 in Arabidopsis guard cells.

Imes D , Mumm P , Böhm J , Al-Rasheid KA , Marten I , Geiger D , Hedrich R .


Abstract
Under drought stress, the stress hormone ABA addresses the SnR kinase OST1 via its cytosolic receptor and the protein phosphatase ABI1. Upon activation, OST1 phosphorylates the guard cell S-type anion channel SLAC1. Arabidopsis ABI1 and OST1 loss-of-function mutants are characterized by an extreme wilting ''open stomata'' phenotype. Given the fact that guard cells express both SLAC- and R-/QUAC-type anion channels, we questioned whether OST1, besides SLAC1, also controls the QUAC1 channel. In other words, are ABI1/OST1 defects preventing both of the guard cell anion channel types from operating properly in terms of stomatal closure? The activation of the R-/QUAC-type anion channel by ABA signaling kinase OST1 and phosphatase ABI1 was analyzed in two experimental systems: Arabidopsis guard cells and the plant cell-free background of Xenopus oocytes. Patch-clamp studies on guard cells show that ABA activates R-/QUAC-type currents of wild-type plants, but to a much lesser extent in those of abi1-1 and ost1-2 mutants. In the oocyte system the co-expression of QUAC1 and OST1 resulted in a pronounced activation of the R-type anion channel. These studies indicate that OST1 is addressing both S-/SLAC- and R-/QUAC-type guard cell anion channels, and explain why the ost1-2 mutant is much more sensitive to drought than single slac1 or quac1 mutants.

PubMed ID: 23452338
Article link: Plant J

Genes referenced: abi1 rpn1



Xenbase: The Xenopus Model Organism Knowledgebase.
Version: 4.15.0
Major funding for Xenbase is provided by grant P41 HD064556