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At ALMT12 represents an R‐type anion channel required for stomatal movement in Arabidopsis guard cells
Author(s) -
Meyer Stefan,
Mumm Patrick,
Imes Dennis,
Endler Anne,
Weder Barbara,
AlRasheid Khaled A.S.,
Geiger Dietmar,
Marten Irene,
Martinoia Enrico,
Hedrich Rainer
Publication year - 2010
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04302.x
Subject(s) - guard cell , microbiology and biotechnology , biophysics , patch clamp , chemistry , arabidopsis , biology , biochemistry , mutant , gene , receptor
Summary Stomatal pores formed by a pair of guard cells in the leaf epidermis control gas exchange and transpirational water loss. Stomatal closure is mediated by the release of potassium and anions from guard cells. Anion efflux from guard cells involves slow (S‐type) and rapid (R‐type) anion channels. Recently the SLAC1 gene has been shown to encode the slow, voltage‐independent anion channel component in guard cells. In contrast, the R‐type channel still awaits identification. Here, we show that At ALMT12, a member of the aluminum activated malate transporter family in Arabidopsis, represents a guard cell R‐type anion channel. At ALMT12 is highly expressed in guard cells and is targeted to the plasma membrane. Plants lacking At ALMT12 are impaired in dark‐ and CO 2 ‐induced stomatal closure, as well as in response to the drought‐stress hormone abscisic acid. Patch‐clamp studies on guard cell protoplasts isolated from atalmt12 mutants revealed reduced R‐type currents compared with wild‐type plants when malate is present in the bath media. Following expression of At ALMT12 in Xenopus oocytes, voltage‐dependent anion currents reminiscent to R‐type channels could be activated. In line with the features of the R‐type channel, the activity of heterologously expressed At ALMT12 depends on extracellular malate. Thereby this key metabolite and osmolite of guard cells shifts the threshold for voltage activation of At ALMT12 towards more hyperpolarized potentials. R‐Type channels, like voltage‐dependent cation channels in nerve cells, are capable of transiently depolarizing guard cells, and thus could trigger membrane potential oscillations, action potentials and initiate long‐term anion and K + efflux via SLAC1 and GORK, respectively.