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Induction of RAB18 gene expression and activation of K + outward rectifying channels depend on an extracellular perception of ABA in Arabidopsis thaliana suspension cells
Author(s) -
Jeannette Emmanuelle,
Rona JeanPierre,
Bardat Françoise,
Cornel Daniel,
Sotta Bruno,
Miginiac Emile
Publication year - 1999
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 - 10.1046/j.1365-313x.1999.00423.x
Subject(s) - tetraethylammonium , arabidopsis thaliana , extracellular , biophysics , microbiology and biotechnology , gene expression , arabidopsis , chemistry , depolarization , abscisic acid , gene , biochemistry , biology , potassium , mutant , organic chemistry
Summary Important progress has been made regarding the characterization of the ABA signalling components using genetic and molecular approaches ( Leung & Giraudat 1998). However, we do not yet know the mechanism of ABA perception. Conflicting results concerning the site of ABA perception have been published. The prevailing view is that since ABA controls many responses, different sites of perception for ABA might exist. In order to establish the cellular localisation of the ABA receptors in Arabidopsis thaliana suspension cells, we developed two physiological tests based upon the capacity of impermeant ABA‐BSA conjugate to mimic permeant free ABA effects. We show that purified ABA‐BSA conjugate is able to trigger RAB18 gene expression and that this response is strictly due to the natural (+)‐ABA enantiomer. The rate of RAB18 gene expression was independent of the level of ABA uptake by the cells. Using the voltage‐clamp technique we show that ABA‐BSA, similarly to ABA, evokes a membrane depolarization and activates time‐and voltage‐dependent outward rectifying currents (ORC). We demonstrate that these ORC are due to a K + efflux as assessed by tail currents and specific inhibition by both tetraethylammonium (TEA) and Ba 2+ . These observations provide evidence in favour of an extracellular site for ABA perception.