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A mechanism of growth inhibition by abscisic acid in germinating seeds of Arabidopsis thaliana based on inhibition of plasma membrane \(H^+\)-ATPase and decreased cytosolic pH, \(K^+\), and anions

Please always quote using this URN: urn:nbn:de:bvb:20-opus-121221
  • The stress hormone abscisic acid (ABA) induces expression of defence genes in many organs, modulates ion homeostasis and metabolism in guard cells, and inhibits germination and seedling growth. Concerning the latter effect, several mutants of Arabidopsis thaliana with improved capability for \(H^+\) efflux (wat1-1D, overexpression of AKT1 and ost2-1D) are less sensitive to inhibition by ABA than the wild type. This suggested that ABA could inhibit \(H^+\) efflux (\(H^+\)-ATPase) and induce cytosolic acidification as a mechanism of growthThe stress hormone abscisic acid (ABA) induces expression of defence genes in many organs, modulates ion homeostasis and metabolism in guard cells, and inhibits germination and seedling growth. Concerning the latter effect, several mutants of Arabidopsis thaliana with improved capability for \(H^+\) efflux (wat1-1D, overexpression of AKT1 and ost2-1D) are less sensitive to inhibition by ABA than the wild type. This suggested that ABA could inhibit \(H^+\) efflux (\(H^+\)-ATPase) and induce cytosolic acidification as a mechanism of growth inhibition. Measurements to test this hypothesis could not be done in germinating seeds and we used roots as the most convenient system. ABA inhibited the root plasma-membrane H+-ATPase measured in vitro (ATP hydrolysis by isolated vesicles) and in vivo (\(H^+\) efflux from seedling roots). This inhibition involved the core ABA signalling elements: PYR/PYL/RCAR ABA receptors, ABA-inhibited protein phosphatases (HAB1), and ABA-activated protein kinases (SnRK2.2 and SnRK2.3). Electrophysiological measurements in root epidermal cells indicated that ABA, acting through the PYR/PYL/RCAR receptors, induced membrane hyperpolarization (due to \(K^+\) efflux through the GORK channel) and cytosolic acidification. This acidification was not observed in the wat1-1D mutant. The mechanism of inhibition of the \(H^+\)-ATPase by ABA and its effects on cytosolic pH and membrane potential in roots were different from those in guard cells. ABA did not affect the in vivo phosphorylation level of the known activating site (penultimate threonine) of (\(H^+\)-ATPase in roots, and SnRK2.2 phosphorylated in vitro the C-terminal regulatory domain of (\(H^+\)-ATPase while the guard-cell kinase SnRK2.6/OST1 did not.show moreshow less

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Metadaten
Author: Maria D. Planes, Regina Niñoles, Lourdes Rubio, Gaetano Bissoli, Eduardo Bueso, María J. García-Sánchez, Santiago Alejandro, Miguel Gonzalez-Guzmán, Rainer Hedrich, Pedro L. Rodriguez, José A. Fernández, Ramón Serrano
URN:urn:nbn:de:bvb:20-opus-121221
Document Type:Journal article
Faculties:Fakultät für Biologie / Julius-von-Sachs-Institut für Biowissenschaften
Language:English
Parent Title (English):Journal of Experimental Botany
Year of Completion:2015
Volume:66
Issue:3
Pagenumber:813-25
Source:Journal of Experimental Botany, Vol. 66, No. 3 pp. 813–825, 2015. doi:10.1093/jxb/eru442
DOI:https://doi.org/10.1093/jxb/eru442
Pubmed Id:http://www.ncbi.nlm.nih.gov/pubmed?term=25371509
Dewey Decimal Classification:5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie
Tag:ABA receptors; cytosolic pH; ion channels; microelectrodes; protein kinase; proton efflux
Release Date:2016/02/17
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung