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Mutations in the Arabidopsis ROL17/isopropylmalate synthase 1 locus alter amino acid content, modify the TOR network, and suppress the root hair cell development mutant lrx1

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Schaufelberger Myriam, Galbier Florian, Herger Aline, de Brito Francisco Rita, Roffler Stefan, Clement Gilles, Diet Anouck, Hörtensteiner Stefan, Wicker Thomas, Ringli Christoph,
Project Analysis of LRX proteins as potential regulators of Ca2+ fluxes
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Original article (peer-reviewed)

Journal Journal of Experimental Botany
Volume (Issue) 70(8)
Page(s) 2313 - 2323
Title of proceedings Journal of Experimental Botany
DOI 10.1093/jxb/ery463

Open Access

URL http://doi.org/10.1093/jxb/ery463
Type of Open Access Publisher (Gold Open Access)

Abstract

Growth and development of organisms must be tightly controlled and adjusted to nutrient availability and metabolic activities. The Target of Rapamycin (TOR) network is a major control mechanism in eukaryotes and influences processes such as translation, mitochondrial activity, ROS production, and the cytoskeleton. In Arabidopsis thaliana, inhibition of the TOR kinase causes changes in cell wall architecture and suppression of phenotypic defects of the cell wall formation mutant lrx1 (leucine-rich repeat extensin 1). The rol17 (repressor of lrx1 17) mutant was identified as a new suppressor of lrx1 that induces also a short root phenotype. The ROL17 locus encodes IPMS1 (isopropylmalate synthase 1), a protein involved in leucine biosynthesis. Dependent on growth conditions, mutations in ROL17 do not necessarily alter the level of leucine, but always cause development of the rol17 mutant phenotypes, suggesting that the mutation does not only influence leucine biosynthesis. Changes in the metabolome of rol17 mutants are also found in plants with inhibited TOR kinase activity. Furthermore, rol17 mutants show reduced sensitivity to the TOR kinase inhibitor AZD-8055, indicative for a modified TOR network. Together, these data suggest that suppression of lrx1 by rol17 is the result of an alteration of the TOR network.
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