SORTING NEXIN1 Is Required for Modulating the Trafficking and Stability of the Arabidopsis IRON-REGULATED TRANSPORTER1

Dicotyledonous plants growing under limited iron availability initiate a response resulting in the solubilization, reduction, and uptake of soil iron. The protein factors responsible for these steps are transmembrane proteins, suggesting that the intracellular trafficking machinery may be involved i...

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Bibliographic Details
Published in:The Plant cell 2014-03, Vol.26 (3), p.1294-1307
Main Authors: Ivanov, Rumen, Brumbarova, Tzvetina, Blum, Ailisa, Jantke, Anna-Maria, Fink-Straube, Claudia, Bauer, Petra
Format: Article
Language:English
Subjects:
Arabidopsis - genetics
Arabidopsis - metabolism
Arabidopsis Proteins - genetics
Arabidopsis Proteins - metabolism
Arabidopsis Proteins - physiology
Cation Transport Proteins - metabolism
Endosomes
Gene expression regulation
Gene Expression Regulation, Plant
Genes
Iron
Iron - metabolism
Iron regulatory proteins
Mutation
Phenotypes
Plant cells
Plant roots
Plants
Protein Transport
Sorting Nexins - genetics
Sorting Nexins - physiology
Statistical significance
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Summary:Dicotyledonous plants growing under limited iron availability initiate a response resulting in the solubilization, reduction, and uptake of soil iron. The protein factors responsible for these steps are transmembrane proteins, suggesting that the intracellular trafficking machinery may be involved in iron acquisition. In search for components involved in the regulation of Arabidopsis thaliana iron deficiency responses, we identified the members of the SORTING NEXIN (SNX) protein family. SNX loss-of-function plants display enhanced susceptibility to iron deficiency in comparison to the wild type. The absence of SNX led to reduced iron import efficiency into the root. SNX1 showed partial colocalization with the principal root iron importer IRON-REGULATED TRANSPORTER1 (IRT1). In SNX loss-of-function plants, IRT1 protein levels were decreased compared with the wild type due to enhanced IRT1 degradation. This resulted in diminished amounts of the IRT1 protein at the plasma membrane, snx mutants exhibited enhanced iron deficiency responses compared with the wild type, presumably due to the lower iron uptake through IRT1. Our results reveal a role of SNX1 for the correct trafficking of IRT1 and, thus, for modulating the activity of the iron uptake machinery.
ISSN:1040-4651
1532-298X
DOI:10.1105/tpc.113.116244