Phosphorylation of a malate transporter promotes malate excretion and reduces cadmium uptake in apple.
ALMT14
SOS2L1
apple
cadmium
heavy metal
malic acid
Journal
Journal of experimental botany
ISSN: 1460-2431
Titre abrégé: J Exp Bot
Pays: England
ID NLM: 9882906
Informations de publication
Date de publication:
22 06 2020
22 06 2020
Historique:
received:
15
10
2019
accepted:
02
03
2020
pubmed:
10
3
2020
medline:
15
5
2021
entrez:
10
3
2020
Statut:
ppublish
Résumé
Heavy metal contamination is a major environmental and human health hazard in many areas of the world. Organic acids sequester heavy metals and protect plant roots from the effects of toxicity; however, it is largely unknown how these acids are regulated in response to heavy metal stress. Here, protein kinase SOS2L1 from apple was functionally characterized. MdSOS2L1 was found to be involved in the regulation of malate excretion, and to inhibit cadmium uptake into roots. Using the DUAL membrane system in a screen of an apple cDNA library with MdSOS2L1 as bait, a malate transporter, MdALMT14, was identified as an interactor. Bimolecular fluorescence complementation, pull-down, and co-immunoprecipitation assays further indicated the interaction of the two proteins. Transgenic analyses showed that MdSOS2L1 is required for cadmium-induced phosphorylation at the Ser358 site of MdALMT14, a modification that enhanced the stability of the MdALMT14 protein. MdSOS2L1 was also shown to enhance cadmium tolerance in an MdALMT14-dependent manner. This study sheds light on the roles of the MdSOS2L1-MdALMT14 complex in physiological responses to cadmium toxicity.
Identifiants
pubmed: 32147696
pii: 5799229
doi: 10.1093/jxb/eraa121
pmc: PMC7475249
doi:
Substances chimiques
Malates
0
Plant Proteins
0
Cadmium
00BH33GNGH
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3437-3449Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
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