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New insights into plant salt acclimation: the roles of vesicle trafficking and reactive oxygen species signalling in mitochondria and the endomembrane system
Author(s) -
Garcia de la Garma Jesus,
FernandezGarcia Nieves,
Bardisi Enas,
Pallol Beatriz,
AsensioRubio Jose Salvador,
Bru Roque,
Olmos Enrique
Publication year - 2015
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12997
Subject(s) - endomembrane system , microbiology and biotechnology , reactive oxygen species , endoplasmic reticulum , mitochondrion , vacuole , biology , compartmentalization (fire protection) , golgi apparatus , abscisic acid , biochemistry , cytoplasm , enzyme , gene
Summary In this study, we investigated the cellular and molecular mechanisms that regulate salt acclimation. The main objective was to obtain new insights into the molecular mechanisms that control salt acclimation. Therefore, we carried out a multidisciplinary study using proteomic, transcriptomic, subcellular and physiological techniques. We obtained a Nicotiana tabacum BY‐2 cell line acclimated to be grown at 258  mM NaCl as a model for this study. The proteomic and transcriptomic data indicate that the molecular response to stress (chaperones, defence proteins, etc.) is highly induced in these salt‐acclimated cells. The subcellular results show that salt induces sodium compartmentalization in the cell vacuoles and seems to be mediated by vesicle trafficking in tobacco salt‐acclimated cells. Our results demonstrate that abscisic acid ( ABA ) and proline metabolism are crucial in the cellular signalling of salt acclimation, probably regulating reactive oxygen species ( ROS ) production in the mitochondria. ROS may act as a retrograde signal, regulating the cell response. The network of endoplasmic reticulum and Golgi apparatus is highly altered in salt‐acclimated cells. The molecular and subcellular analysis suggests that the unfolded protein response is induced in salt‐acclimated cells. Finally, we propose that this mechanism may mediate cell death in salt‐acclimated cells.

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