Patellin1 Negatively Modulates Salt Tolerance by Regulating PM Na+/H+ Antiport Activity and Cellular Redox Homeostasis in Arabidopsis

Patellin1 Negatively Modulates Salt Tolerance by Regulating PM Na+/H+ Antiport Activity and... Abstract Soil salinity significantly represses plant development and growth. Mechanisms involved sodium (Na+) extrusion and compartmentation, intracellular membrane trafficking as well as redox homeostasis regulation play important roles in plant salt tolerance. In this study, we report that Patellin1 (PATL1), a membrane trafficking-related protein, modulates salt tolerance in Arabidopsis. The T-DNA insertion mutant of PATL1 (patl1) with elevated PATL1 transcription level displays salt-sensitive phenotype. PATL1 partially associates with plasma membrane (PM) and endosomal system, and might participate in regulating membrane trafficking. Interestingly, PATL1 interacts with SOS1, a PM Na+/H+ antiporter in Salt-Overly-Sensitive (SOS) pathway, and the PM Na+/H+ antiport activity is lower in patl1 than that in Col-0. Furthermore, reactive oxygen species (ROS) content is higher in patl1 and the antioxidants redox signaling is partially disrupted in patl1 under salt stress condition. Artificially elimination of ROS could partially rescue the salt-sensitive phenotype of patl1. Taken together, our results indicate that PATL1 participates in plant salt tolerance by regulating Na+ transport at least in part via SOS1, and by modulating cellular redox homeostasis during salt stress. © The Author(s) 2018. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant and Cell Physiology Oxford University Press

Patellin1 Negatively Modulates Salt Tolerance by Regulating PM Na+/H+ Antiport Activity and Cellular Redox Homeostasis in Arabidopsis

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Publisher
Oxford University Press
Copyright
© The Author(s) 2018. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oup.com.
ISSN
0032-0781
eISSN
1471-9053
D.O.I.
10.1093/pcp/pcy081
Publisher site
See Article on Publisher Site

Abstract

Abstract Soil salinity significantly represses plant development and growth. Mechanisms involved sodium (Na+) extrusion and compartmentation, intracellular membrane trafficking as well as redox homeostasis regulation play important roles in plant salt tolerance. In this study, we report that Patellin1 (PATL1), a membrane trafficking-related protein, modulates salt tolerance in Arabidopsis. The T-DNA insertion mutant of PATL1 (patl1) with elevated PATL1 transcription level displays salt-sensitive phenotype. PATL1 partially associates with plasma membrane (PM) and endosomal system, and might participate in regulating membrane trafficking. Interestingly, PATL1 interacts with SOS1, a PM Na+/H+ antiporter in Salt-Overly-Sensitive (SOS) pathway, and the PM Na+/H+ antiport activity is lower in patl1 than that in Col-0. Furthermore, reactive oxygen species (ROS) content is higher in patl1 and the antioxidants redox signaling is partially disrupted in patl1 under salt stress condition. Artificially elimination of ROS could partially rescue the salt-sensitive phenotype of patl1. Taken together, our results indicate that PATL1 participates in plant salt tolerance by regulating Na+ transport at least in part via SOS1, and by modulating cellular redox homeostasis during salt stress. © The Author(s) 2018. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Plant and Cell PhysiologyOxford University Press

Published: Apr 19, 2018

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