4.7 Article

TheArabidopsisphosphatase PP2C49 negatively regulates salt tolerance through inhibition of AtHKT1;1

Journal

JOURNAL OF INTEGRATIVE PLANT BIOLOGY
Volume 63, Issue 3, Pages 528-542

Publisher

WILEY
DOI: 10.1111/jipb.13008

Keywords

Arabidopsis; AtHKT1; 1; Na plus distribution; translocation; PP2C; salt stress

Funding

  1. Jiangsu Collaborative Innovation Center for Modern Crop Production
  2. Doctoral Fund of Ministry of Education of China [20130091110038]

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The study revealed that PP2C49 negatively regulates the activity of AtHKT1;1 during salt stress, determining the systemic Na(+) allocation by interacting with AtHKT1;1 and inhibiting its Na(+) permeability.
Type 2C protein phosphatases (PP2Cs) are the largest protein phosphatase family. PP2Cs dephosphorylate substrates for signaling inArabidopsis, but the functions of most PP2Cs remain unknown. Here, we characterized PP2C49 (AT3G62260, a Group G PP2C), which regulates Na(+)distribution under salt stress and is localized to the cytoplasm and nucleus.PP2C49was highly expressed in root vascular tissues and its disruption enhanced plant tolerance to salt stress. Compared with wild type, thepp2c49mutant contained more Na(+)in roots but less Na(+)in shoots and xylem sap, suggesting that PP2C49 regulates shoot Na(+)extrusion. Reciprocal grafting revealed a root-based mechanism underlying the salt tolerance ofpp2c49. Systemic Na(+)distribution largely depends on AtHKT1;1 and loss of function ofAtHKT1;1in thepp2c49background overrode the salt tolerance ofpp2c49, resulting in salt sensitivity. Furthermore, compared with plants overexpressingPP2C49in the wild-type background, plants overexpressingPP2C49in theathtk1;1mutant background were sensitive to salt, like theathtk1;1mutants. Moreover, protein-protein interaction and two-voltage clamping assays demonstrated that PP2C49 physically interacts with AtHKT1;1 and inhibits the Na(+)permeability of AtHKT1;1. This study reveals that PP2C49 negatively regulates AtHKT1;1 activity and thus determines systemic Na(+)allocation during salt stress.

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