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Salinity-Induced Calcium Signaling and Root Adaptation in Arabidopsis Require the Calcium Regulatory Protein Annexin1
Author(s) -
Anuphon Laohavisit,
Siân L. Richards,
Lana Shabala,
Chen Chen,
Renato Colaço,
Stéphanie M. Swarbreck,
Emma Shaw,
Adeeba Dark,
Sergey Shabala,
Zhonglin Shang,
Julia M. Davies
Publication year - 2013
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.113.217810
Subject(s) - arabidopsis , arabidopsis thaliana , cytosol , microbiology and biotechnology , extracellular , calcium , reactive oxygen species , nadph oxidase , biochemistry , plasma membrane ca2+ atpase , biology , second messenger system , signal transduction , oxidase test , nicotinamide adenine dinucleotide phosphate , calcium signaling , mutant , chemistry , biophysics , enzyme , gene , atpase , organic chemistry
Salinity (NaCl) stress impairs plant growth and inflicts severe crop losses. In roots, increasing extracellular NaCl causes Ca2+ influx to elevate cytosolic free Ca2+ ([Ca2+]cyt) as a second messenger for adaptive signaling. Amplification of the signal involves plasma membrane reduced nicotinamide adenine dinucleotide phosphate oxidase activation, with the resultant reactive oxygen species triggering Ca2+ influx. The genetic identities of the Ca2+-permeable channels involved in generating the [Ca2+]cyt signal are unknown. Potential candidates in the model plant Arabidopsis (Arabidopsis thaliana) include annexin1 (AtANN1). Here, luminescent detection of [Ca2+]cyt showed that AtANN1 responds to high extracellular NaCl by mediating reactive oxygen species-activated Ca2+ influx across the plasma membrane of root epidermal protoplasts. Electrophysiological analysis revealed that root epidermal plasma membrane Ca2+ influx currents activated by NaCl are absent from the Atann1 loss-of-function mutant. Both adaptive signaling and salt-responsive production of secondary roots are impaired in the loss-of-function mutant, thus identifying AtANN1 as a key component of root cell adaptation to salinity.

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