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Systemin triggers an increase of cytoplasmic calcium in tomato mesophyll cells: Ca 2+ mobilization from intra‐ and extracellular compartments
Author(s) -
Moyen C.,
HammondKosack * K. E.,
Jones J.,
Knight M. R.,
Johannes E.
Publication year - 1998
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1046/j.1365-3040.1998.00378.x
Subject(s) - ruthenium red , extracellular , egta , channel blocker , intracellular , calcium , chemistry , biochemistry , thapsigargin , ionomycin , cytoplasm , cyclic adp ribose , cyclopiazonic acid , cytosol , biophysics , microbiology and biotechnology , biology , enzyme , organic chemistry , cd38 , stem cell , cd34
We show here that, within 1–2 min of application, systemin triggers a transient increase of cytoplasmic free calcium concentration ([Ca 2+ ] c ) in cells from Lycopersicon esculentum mesophyll. The systemin‐induced Ca 2+ increase was slightly but not significantly reduced by L‐type Ca 2+ channel blockers (nifedipine, verapamil and diltiazem) and the Ca 2+ chelator [ethylene glycol tetraacetic acid (EGTA)], whereas inorganic Ca 2+ channel blockers (LaCl 3 , CdCl 2 and GdCl 3 ) and compounds affecting the release of intracellular Ca 2+ from the vacuole (ruthenium red, LiCl, neomycin) strongly reduced the systemin‐induced [Ca 2+ ] c increase. By contrast, no inhibitory effect was seen with the potassium and chloride channel blockers tested. Unlike systemin, other inducers of proteinase inhibitor (PI) and of wound‐induced protein synthesis, such as jasmonic acid (JA) and bestatin, did not trigger an increase of cytoplasmic Ca 2+ . The systemin‐induced elevation of cytoplasmic Ca 2+ which might be an early step in the systemin signalling pathway, appears to involve an influx of extracellular Ca 2+ simultaneously through several types of Ca 2+ permeable channels, and a release of Ca 2+ from intracellular stores sensitive to blockers of inositol 1,4,5‐triphosphate (IP 3 )‐ and cyclic adenasine 5’‐diphosphoribose (cADPR)‐mediated Ca 2+ release.