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Nitric oxide‐induced phosphatidic acid accumulation: a role for phospholipases C and D in stomatal closure
Author(s) -
DISTÉFANO AYELEN M.,
GARCÍAMATA CARLOS,
LAMATTINA LORENZO,
LAXALT ANA M.
Publication year - 2008
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 - 10.1111/j.1365-3040.2007.01756.x
Subject(s) - phosphatidic acid , nitric oxide , chemistry , closure (psychology) , biophysics , microbiology and biotechnology , biochemistry , biology , organic chemistry , phospholipid , membrane , economics , market economy
Stomatal closure is regulated by a complex network of signalling events involving numerous intermediates, among them nitric oxide (NO). Little is known about the signalling events occurring downstream of NO. Previous studies have shown that NO modulates cytosolic calcium concentration and the activation of plasma membrane ion channels. Here we provide evidence that supports the involvement of the lipid second messenger phosphatidic acid (PA) in NO signalling during stomatal closure. PA levels in Vicia faba epidermal peels increased upon NO treatment to maximum levels within 30 min, subsequently decreasing to control levels at 60 min. PA can be generated via phospholipase D (PLD) or via phospholipase C (PLC) in concerted action with diacylglycerol kinase (DGK). Our results showed that NO‐induced PA is produced via the activation of both pathways. NO‐induced stomatal closure was blocked either when PLC or PLD activity was inhibited. We have shown that PLC‐ and PLD‐derived PA represents a downstream component of NO signalling cascade during stomatal closure.