Nitric oxide production occurs after cytosolic alkalinization during stomatal closure induced by abscisic acid

Abscisic acid (ABA) raised the cytosolic pH and nitric oxide (NO) levels in guard cells while inducing stomatal closure in epidermis of Pisum sativum. Butyrate (a weak acid) reduced the cytosolic pH/NO production and prevented stomatal closure by ABA. Methylamine (a weak base) enhanced the cytosolic...

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Published in:Plant, cell and environment cell and environment, 2008-11, Vol.31 (11), p.1717-1724
Main Authors: GONUGUNTA, VIJAY K, SRIVASTAVA, NUPUR, PULI, MALLIKARJUNA R, RAGHAVENDRA, AGEPATI S
Format: Article
Language:English
Subjects:
abscisic acid
Abscisic Acid - pharmacology
Biological and medical sciences
calcium
Calcium - metabolism
Cytosol - chemistry
cytosolic pH
Fundamental and applied biological sciences. Psychology
guard cells
Hydrogen-Ion Concentration
nitric oxide
Nitric Oxide - biosynthesis
Pisum sativum
Pisum sativum - drug effects
Pisum sativum - metabolism
Plant Growth Regulators - pharmacology
Plant Stomata - drug effects
Plant Stomata - metabolism
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Summary:Abscisic acid (ABA) raised the cytosolic pH and nitric oxide (NO) levels in guard cells while inducing stomatal closure in epidermis of Pisum sativum. Butyrate (a weak acid) reduced the cytosolic pH/NO production and prevented stomatal closure by ABA. Methylamine (a weak base) enhanced the cytosolic alkalinization and aggravated stomatal closure by ABA. The rise in guard cell pH because of ABA became noticeable after 6 min and peaked at 12 min, while NO production started at 9 min and peaked at 18 min. These results suggested that NO production was downstream of the rise in cytosolic pH. The ABA-induced increase in NO of guard cells and stomatal closure was prevented by 2-phenyl-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide (cPTIO, a NO scavenger) and partially by N-nitro-L-Arg-methyl ester (L-NAME, an inhibitor of NO synthase). In contrast, cPTIO or L-NAME had only a marginal effect on the pH rise induced by ABA. Ethylene glycol tetraacetic acid (EGTA, a calcium chelator) prevented ABA-induced stomatal closure while restricting cytosolic pH rise and NO production. We suggest that during ABA-induced stomatal closure, a rise in cytosolic pH is necessary for NO production. Calcium may act upstream of cytosolic alkalinization and NO production, besides its known function as a downstream component.
ISSN:0140-7791
1365-3040
DOI:10.1111/j.1365-3040.2008.01872.x