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A new role for an old enzyme: Nitrate reductase-mediated nitric oxide generation is required for abscisic acid-induced stomatal closure in Arabidopsis thaliana

Desikan, Radhika; Griffiths, Rachael; Hancock, John T.; Neill, Steven

Authors

Radhika Desikan

Rachael Griffiths

Profile image of John Hancock

John Hancock John.Hancock@uwe.ac.uk
Professor in Cell Signalling

Steven Neill



Abstract

The plant hormone abscisic acid (ABA), synthesized in response to water-deficit stress, induces stomatal closure via activation of complex signaling cascades. Recent work has established that nitric oxide (NO) is a key signaling molecule mediating ABA-induced stomatal closure. However, the biosynthetic origin of NO in guard cells has not yet been resolved. Here, we provide pharmacological, physiological, and genetic evidence that NO synthesis in Arabidopsis guard cells is mediated by the enzyme nitrate reductase (NR). Guard cells of wild-type Arabidopsis generate NO in response to treatment with ABA and nitrite, a substrate for NR. Moreover, NR-mediated NO synthesis is required for ABA-induced stomatal closure. However, in the NR double mutant, nia1, nia2 that has diminished NR activity, guard cells do not synthesize NO nor do the stomata close in response to ABA or nitrite, although stomatal opening is still inhibited by ABA. Furthermore, by using the ABA-insensitive (ABI) abi1-1 and abi2-1 mutants, we show that the ABI1 and ABI2 protein phosphatases are downstream of NO in the ABA signal-transduction cascade. These data demonstrate a previously uncharacterized signaling role for NR, that of mediating ABA-induced NO synthesis in Arabidopsis guard cells.

Journal Article Type Article
Publication Date Dec 10, 2002
Journal Proceedings of the National Academy of Sciences of the United States of America
Print ISSN 0027-8424
Publisher National Academy of Sciences
Peer Reviewed Peer Reviewed
Volume 99
Issue 25
Pages 16314-16318
DOI https://doi.org/10.1073/pnas.252461999
Public URL https://uwe-repository.worktribe.com/output/1082563
Publisher URL http://dx.doi.org/10.1073/pnas.252461999