Nitric oxide negatively regulates abscisic acid signaling in guard cells by S-nitrosylation of OST1.
Proc Natl Acad Sci U S A
; 112(2): 613-8, 2015 Jan 13.
Article
em En
| MEDLINE
| ID: mdl-25550508
ABSTRACT
The phytohormone abscisic acid (ABA) plays important roles in plant development and adaptation to environmental stress. ABA induces the production of nitric oxide (NO) in guard cells, but how NO regulates ABA signaling is not understood. Here, we show that NO negatively regulates ABA signaling in guard cells by inhibiting open stomata 1 (OST1)/sucrose nonfermenting 1 (SNF1)-related protein kinase 2.6 (SnRK2.6) through S-nitrosylation. We found that SnRK2.6 is S-nitrosylated at cysteine 137, a residue adjacent to the kinase catalytic site. Dysfunction in the S-nitrosoglutathione (GSNO) reductase (GSNOR) gene in the gsnor1-3 mutant causes NO overaccumulation in guard cells, constitutive S-nitrosylation of SnRK2.6, and impairment of ABA-induced stomatal closure. Introduction of the Cys137 to Ser mutated SnRK2.6 into the gsnor1-3/ost1-3 double-mutant partially suppressed the effect of gsnor1-3 on ABA-induced stomatal closure. A cysteine residue corresponding to Cys137 of SnRK2.6 is present in several yeast and human protein kinases and can be S-nitrosylated, suggesting that the S-nitrosylation may be an evolutionarily conserved mechanism for protein kinase regulation.
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Base de dados:
MEDLINE
Assunto principal:
Proteínas Quinases
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Arabidopsis
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Ácido Abscísico
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Proteínas de Arabidopsis
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Óxido Nítrico
Limite:
Humans
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article