In:
The Plant Journal, Wiley, Vol. 43, No. 4 ( 2005-08), p. 520-529
Abstract:
Recent work has indicated that nitric oxide (NO) and its synthesis are important elements of signal cascades in plant–pathogen defence, and are a prerequisite for drought and abscisic acid (ABA) responses in Arabidopsis thaliana and Vicia faba guard cells. NO regulates inward‐rectifying K + channels and Cl − channels of Vicia guard cells via intracellular Ca 2+ release. However, its integration with related signals, including the actions of serine–threonine protein kinases, is less well defined. We report here that the elevation of cytosolic‐free [Ca 2+ ] ([Ca 2+ ] i ) mediated by NO in guard cells is reversibly inhibited by the broad‐range protein kinase antagonists staurosporine and K252A, but not by the tyrosine kinase antagonist genistein. The effects of kinase antagonism translate directly to a loss of NO‐sensitivity of the inward‐rectifying K + channels and background (Cl − channel) current, and to a parallel loss in sensitivity of the K + channels to ABA. These results demonstrate that NO‐dependent signals can be modulated through protein phosphorylation upstream of intracellular Ca 2+ release, and they implicate a target for protein kinase control in ABA signalling that feeds into NO‐dependent Ca 2+ release.
Type of Medium:
Online Resource
ISSN:
0960-7412
,
1365-313X
DOI:
10.1111/tpj.2005.43.issue-4
DOI:
10.1111/j.1365-313X.2005.02471.x
Language:
English
Publisher:
Wiley
Publication Date:
2005
detail.hit.zdb_id:
2020961-7
SSG:
12
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