期刊
PLANT JOURNAL
卷 43, 期 4, 页码 520-529出版社
WILEY
DOI: 10.1111/j.1365-313X.2005.02471.x
关键词
K+ channel; inward-rectifying; Cl- channel; Vicia faba stomatal guard cell; oxidative stress; protein kinase; cytosolic-free Ca2+ concentration
资金
- Biotechnology and Biological Sciences Research Council [BB/C500595/1, P12750] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [P12750, BB/C500595/1] Funding Source: researchfish
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 Ca2+ 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 [Ca2+] ([Ca2+](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 Ca2+ release, and they implicate a target for protein kinase control in ABA signalling that feeds into NO-dependent Ca2+ release.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据