4.7 Review

Roles of Ca2+ and cyclic nucleotide gated channel in plant innate immunity

期刊

PLANT SCIENCE
卷 181, 期 4, 页码 342-346

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.plantsci.2011.06.002

关键词

Arabidopsis; Calcium; Cyclic nucleotide gated channel; Nitric oxide; Plant innate immunity; Signal transduction

向作者/读者索取更多资源

The increase of cytosolic Ca2+ is a vital event in plant pathogen signaling cascades. Molecular components linking pathogen signal perception to cytosolic Ca2+ increase have not been well characterized. Plant cyclic nucleotide gated channels (CNGCs) play important roles in the pathogen signaling cascade, in terms of facilitating Ca2+ uptake into the cytosol in response to pathogen and pathogen associated molecular pattern (PAMP) signals. Perception of pathogens leads to cyclic nucleotide production and the activation of CNGCs. The Ca2+ signal is transduced through Ca2+ sensors (Calmodulin (CaM) and CaM-like proteins (CMLs)), which regulates the production of nitric oxide (NO). In addition, roles of Ca2+/CaM interacting proteins such as CaM binding Protein (CBP) and CaM-binding transcription activators (CAMTAs)) have been recently identified in the plant defense signaling cascade as well. Furthermore, Ca2+-dependent protein kinases (CDPKs) have been found to function as components in terms of transcriptional activation in response to a pathogen (PAMP) signal. Although evidence shows that Ca2+ is an essential signaling component upstream from many vital signaling molecules (such as NO), some work also indicates that these downstream signaling components can also regulate Ca2+ homeostasis. NO can induce cytosolic Ca2+ increase (through activation of plasma membrane- and intracellular membrane-localized Ca2+ channels) during pathogen signaling cascades. Thus, much work is needed to further elucidate the complexity of the plant pathogen signaling network in the future. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

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。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据