Wei Ma
Journal: Plant science : an international journal of experimental plant biology 2011;181(4):342-6
PMID: 21889039
The increase of cytosolic Ca(2+) is a vital event in plant pathogen signaling cascades. Molecular components linking pathogen signal perception to cytosolic Ca(2+) increase have not been well characterized. Plant cyclic nucleotide gated channels (CNGCs) play important roles in the pathogen signaling cascade, in terms of facilitating Ca(2+) 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 Ca(2+) signal is transduced through Ca(2+) sensors (Calmodulin (CaM) and CaM-like proteins (CMLs)), which regulates the production of nitric oxide (NO). In addition, roles of Ca(2+)/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, Ca(2+)-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 Ca(2+) 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 Ca(2+) homeostasis. NO can induce cytosolic Ca(2+) increase (through activation of plasma membrane- and intracellular membrane-localized Ca(2+) channels) during pathogen signaling cascades. Thus, much work is needed to further elucidate the complexity of the plant pathogen signaling network in the future.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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