کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2017515 | 1067801 | 2011 | 5 صفحه PDF | دانلود رایگان |

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.
► CNGCs play important roles in facilitating Ca2+ uptake into plant cells and plant innate immunity.
► Ca2+ sensors, NO and other associate signaling components play pivotal roles in plant innate immune signaling cascade.
► Ca2+ homeostasis can be regulated by downstream signaling components.
Journal: Plant Science - Volume 181, Issue 4, October 2011, Pages 342–346