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The grateful dead: calcium and cell death in plant innate immunity

The grateful dead: calcium and cell death in plant innate immunity Summary Plant cells sensing pathogenic microorganisms evoke defence systems that can confer resistance to infection. This innate immune reaction can include triggering of basal defence responses as well as programmed cell death, or hypersensitive response (HR). In both cases (basal defence and HR), pathogen perception is translated into elevated cytosolic Ca2+ (mediated by plasma membrane and intracellular channels) as an early step in a signalling cascade. Cyclic nucleotide‐gated channels contribute to this influx of Ca2+ into the cell. The molecular nature of other transport proteins contributing to the Ca2+ elevation is unclear. Pathogen recognition occurs at two levels: the perception of pathogen‐associated molecular pattern (PAMP) molecules widely present in microorganisms, and an interaction between pathogen avirulence gene products (if present) and corresponding plant R (resistance) gene products. The Ca2+ elevation occurring in response to PAMP perception or R gene interactions could occur due to phosphorylation events, G‐protein signalling and/or an increase in cyclic nucleotides. Downstream from the initial Ca2+ rise, the signalling cascade includes: activation of calmodulin and protein kinases, and nitric oxide and reactive oxygen species generation. Some of these downstream events amplify the Ca2+ signal by further activation of Ca2+ transporters. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cellular Microbiology Wiley

The grateful dead: calcium and cell death in plant innate immunity

Cellular Microbiology , Volume 9 (11) – Nov 1, 2007

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References (136)

Publisher
Wiley
Copyright
Copyright © 2007 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1462-5814
eISSN
1462-5822
DOI
10.1111/j.1462-5822.2007.01031.x
pmid
17714518
Publisher site
See Article on Publisher Site

Abstract

Summary Plant cells sensing pathogenic microorganisms evoke defence systems that can confer resistance to infection. This innate immune reaction can include triggering of basal defence responses as well as programmed cell death, or hypersensitive response (HR). In both cases (basal defence and HR), pathogen perception is translated into elevated cytosolic Ca2+ (mediated by plasma membrane and intracellular channels) as an early step in a signalling cascade. Cyclic nucleotide‐gated channels contribute to this influx of Ca2+ into the cell. The molecular nature of other transport proteins contributing to the Ca2+ elevation is unclear. Pathogen recognition occurs at two levels: the perception of pathogen‐associated molecular pattern (PAMP) molecules widely present in microorganisms, and an interaction between pathogen avirulence gene products (if present) and corresponding plant R (resistance) gene products. The Ca2+ elevation occurring in response to PAMP perception or R gene interactions could occur due to phosphorylation events, G‐protein signalling and/or an increase in cyclic nucleotides. Downstream from the initial Ca2+ rise, the signalling cascade includes: activation of calmodulin and protein kinases, and nitric oxide and reactive oxygen species generation. Some of these downstream events amplify the Ca2+ signal by further activation of Ca2+ transporters.

Journal

Cellular MicrobiologyWiley

Published: Nov 1, 2007

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