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A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype
Lesion mimic mutants (LMMs) are a class of mutants in which hypersensitive cell death and defence responses are constitutively activated in the absence of pathogen attack. Various signalling molecules, such as salicylic acid (SA), reactive oxygen species (ROS), nitric oxide (NO), Ca(2+), ethylene, a...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3808314/ https://www.ncbi.nlm.nih.gov/pubmed/23963675 http://dx.doi.org/10.1093/jxb/ert237 |
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author | Landoni, Michela De Francesco, Alessandra Bellatti, Silvia Delledonne, Massimo Ferrarini, Alberto Venturini, Luca Pilu, Roberto Bononi, Monica Tonelli, Chiara |
author_facet | Landoni, Michela De Francesco, Alessandra Bellatti, Silvia Delledonne, Massimo Ferrarini, Alberto Venturini, Luca Pilu, Roberto Bononi, Monica Tonelli, Chiara |
author_sort | Landoni, Michela |
collection | PubMed |
description | Lesion mimic mutants (LMMs) are a class of mutants in which hypersensitive cell death and defence responses are constitutively activated in the absence of pathogen attack. Various signalling molecules, such as salicylic acid (SA), reactive oxygen species (ROS), nitric oxide (NO), Ca(2+), ethylene, and jasmonate, are involved in the regulation of multiple pathways controlling hypersensitive response (HR) activation, and LMMs are considered useful tools to understand the role played by the key elements of the HR cell death signalling cascade. Here the characterization of an Arabidopsis LMM lacking the function of the FZL gene is reported. This gene encodes a membrane-remodelling GTPase playing an essential role in the determination of thylakoid and chloroplast morphology. The mutant displayed alteration in chloroplast number, size, and shape, and the typical characteristics of an LMM, namely development of chlorotic lesions on rosette leaves and constitutive expression of genetic and biochemical markers associated with defence responses. The chloroplasts are a major source of ROS, and the characterization of this mutant suggests that their accumulation, triggered by damage to the chloroplast membranes, is a signal sufficient to start the HR signalling cascade, thus confirming the central role of the chloroplast in HR activation. |
format | Online Article Text |
id | pubmed-3808314 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-38083142013-10-26 A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype Landoni, Michela De Francesco, Alessandra Bellatti, Silvia Delledonne, Massimo Ferrarini, Alberto Venturini, Luca Pilu, Roberto Bononi, Monica Tonelli, Chiara J Exp Bot Research Paper Lesion mimic mutants (LMMs) are a class of mutants in which hypersensitive cell death and defence responses are constitutively activated in the absence of pathogen attack. Various signalling molecules, such as salicylic acid (SA), reactive oxygen species (ROS), nitric oxide (NO), Ca(2+), ethylene, and jasmonate, are involved in the regulation of multiple pathways controlling hypersensitive response (HR) activation, and LMMs are considered useful tools to understand the role played by the key elements of the HR cell death signalling cascade. Here the characterization of an Arabidopsis LMM lacking the function of the FZL gene is reported. This gene encodes a membrane-remodelling GTPase playing an essential role in the determination of thylakoid and chloroplast morphology. The mutant displayed alteration in chloroplast number, size, and shape, and the typical characteristics of an LMM, namely development of chlorotic lesions on rosette leaves and constitutive expression of genetic and biochemical markers associated with defence responses. The chloroplasts are a major source of ROS, and the characterization of this mutant suggests that their accumulation, triggered by damage to the chloroplast membranes, is a signal sufficient to start the HR signalling cascade, thus confirming the central role of the chloroplast in HR activation. Oxford University Press 2013-11 2013-08-19 /pmc/articles/PMC3808314/ /pubmed/23963675 http://dx.doi.org/10.1093/jxb/ert237 Text en © The Author 2013. Published by Oxford University Press on behalf of the Society for Experimental Biology. http://creativecommons.org/licenses/by/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Landoni, Michela De Francesco, Alessandra Bellatti, Silvia Delledonne, Massimo Ferrarini, Alberto Venturini, Luca Pilu, Roberto Bononi, Monica Tonelli, Chiara A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title | A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title_full | A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title_fullStr | A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title_full_unstemmed | A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title_short | A mutation in the FZL gene of Arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
title_sort | mutation in the fzl gene of arabidopsis causing alteration in chloroplast morphology results in a lesion mimic phenotype |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3808314/ https://www.ncbi.nlm.nih.gov/pubmed/23963675 http://dx.doi.org/10.1093/jxb/ert237 |
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