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VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
The intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence. We addressed this phenomenon by using AM‐defective vapyrin (vpy) m...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7986166/ https://www.ncbi.nlm.nih.gov/pubmed/33231304 http://dx.doi.org/10.1111/nph.17109 |
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author | Chen, Min Bruisson, Sébastien Bapaume, Laure Darbon, Geoffrey Glauser, Gaëtan Schorderet, Martine Reinhardt, Didier |
author_facet | Chen, Min Bruisson, Sébastien Bapaume, Laure Darbon, Geoffrey Glauser, Gaëtan Schorderet, Martine Reinhardt, Didier |
author_sort | Chen, Min |
collection | PubMed |
description | The intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence. We addressed this phenomenon by using AM‐defective vapyrin (vpy) mutants in Petunia hybrida, including a new allele (vpy‐3) with a transposon insertion close to the ATG start codon. We explore whether abortion of fungal infection in vpy mutants is associated with the induction of defence markers, such as cell wall alterations, accumulation of reactive oxygen species (ROS), defence hormones and induction of pathogenesis‐related (PR) genes. We show that vpy mutants exhibit a strong resistance against intracellular colonization, which is associated with the generation of cell wall appositions (papillae) with lignin impregnation at fungal entry sites, while no accumulation of defence hormones, ROS or callose was observed. Systematic analysis of PR gene expression revealed that several PR genes are induced in mycorrhizal roots of the wild‐type, and even more in vpy plants. Some PR genes are induced exclusively in vpy mutants. Our results suggest that VPY is involved in avoiding or suppressing the induction of a cellular defence syndrome that involves localized lignin deposition and PR gene induction. |
format | Online Article Text |
id | pubmed-7986166 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-79861662021-03-25 VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida Chen, Min Bruisson, Sébastien Bapaume, Laure Darbon, Geoffrey Glauser, Gaëtan Schorderet, Martine Reinhardt, Didier New Phytol Research The intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence. We addressed this phenomenon by using AM‐defective vapyrin (vpy) mutants in Petunia hybrida, including a new allele (vpy‐3) with a transposon insertion close to the ATG start codon. We explore whether abortion of fungal infection in vpy mutants is associated with the induction of defence markers, such as cell wall alterations, accumulation of reactive oxygen species (ROS), defence hormones and induction of pathogenesis‐related (PR) genes. We show that vpy mutants exhibit a strong resistance against intracellular colonization, which is associated with the generation of cell wall appositions (papillae) with lignin impregnation at fungal entry sites, while no accumulation of defence hormones, ROS or callose was observed. Systematic analysis of PR gene expression revealed that several PR genes are induced in mycorrhizal roots of the wild‐type, and even more in vpy plants. Some PR genes are induced exclusively in vpy mutants. Our results suggest that VPY is involved in avoiding or suppressing the induction of a cellular defence syndrome that involves localized lignin deposition and PR gene induction. John Wiley and Sons Inc. 2020-12-25 2021-03 /pmc/articles/PMC7986166/ /pubmed/33231304 http://dx.doi.org/10.1111/nph.17109 Text en © 2020 The Authors New Phytologist © 2020 New Phytologist Foundation This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Chen, Min Bruisson, Sébastien Bapaume, Laure Darbon, Geoffrey Glauser, Gaëtan Schorderet, Martine Reinhardt, Didier VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida |
title | VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
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title_full | VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
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title_fullStr | VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
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title_full_unstemmed | VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
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title_short | VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrida
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title_sort | vapyrin attenuates defence by repressing pr gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of petunia hybrida |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7986166/ https://www.ncbi.nlm.nih.gov/pubmed/33231304 http://dx.doi.org/10.1111/nph.17109 |
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