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Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis

The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death...

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Autores principales: Dvořák Tomaštíková, Eva, Hafrén, Anders, Trejo-Arellano, Minerva S, Rasmussen, Sheena Ricafranca, Sato, Hikaru, Santos-González, Juan, Köhler, Claudia, Hennig, Lars, Hofius, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8133635/
https://www.ncbi.nlm.nih.gov/pubmed/33566101
http://dx.doi.org/10.1093/plphys/kiab035
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author Dvořák Tomaštíková, Eva
Hafrén, Anders
Trejo-Arellano, Minerva S
Rasmussen, Sheena Ricafranca
Sato, Hikaru
Santos-González, Juan
Köhler, Claudia
Hennig, Lars
Hofius, Daniel
author_facet Dvořák Tomaštíková, Eva
Hafrén, Anders
Trejo-Arellano, Minerva S
Rasmussen, Sheena Ricafranca
Sato, Hikaru
Santos-González, Juan
Köhler, Claudia
Hennig, Lars
Hofius, Daniel
author_sort Dvořák Tomaštíková, Eva
collection PubMed
description The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD.
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spelling pubmed-81336352021-05-25 Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis Dvořák Tomaštíková, Eva Hafrén, Anders Trejo-Arellano, Minerva S Rasmussen, Sheena Ricafranca Sato, Hikaru Santos-González, Juan Köhler, Claudia Hennig, Lars Hofius, Daniel Plant Physiol Regular Issue The Polycomb Repressive Complex 2 (PRC2) is well-known for its role in controlling developmental transitions by suppressing the premature expression of key developmental regulators. Previous work revealed that PRC2 also controls the onset of senescence, a form of developmental programmed cell death (PCD) in plants. Whether the induction of PCD in response to stress is similarly suppressed by the PRC2 remained largely unknown. In this study, we explored whether PCD triggered in response to immunity- and disease-promoting pathogen effectors is associated with changes in the distribution of the PRC2-mediated histone H3 lysine 27 trimethylation (H3K27me3) modification in Arabidopsis thaliana. We furthermore tested the distribution of the heterochromatic histone mark H3K9me2, which is established, to a large extent, by the H3K9 methyltransferase KRYPTONITE, and occupies chromatin regions generally not targeted by PRC2. We report that effector-induced PCD caused major changes in the distribution of both repressive epigenetic modifications and that both modifications have a regulatory role and impact on the onset of PCD during pathogen infection. Our work highlights that the transition to pathogen-induced PCD is epigenetically controlled, revealing striking similarities to developmental PCD. Oxford University Press 2021-02-04 /pmc/articles/PMC8133635/ /pubmed/33566101 http://dx.doi.org/10.1093/plphys/kiab035 Text en © The Author(s) 2021. Published by Oxford University Press on behalf of American Society of Plant Biologists. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Regular Issue
Dvořák Tomaštíková, Eva
Hafrén, Anders
Trejo-Arellano, Minerva S
Rasmussen, Sheena Ricafranca
Sato, Hikaru
Santos-González, Juan
Köhler, Claudia
Hennig, Lars
Hofius, Daniel
Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title_full Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title_fullStr Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title_full_unstemmed Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title_short Polycomb Repressive Complex 2 and KRYPTONITE regulate pathogen-induced programmed cell death in Arabidopsis
title_sort polycomb repressive complex 2 and kryptonite regulate pathogen-induced programmed cell death in arabidopsis
topic Regular Issue
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8133635/
https://www.ncbi.nlm.nih.gov/pubmed/33566101
http://dx.doi.org/10.1093/plphys/kiab035
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