Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.

Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The a...

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Autores principales: Kristoffer Palma, Stephan Thorgrimsen, Frederikke Gro Malinovsky, Berthe Katrine Fiil, H Bjørn Nielsen, Peter Brodersen, Daniel Hofius, Morten Petersen, John Mundy
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Publicado: Public Library of Science (PLoS) 2010
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spelling oai:doaj.org-article:81b1cd5bc0de42a3987ec3b633a1ce8b2021-11-18T06:03:50ZAutoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.1553-73661553-737410.1371/journal.ppat.1001137https://doaj.org/article/81b1cd5bc0de42a3987ec3b633a1ce8b2010-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20949080/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The accelerated cell death 11 (acd11) "lesion mimic" mutant of Arabidopsis thaliana exhibits autoimmune phenotypes such as constitutive defense responses and cell death without pathogen perception. ACD11 encodes a putative sphingosine transfer protein, but its precise role during these processes is unknown. In a screen for lazarus (laz) mutants that suppress acd11 death we identified two genes, LAZ2 and LAZ5. LAZ2 encodes the histone lysine methyltransferase SDG8, previously shown to epigenetically regulate flowering time via modification of histone 3 (H3). LAZ5 encodes an RPS4-like R-protein, defined by several dominant negative alleles. Microarray and chromatin immunoprecipitation analyses showed that LAZ2/SDG8 is required for LAZ5 expression and H3 lysine 36 trimethylation at LAZ5 chromatin to maintain a transcriptionally active state. We hypothesize that LAZ5 triggers cell death in the absence of ACD11, and that cell death in other lesion mimic mutants may also be caused by inappropriate activation of R genes. Moreover, SDG8 is required for basal and R protein-mediated pathogen resistance in Arabidopsis, revealing the importance of chromatin remodeling as a key process in plant innate immunity.Kristoffer PalmaStephan ThorgrimsenFrederikke Gro MalinovskyBerthe Katrine FiilH Bjørn NielsenPeter BrodersenDaniel HofiusMorten PetersenJohn MundyPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 6, Iss 10, p e1001137 (2010)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Kristoffer Palma
Stephan Thorgrimsen
Frederikke Gro Malinovsky
Berthe Katrine Fiil
H Bjørn Nielsen
Peter Brodersen
Daniel Hofius
Morten Petersen
John Mundy
Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
description Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The accelerated cell death 11 (acd11) "lesion mimic" mutant of Arabidopsis thaliana exhibits autoimmune phenotypes such as constitutive defense responses and cell death without pathogen perception. ACD11 encodes a putative sphingosine transfer protein, but its precise role during these processes is unknown. In a screen for lazarus (laz) mutants that suppress acd11 death we identified two genes, LAZ2 and LAZ5. LAZ2 encodes the histone lysine methyltransferase SDG8, previously shown to epigenetically regulate flowering time via modification of histone 3 (H3). LAZ5 encodes an RPS4-like R-protein, defined by several dominant negative alleles. Microarray and chromatin immunoprecipitation analyses showed that LAZ2/SDG8 is required for LAZ5 expression and H3 lysine 36 trimethylation at LAZ5 chromatin to maintain a transcriptionally active state. We hypothesize that LAZ5 triggers cell death in the absence of ACD11, and that cell death in other lesion mimic mutants may also be caused by inappropriate activation of R genes. Moreover, SDG8 is required for basal and R protein-mediated pathogen resistance in Arabidopsis, revealing the importance of chromatin remodeling as a key process in plant innate immunity.
format article
author Kristoffer Palma
Stephan Thorgrimsen
Frederikke Gro Malinovsky
Berthe Katrine Fiil
H Bjørn Nielsen
Peter Brodersen
Daniel Hofius
Morten Petersen
John Mundy
author_facet Kristoffer Palma
Stephan Thorgrimsen
Frederikke Gro Malinovsky
Berthe Katrine Fiil
H Bjørn Nielsen
Peter Brodersen
Daniel Hofius
Morten Petersen
John Mundy
author_sort Kristoffer Palma
title Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
title_short Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
title_full Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
title_fullStr Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
title_full_unstemmed Autoimmunity in Arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
title_sort autoimmunity in arabidopsis acd11 is mediated by epigenetic regulation of an immune receptor.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/81b1cd5bc0de42a3987ec3b633a1ce8b
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AT berthekatrinefiil autoimmunityinarabidopsisacd11ismediatedbyepigeneticregulationofanimmunereceptor
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