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Next generation systemic acquired resistance

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Next generation systemic acquired resistance. / Luna, Estrella; Bruce, Toby; Roberts, Michael et al.
In: Plant Physiology, Vol. 158, No. 2, 02.2012, p. 844-853.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

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Luna, E, Bruce, T, Roberts, M, Flors, V & Ton, J 2012, 'Next generation systemic acquired resistance', Plant Physiology, vol. 158, no. 2, pp. 844-853. https://doi.org/10.1104/pp.111.187468

APA

Luna, E., Bruce, T., Roberts, M., Flors, V., & Ton, J. (2012). Next generation systemic acquired resistance. Plant Physiology, 158(2), 844-853. https://doi.org/10.1104/pp.111.187468

Vancouver

Luna E, Bruce T, Roberts M, Flors V, Ton J. Next generation systemic acquired resistance. Plant Physiology. 2012 Feb;158(2):844-853. Epub 2011 Dec 6. doi: 10.1104/pp.111.187468

Author

Luna, Estrella ; Bruce, Toby ; Roberts, Michael et al. / Next generation systemic acquired resistance. In: Plant Physiology. 2012 ; Vol. 158, No. 2. pp. 844-853.

Bibtex

@article{909f960eea7b406a99e8c804ad84c9f2,
title = "Next generation systemic acquired resistance",
abstract = "Systemic acquired resistance (SAR) is a plant immune response to pathogen attack. Recent evidence suggests that plant immunity involves regulation by chromatin remodeling and DNA methylation. We have investigated whether SAR can be inherited epigenetically following disease pressure by Pseudomonas syringae pv. tomato DC3000 (PstDC3000). Compared to progeny from control-treated Arabidopsis (C1), progeny from PstDC3000-inoculated Arabidopsis (P1) were primed to activate salicylic acid (SA)-inducible defense genes and were more resistant to the (hemi-)biotrophic pathogens Hyaloperonospora arabidopsidis and PstDC3000. This trans-generational SAR was sustained over one stress-free generation, indicating an epigenetic basis of the phenomenon. Furthermore, P1 progeny displayed reduced responsiveness of jasmonic acid (JA)-inducible genes and enhanced susceptibility to the necrotrophic fungus Alternaria brassicicola. This shift in SA- and JA-dependent gene responsiveness was not associated with changes in corresponding hormone levels. Instead, chromatin-immunoprecipitation analyses revealed that SA-inducible promoters of PR-1, WRKY6 and WRKY53 in P1 plants are enriched with acetylated histone H3 at lysine9, a chromatin mark associated with a permissive state of transcription. Conversely, the JA-inducible PDF1.2 promoter showed increased H3 triple-methylation at lysine27, a mark related to repressed gene transcription. P1 progeny from the defense regulatory mutant npr1-1 failed to develop trans-generational defense phenotypes, demonstrating a critical role for NPR1 in expression of trans-generational SAR. Furthermore, the drm1drm2cmt3 mutant that is affected in non-CpG DNA methylation mimicked the trans-generational SAR phenotype. Since PstDC3000 induces DNA hypomethylation in Arabidopsis, our results suggest that trans-generational SAR is transmitted by hypomethylated genes that direct priming of SA-dependent defenses in following generations. ",
keywords = "priming, systemic acquired resistance, epigenetic inheritance, plant immunity",
author = "Estrella Luna and Toby Bruce and Michael Roberts and Victor Flors and Jurriaan Ton",
year = "2012",
month = feb,
doi = "10.1104/pp.111.187468",
language = "English",
volume = "158",
pages = "844--853",
journal = "Plant Physiology",
issn = "0032-0889",
publisher = "American Society of Plant Biologists",
number = "2",

}

RIS

TY - JOUR

T1 - Next generation systemic acquired resistance

AU - Luna, Estrella

AU - Bruce, Toby

AU - Roberts, Michael

AU - Flors, Victor

AU - Ton, Jurriaan

PY - 2012/2

Y1 - 2012/2

N2 - Systemic acquired resistance (SAR) is a plant immune response to pathogen attack. Recent evidence suggests that plant immunity involves regulation by chromatin remodeling and DNA methylation. We have investigated whether SAR can be inherited epigenetically following disease pressure by Pseudomonas syringae pv. tomato DC3000 (PstDC3000). Compared to progeny from control-treated Arabidopsis (C1), progeny from PstDC3000-inoculated Arabidopsis (P1) were primed to activate salicylic acid (SA)-inducible defense genes and were more resistant to the (hemi-)biotrophic pathogens Hyaloperonospora arabidopsidis and PstDC3000. This trans-generational SAR was sustained over one stress-free generation, indicating an epigenetic basis of the phenomenon. Furthermore, P1 progeny displayed reduced responsiveness of jasmonic acid (JA)-inducible genes and enhanced susceptibility to the necrotrophic fungus Alternaria brassicicola. This shift in SA- and JA-dependent gene responsiveness was not associated with changes in corresponding hormone levels. Instead, chromatin-immunoprecipitation analyses revealed that SA-inducible promoters of PR-1, WRKY6 and WRKY53 in P1 plants are enriched with acetylated histone H3 at lysine9, a chromatin mark associated with a permissive state of transcription. Conversely, the JA-inducible PDF1.2 promoter showed increased H3 triple-methylation at lysine27, a mark related to repressed gene transcription. P1 progeny from the defense regulatory mutant npr1-1 failed to develop trans-generational defense phenotypes, demonstrating a critical role for NPR1 in expression of trans-generational SAR. Furthermore, the drm1drm2cmt3 mutant that is affected in non-CpG DNA methylation mimicked the trans-generational SAR phenotype. Since PstDC3000 induces DNA hypomethylation in Arabidopsis, our results suggest that trans-generational SAR is transmitted by hypomethylated genes that direct priming of SA-dependent defenses in following generations.

AB - Systemic acquired resistance (SAR) is a plant immune response to pathogen attack. Recent evidence suggests that plant immunity involves regulation by chromatin remodeling and DNA methylation. We have investigated whether SAR can be inherited epigenetically following disease pressure by Pseudomonas syringae pv. tomato DC3000 (PstDC3000). Compared to progeny from control-treated Arabidopsis (C1), progeny from PstDC3000-inoculated Arabidopsis (P1) were primed to activate salicylic acid (SA)-inducible defense genes and were more resistant to the (hemi-)biotrophic pathogens Hyaloperonospora arabidopsidis and PstDC3000. This trans-generational SAR was sustained over one stress-free generation, indicating an epigenetic basis of the phenomenon. Furthermore, P1 progeny displayed reduced responsiveness of jasmonic acid (JA)-inducible genes and enhanced susceptibility to the necrotrophic fungus Alternaria brassicicola. This shift in SA- and JA-dependent gene responsiveness was not associated with changes in corresponding hormone levels. Instead, chromatin-immunoprecipitation analyses revealed that SA-inducible promoters of PR-1, WRKY6 and WRKY53 in P1 plants are enriched with acetylated histone H3 at lysine9, a chromatin mark associated with a permissive state of transcription. Conversely, the JA-inducible PDF1.2 promoter showed increased H3 triple-methylation at lysine27, a mark related to repressed gene transcription. P1 progeny from the defense regulatory mutant npr1-1 failed to develop trans-generational defense phenotypes, demonstrating a critical role for NPR1 in expression of trans-generational SAR. Furthermore, the drm1drm2cmt3 mutant that is affected in non-CpG DNA methylation mimicked the trans-generational SAR phenotype. Since PstDC3000 induces DNA hypomethylation in Arabidopsis, our results suggest that trans-generational SAR is transmitted by hypomethylated genes that direct priming of SA-dependent defenses in following generations.

KW - priming

KW - systemic acquired resistance

KW - epigenetic inheritance

KW - plant immunity

UR - http://www.scopus.com/inward/record.url?scp=84856575118&partnerID=8YFLogxK

U2 - 10.1104/pp.111.187468

DO - 10.1104/pp.111.187468

M3 - Journal article

AN - SCOPUS:84856575118

VL - 158

SP - 844

EP - 853

JO - Plant Physiology

JF - Plant Physiology

SN - 0032-0889

IS - 2

ER -