Seminar Dr Jurriaan Ton
From recall to reset: the role of DNA (de)methylation in plant immune memory - Wednesday 20 May 2026 11 am, INRAE, Versailles
Plants recovering from pest or pathogen attack often develop a heightened defensive state, known as induced resistance (IR). This state is typically driven by a priming of the plant’s innate immune system, enabling faster and stronger defence reactions to subsequent attacks. Our lab studies the epigenetic basis of this immune memory. We have previously shown that early exposure of Arabidopsis seedlings to biotic stress triggers IR that persists throughout the plant's life cycle and, in some cases, into the next generation. These long-lasting IR phenomena are specific to the type of stress encountered previously, are associated with reductions in DNA methylation, and require the activity of the DNA demethylase ROS1.
To dissect how DNA demethylation contributes to immune memory, we employ genetic approaches to manipulate the plant methylome. Using epigenetic recombinant inbred lines (epiRILs), which share the same genetic (wild-type) background but vary in heritable DNA methylation of TE-rich regions, we have previously identified epialleles that prime defence gene expression, resulting in high levels of disease resistance without growth penalties.
Building on these findings, we have developed an XVE-based transactivation system to introduce dosed amounts of ROS1-dependent DNA hypo-methylation into plant genomes, providing a powerful tool to investigate how plants establish, maintain, and reset stress-specific immune memory. Using this system in Arabidopsis, we present new evidence that transient ROS1 activity drives contrasting epigenetic responses between gene-rich chromosome arms and transposon-rich (peri)centromeric regions. The onset and maintenance of ROS1-induced immune memory was associated with reduced levels of DNA methylation and small RNA accumulation along the chromosome arms, promoting expression of genes controlling salicylic acid–dependent immunity and DNA damage repair. These changes were progressively reversed during the erasure of the immune memory. By contrast, the epigenetic changes in the (peri)centromeres were retained beyond the duration of the immune memory, involving elevated accumulation of small RNA and DNA hypermethylation that are partially mediated by a CLSY3-dependent redistribution of RNA-directed DNA methylation activity.
Current research is focusing on the translation of our results into crops with a particular focus on developing methods to engineer stable immune memory and disease resistance in vegetable crops.
Jurriaan Ton, Ton Lab "plant environmental signalling", School of Biosciences, University of Sheffield,UK
Invitation: Nicolas Bouché, "Epigenetic Natural Variation" VarEpi team
Seminar in connection with the research developed at the Institute Jean-Pierre Bourgin for Plant Sciences.
To dissect how DNA demethylation contributes to immune memory, we employ genetic approaches to manipulate the plant methylome. Using epigenetic recombinant inbred lines (epiRILs), which share the same genetic (wild-type) background but vary in heritable DNA methylation of TE-rich regions, we have previously identified epialleles that prime defence gene expression, resulting in high levels of disease resistance without growth penalties.
Building on these findings, we have developed an XVE-based transactivation system to introduce dosed amounts of ROS1-dependent DNA hypo-methylation into plant genomes, providing a powerful tool to investigate how plants establish, maintain, and reset stress-specific immune memory. Using this system in Arabidopsis, we present new evidence that transient ROS1 activity drives contrasting epigenetic responses between gene-rich chromosome arms and transposon-rich (peri)centromeric regions. The onset and maintenance of ROS1-induced immune memory was associated with reduced levels of DNA methylation and small RNA accumulation along the chromosome arms, promoting expression of genes controlling salicylic acid–dependent immunity and DNA damage repair. These changes were progressively reversed during the erasure of the immune memory. By contrast, the epigenetic changes in the (peri)centromeres were retained beyond the duration of the immune memory, involving elevated accumulation of small RNA and DNA hypermethylation that are partially mediated by a CLSY3-dependent redistribution of RNA-directed DNA methylation activity.
Current research is focusing on the translation of our results into crops with a particular focus on developing methods to engineer stable immune memory and disease resistance in vegetable crops.
Jurriaan Ton, Ton Lab "plant environmental signalling", School of Biosciences, University of Sheffield,UK
Invitation: Nicolas Bouché, "Epigenetic Natural Variation" VarEpi team
Seminar in connection with the research developed at the Institute Jean-Pierre Bourgin for Plant Sciences.
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