Study : PRC2-mediated epigenetic signatures associate with pathogn-induced programmed cell death in Arabidopsis
PRC2-mediated epigenetic signatures associate with pathogn-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 (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 H3K27me3 histone 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. Overall design: With modification of two-component vector system (Brand et al., 2006) we designed system for inducible expression of two different constructs mimicking the pathogen infection. The activator vector (pMDC150::XVE) contains chimeric transcription factor XVE under control of minimal 35S promoter. Both respondant vectors (pMDC160::NPP1 and pMDC160::RPT2) contain XVE-responsive promoter OlexA TATA. Constructs were introduced to Arabidopsis thaliana Columbia ecotype containing activator vector pMDC150::XVE by Agrobacterium-mediated transformation (Clough and Bent, 1998). Each ChIP-seq *.bed file was generated from all replicates together and is linked to the corresponding rep1 sample records. The RNA-seq DESeq*.txt files (linked as Series supplementary files) are comparison between different sample groups as indicated in the corresponding sample description field.