Epigenetic control of T-DNA during transgenesis and pathogenesis.

Mobile elements known as T-DNAs are transferred from pathogenic Agrobacterium to plants and reprogram the host cell to form hairy roots or tumors. Disarmed nononcogenic T-DNAs are extensively used to deliver transgenes in plant genetic engineering. Such T-DNAs were the first known targets of RNA silencing mechanisms, which detect foreign RNA in plant cells and produce small RNAs that induce transcript degradation.

Role of Polycomb in the control of transposable elements.

It is generally considered that Polycomb Repressive Complex (PRC)2 deposits the histone mark H3K27me3 on silent protein-coding genes, while transposable elements are repressed by DNA and/or H3K9 methylation. Yet, there is increasing evidence that PRC2 also targets and even silences transposable elements in representatives of several distantly related eukaryotic lineages. In plants and animals, H3K27me3 is present on transposable elements in mutants and specific cell types devoid of DNA methylation.

Polycomb mutant partially suppresses DNA hypomethylation-associated phenotypes in Arabidopsis.

In plants and mammals, DNA methylation and histone H3 lysine 27 trimethylation (H3K27me3), which is deposited by the polycomb repressive complex 2, are considered as two specialized systems for the epigenetic silencing of transposable element (TE) and genes, respectively. Nevertheless, many TE sequences acquire H3K27me3 when DNA methylation is lost. Here, we show in that the gain of H3K27me3 observed at hundreds of TEs in the mutant defective in the maintenance of DNA methylation, essentially depends on CURLY LEAF (CLF), one of two partially redundant H3K27 methyltransferases active in vegetative tissues.

Transcriptional control and exploitation of an immune-responsive family of plant retrotransposons.

Mobilization of transposable elements (TEs) in plants has been recognized as a driving force of evolution and adaptation, in particular by providing genes with regulatory modules that impact their transcription. In this study, we employed an long-terminal repeat (LTR) promoter- fusion to show that this retrotransposon behaves like an immune-responsive gene during pathogen defense in We also showed that the endogenous copy "", which is activated in the presence of bacterial stress, is negatively regulated by both DNA methylation and polycomb-mediated silencing, a mode of repression typically found at protein-coding and microRNA genes. Interestingly, an -derived soloLTR is located upstream of the disease resistance gene and is devoid of DNA methylation and H3K27m3 marks.

C-terminal domains of a histone demethylase interact with a pair of transcription factors and mediate specific chromatin association.

JmjC domain containing protein 14 (JMJ14) is an H3K4-specific histone demethylase that plays important roles in RNA-mediated gene silencing and flowering time regulation in . However, how JMJ14 is recruited to its target genes remains unclear. Here, we show that the C-terminal FYRN and FYRC domains of JMJ14 are required for RNA silencing and flowering time regulation.

Interplay between active chromatin marks and RNA-directed DNA methylation in Arabidopsis thaliana.

DNA methylation is an epigenetic mark that is associated with transcriptional repression of transposable elements and protein-coding genes. Conversely, transcriptionally active regulatory regions are strongly correlated with histone 3 lysine 4 di- and trimethylation (H3K4m2/m3). We previously showed that Arabidopsis thaliana plants with mutations in the H3K4m2/m3 demethylase JUMONJI 14 (JMJ14) exhibit a mild reduction in RNA-directed DNA methylation (RdDM) that is associated with an increase in H3K4m2/m3 levels.

Loss of the DNA methyltransferase MET1 Induces H3K9 hypermethylation at PcG target genes and redistribution of H3K27 trimethylation to transposons in Arabidopsis thaliana.

Dimethylation of histone H3 lysine 9 (H3K9m2) and trimethylation of histone H3 lysine 27 (H3K27m3) are two hallmarks of transcriptional repression in many organisms. In Arabidopsis thaliana, H3K27m3 is targeted by Polycomb Group (PcG) proteins and is associated with silent protein-coding genes, while H3K9m2 is correlated with DNA methylation and is associated with transposons and repetitive sequences. Recently, ectopic genic DNA methylation in the CHG context (where H is any base except G) has been observed in globally DNA hypomethylated mutants such as met1, but neither the nature of the hypermethylated loci nor the biological significance of this epigenetic phenomenon have been investigated.

The de novo cytosine methyltransferase DRM2 requires intact UBA domains and a catalytically mutated paralog DRM3 during RNA-directed DNA methylation in Arabidopsis thaliana.

Eukaryotic DNA cytosine methylation can be used to transcriptionally silence repetitive sequences, including transposons and retroviruses. This silencing is stable between cell generations as cytosine methylation is maintained epigenetically through DNA replication. The Arabidopsis thaliana Dnmt3 cytosine methyltransferase ortholog DOMAINS rearranged methyltransferase2 (DRM2) is required for establishment of small interfering RNA (siRNA) directed DNA methylation.

Involvement of a Jumonji-C domain-containing histone demethylase in DRM2-mediated maintenance of DNA methylation.

Histone demethylases-both lysine-specific demethylase 1 (LSD1) and Jumonji-C (JmjC) domain-containing proteins-are broadly implicated in the regulation of chromatin-dependent processes. In Arabidopsis thaliana, histone marks directly affect DNA methylation, and mutations in LSD1 homologues show reduced DNA methylation at some loci. We screened transfer DNA mutations in genes encoding JmjC domains for defects in DNA methylation.

Hierarchical action and inhibition of plant Dicer-like proteins in antiviral defense.

The mechanisms underlying induction and suppression of RNA silencing in the ongoing plant-virus arms race are poorly understood. We show here that virus-derived small RNAs produced by Arabidopsis Dicer-like 4 (DCL4) program an effector complex conferring antiviral immunity. Inhibition of DCL4 by a viral-encoded suppressor revealed the subordinate antiviral activity of DCL2.