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Transposable elements (TEs) are robustly silenced by multiple epigenetic marks, but dynamics of crosstalk among these marks remains enigmatic. In Arabidopsis, TEs are silenced by cytosine methylation in both CpG and non-CpG contexts (mCG and mCH) and histone H3 lysine 9 methylation (H3K9me). While mCH and H3K9me are mutually dependent for their maintenance, mCG and mCH/H3K9me are independently maintained. Here, we show that establishment, rather than maintenance, of mCH depends on mCG, accounting for the synergistic colocalization of these silent marks in TEs. When mCG is lost, establishment of mCH is abolished in TEs. mCG also guides mCH in active genes, though the resulting mCH/H3K9me is removed thereafter. Unexpectedly, targeting efficiency of mCH depends on relative, rather than absolute, levels of mCG within the genome, suggesting underlying global negative controls. We propose that local positive feedback in heterochromatin dynamics, together with global negative feedback, drive robust and balanced DNA methylome patterning. In plant genomes, both mCG and H3K9me2/mCH are important for silencing transposable elements (TEs). Here, the authors show that establishment of mCH is abolished in both TE and active genes when mCG is lost and targeting efficiency of mCH depends on relative levels of mCG within the genome.

DNA methylation is important for silencing transposable elements (TEs) in diverse eukaryotes, including plants. In plant genomes, TEs are silenced by methylation of histone H3 lysine 9 (H3K9) and cytosines in both CG and non-CG contexts. The role of RNA interference (RNAi) in establishing TE-specific silent marks has been extensively studied, but the importance of RNAi-independent pathways remains largely unexplored. Here, we directly investigated transgenerational de novo DNA methylation of TEs after the loss of silent marks. Our analyses uncovered potent and precise RNAi-independent pathways for recovering non-CG methylation and H3K9 methylation in most TE genes (that is, coding regions within TEs). Characterization of a subset of TE genes without the recovery revealed the effects of H3K9 demethylation, replacement of histone H2A variants and their interaction with CG methylation, together with feedback from transcription. These chromatin components are conserved among eukaryotes and may contribute to chromatin reprogramming in a conserved manner. A chromatin-based, RNAi-independent mechanism is uncovered that reestablishes DNA methylation on heterochromatin transposable elements and is impacted by multiple factors, including CG methylation, H3K9 demethylation and replacement of H2A variants.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.

DNA methylation is essential for genomic function and transposable element silencing. In plants, DNA methylation occurs in CG, CHG, and CHH contexts (where H = A, T, or C), with the maintenance of CG methylation mediated by the DNA methyltransferase MET1. The molecular mechanism by which MET1 maintains CG methylation, however, remains unclear. Here, we report cryogenic electron microscopy structures of Arabidopsis thaliana MET1. We find that the methyltransferase domain of MET1 specifically methylates hemimethylated DNA in vitro. The structure of MET1 bound to hemimethylated DNA reveals the activation mechanism of MET1 resembling that of mammalian DNMT1. Curiously, the structure of apo-MET1 shows an autoinhibitory state distinct from that of DNMT1, where the RFTS2 domain and the connecting linker inhibit DNA binding. The autoinhibition of MET1 is relieved upon binding of a potential activator, ubiquitinated histone H3. Taken together, our structural analysis demonstrates both conserved and distinct molecular mechanisms regulating CG maintenance methylation in plant and animal DNA methyltransferases. DNA methyltransferase MET1 maintains CG methylation in plants. Kikuchi determined the cryo-EM structure of Arabidopsis MET1, revealing autoinhibition and activation mechanisms, with conserved and plant-specific features distinct from mammalian DNMT1.

A Correction to this paper has been published: https://doi.org/10.1038/s41477-020-00839-0.

Jasmonate (JA) and ethylene (ET) are two major plant hormones that synergistically regulate plant development and tolerance to necrotrophic fungi. Both JA and ET induce the expression of several pathogenesis-related genes, while blocking either signaling pathway abolishes the induction of these genes by JA and ET alone or in combination. However, the molecular basis of JA/ET coaction and signaling interdependency is largely unknown. Here, we report that two Arabidopsis ET-stabilized transcription factors (EIN3 and EIL1) integrate ET and JA signaling in the regulation of gene expression, root development, and necrotrophic pathogen defense. Further studies reveal that JA enhances the transcriptional activity of EIN3/EIL1 by removal of JA-Zim domain (JAZ) proteins, which physically interact with and repress EIN3/EIL1. In addition, we find that JAZ proteins recruit an RPD3-type histone deacetylase (HDA6) as a corepressor that modulates histone acetylation, represses EIN3/EIL1-dependent transcription, and inhibits JA signaling. Our studies identify EIN3/EIL1 as a key integration node whose activation requires both JA and ET signaling, and illustrate transcriptional derepression as a common mechanism to integrate diverse signaling pathways in the regulation of plant development and defense.

Among hymenopteran insects, aculeate species such as bees, ants, and wasps have enlarged and morphologically elaborate mushroom bodies (MBs), a higher-order brain center in the insect, implying their relationship with the advanced behavioral traits of aculeate species. The molecular bases leading to the acquisition of complicated MB functions, however, remains unclear. We previously reported the constitutive and MB-preferential expression of an ecdysone-signaling related transcription factor, Mblk-1/E93, in the honey bee brain. Here, we searched for target genes of Mblk-1 in the worker honey bee MBs using chromatin immunoprecipitation sequence analyses and found that Mblk-1 targets several genes involved in synaptic plasticity, learning, and memory abilities. We also demonstrated that Mblk-1 expression is self-regulated via Mblk-1-binding sites, which are located upstream of Mblk-1 . Furthermore, we showed that the number of the Mblk-1-binding motif located upstream of Mblk-1 homologs increased associated with evolution of hymenopteran insects. Our findings suggest that Mblk-1 , which has been focused on as a developmental gene transiently induced by ecdysone, has acquired a novel expression pattern to play a role in synaptic plasticity in honey bee MBs, raising a possibility that molecular evolution of Mblk-1 may have partly contributed to the elaboration of MB function in insects.

Water deficit caused by global climate changes seriously endangers the survival of organisms and crop productivity, and increases environmental deterioration 1 , 2 . Plants' resistance to drought involves global reprogramming of transcription, cellular metabolism, hormone signalling and chromatin modification 3 – 8 . However, how these regulatory responses are coordinated via the various pathways, and the underlying mechanisms, are largely unknown. Herein, we report an essential drought-responsive network in which plants trigger a dynamic metabolic flux conversion from glycolysis into acetate synthesis to stimulate the jasmonate (JA) signalling pathway to confer drought tolerance. In Arabidopsis , the ON/OFF switching of this whole network is directly dependent on histone deacetylase HDA6. In addition, exogenous acetic acid promotes de novo JA synthesis and enrichment of histone H4 acetylation, which influences the priming of the JA signalling pathway for plant drought tolerance. This novel acetate function is evolutionarily conserved as a survival strategy against environmental changes in plants. Furthermore, the external application of acetic acid successfully enhanced the drought tolerance in Arabidopsis , rapeseed, maize, rice and wheat plants. Our findings highlight a radically new survival strategy that exploits an epigenetic switch of metabolic flux conversion and hormone signalling by which plants adapt to drought. In response to drought, acetate accumulates endogenously through redirection of metabolic fluxes, and stimulates jasmonate pathways controlling Arabidopsis drought tolerance. Application of exogenous acetic acid alone increases drought tolerance of major crops such as maize, wheat and rice.

Exposure to short-term cold stress delays flowering by activating the floral repressor FLOWERING LOCUS C (FLC) in Arabidopsis thaliana. The cold signaling attenuator HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE1 (HOS1) negatively regulates cold responses. Notably, HOS1-deficient mutants exhibit early flowering, and FLC expression is suppressed in the mutants. However, it remains unknown how HOS1 regulates FLC expression. Here, we show that HOS1 induces FLC expression by antagonizing the actions of FVE and its interacting partner histone deacetylase 6 (HDA6) under short-term cold stress. HOS1 binds to FLC chromatin in an FVE-dependent manner, and FVE is essential for the HOS1-mediated activation of FLC transcription. HOS1 also interacts with HDA6 and inhibits the binding of HDA6 to FLC chromatin. Intermittent cold treatments induce FLC expression by activating HOS1, which attenuates the activity of HDA6 in silencing FLC chromatin, and the effects of intermittent cold are diminished in hos1 and fve mutants. These observations indicate that HOS1 acts as a chromatin remodeling factor for FLC regulation under short-term cold stress.

Acetic acid is a simple and universal compound found in various organisms. Recently, acetic acid was found to play an essential role in conferring tolerance to water deficit stress in plants. This novel mechanism of drought stress tolerance mediated by acetic acid via networks involving phytohormones, genes, and chromatin regulation has great potential for solving the global food crisis and preventing desertification caused by global warming. We highlight the functions of acetic acid in conferring tolerance to water deficit stress.