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Post‐translational modification of histones and DNA methylation are important components of chromatin‐level control of genome activity in eukaryotes. However, principles governing the combinatorial association of chromatin marks along the genome remain poorly understood. Here, we have generated epigenomic maps for eight histone modifications (H3K4me2 and 3, H3K27me1 and 2, H3K36me3, H3K56ac, H4K20me1 and H2Bub) in the model plant Arabidopsis and we have combined these maps with others, produced under identical conditions, for H3K9me2, H3K9me3, H3K27me3 and DNA methylation. Integrative analysis indicates that these 12 chromatin marks, which collectively cover ∼90% of the genome, are present at any given position in a very limited number of combinations. Moreover, we show that the distribution of the 12 marks along the genomic sequence defines four main chromatin states, which preferentially index active genes, repressed genes, silent repeat elements and intergenic regions. Given the compact nature of the Arabidopsis genome, these four indexing states typically translate into short chromatin domains interspersed with each other. This first combinatorial view of the Arabidopsis epigenome points to simple principles of organization as in metazoans and provides a framework for further studies of chromatin‐based regulatory mechanisms in plants. This first comprehensive view of the Arabidopsis epigenome reveals that it is organized into four main chromatin types based on the integrative mapping of a broad set of 11 histone marks and DNA methylation in seedlings.

Histone deacetylases have central functions in regulating stress defenses and development in plants. However, the knowledge about the deacetylase functions is largely limited to histones, although these enzymes were found in diverse subcellular compartments. In this study, we determined the proteome‐wide signatures of the RPD3/HDA1 class of histone deacetylases in Arabidopsis . Relative quantification of the changes in the lysine acetylation levels was determined on a proteome‐wide scale after treatment of Arabidopsis leaves with deacetylase inhibitors apicidin and trichostatin A. We identified 91 new acetylated candidate proteins other than histones, which are potential substrates of the RPD3/HDA1‐like histone deacetylases in Arabidopsis , of which at least 30 of these proteins function in nucleic acid binding. Furthermore, our analysis revealed that histone deacetylase 14 (HDA14) is the first organellar‐localized RPD3/HDA1 class protein found to reside in the chloroplasts and that the majority of its protein targets have functions in photosynthesis. Finally, the analysis of HDA14 loss‐of‐function mutants revealed that the activation state of RuBisCO is controlled by lysine acetylation of RuBisCO activase under low‐light conditions. Synopsis A comprehensive lysine acetylome profiling identifies new potential substrate proteins of the Arabidopsis RPD3/HDA1‐KDACs with various subcellular localizations. HDA14 is identified as the first RPD3/HDA1‐KDAC, which is active in organelles. 2,152 lysine acetylation sites are identified on 1,022 Arabidopsis protein groups. Analyses with deacetylase inhibitors identify potential target sites of RPD3/HDA1 class‐KDACs of Arabidopsis . HDA14 is found to be active in Arabidopsis chloroplasts and RuBisCo activase (RCA) Kac‐438 is identified as one of the potential HDA14 substrates. Lysine acetylation on RCA‐K438 decreases the enzyme's ADP‐sensitivity, which is important for RCA inhibition under low‐light conditions. Graphical Abstract A comprehensive lysine acetylome profiling identifies new potential substrate proteins of the Arabidopsis RPD3/HDA1‐KDACs with various subcellular localizations. HDA14 is identified as the first RPD3/HDA1‐KDAC, which is active in organelles.

Priming of defence genes for amplified response to secondary stress can be induced by application of the plant hormone salicylic acid or its synthetic analogue acibenzolar S ‐methyl. In this study, we show that treatment with acibenzolar S ‐methyl or pathogen infection of distal leaves induce chromatin modifications on defence gene promoters that are normally found on active genes, although the genes remain inactive. This is associated with an amplified gene response on challenge exposure to stress. Mutant analyses reveal a tight correlation between histone modification patterns and gene priming. The data suggest a histone memory for information storage in the plant stress response. Plants can acquire systemic resistance to stress or infection after a first localized exposure. The paper provides evidence that histone modifications provide a memory that sensitizes defense genes for stronger responses.

Protein acetylation is a highly frequent protein modification. However, comparatively little is known about its enzymatic machinery. N‐α‐acetylation (NTA) and ε‐lysine acetylation (KA) are known to be catalyzed by distinct families of enzymes (NATs and KATs, respectively), although the possibility that the same GCN5‐related N ‐acetyltransferase (GNAT) can perform both functions has been debated. Here, we discovered a new family of plastid‐localized GNATs, which possess a dual specificity. All characterized GNAT family members display a number of unique features. Quantitative mass spectrometry analyses revealed that these enzymes exhibit both distinct KA and relaxed NTA specificities. Furthermore, inactivation of GNAT2 leads to significant NTA or KA decreases of several plastid proteins, while proteins of other compartments were unaffected. The data indicate that these enzymes have specific protein targets and likely display partly redundant selectivity, increasing the robustness of the acetylation process in vivo . In summary, this study revealed a new layer of complexity in the machinery controlling this prevalent modification and suggests that other eukaryotic GNATs may also possess these previously underappreciated broader enzymatic activities. Synopsis A novel protein acetyltransferase family localized or associated to plant plastids is identified and characterised. These GCN5‐related N ‐acetyltransferases (GNATs) have unique amino acid sequence characteristics and unambiguously possess dual N ‐α‐ and ε‐lysine acetylation activities. An in silico search for putative plastidial N‐terminal and lysine acetyltransferases reveals 10 putative GNAT candidates, showing unique features both at the level of the conserved motifs and key residues. Localization to chloroplasts is confirmed for seven of them, while another one is either associated to chloroplasts or localized within the nucleus. All plastid‐associated GNATs display distinct lysine acetyltransferase and relaxed N‐ terminal acetyltransferase substrate specificities. Inactivation of GNAT2, the plastid GNAT involved in photosynthetic state transitions, results in NTA decreases confined to chloroplast proteins, next to the known decreases on photosynthetic KA target proteins. Graphical Abstract A novel protein acetyltransferase family localized or associated to plant plastids is identified and characterised. These GCN5‐related N ‐acetyltransferases (GNATs) have unique amino acid sequence characteristics and unambiguously possess dual N ‐α‐ and ε‐lysine acetylation activities.

Protein ubiquitylation is a post‐translational modification that controls all aspects of eukaryotic cell functionality, and its defective regulation is manifested in various human diseases. The ubiquitylation process requires a set of enzymes, of which the ubiquitin ligases (E3s) are the substrate recognition components. Modular CULLIN‐RING ubiquitin ligases (CRLs) are the most prevalent class of E3s, comprising hundreds of distinct CRL complexes with the potential to recruit as many and even more protein substrates. Best understood at both structural and functional levels are CRL1 or SCF (SKP1/CUL1/F‐box protein) complexes, representing the founding member of this class of multimeric E3s. Another CRL subfamily, called CRL3, is composed of the molecular scaffold CULLIN3 and the RING protein RBX1, in combination with one of numerous BTB domain proteins acting as substrate adaptors. Recent work has firmly established CRL3s as major regulators of different cellular and developmental processes as well as stress responses in both metazoans and higher plants. In humans, functional alterations of CRL3s have been associated with various pathologies, including metabolic disorders, muscle, and nerve degeneration, as well as cancer. In this review, we summarize recent discoveries on the function of CRL3s in both metazoans and plants, and discuss their mode of regulation and specificities. Pascal Genschik and colleagues review the fascinating array of signalling, cell cycle, and stress response roles that Cullin3/Rbx1/BTB‐protein ubiquitin ligases play in both metazoan organisms and higher plants.

In most eukaryotes, double‐stranded RNA is processed into small RNAs that are potent regulators of gene expression. This gene silencing process is known as RNA silencing or RNA interference (RNAi) and, in plants and nematodes, it is associated with the production of a mobile signal that can travel from cell‐to‐cell and over long distances. The sequence‐specific nature of systemic RNA silencing indicates that a nucleic acid is a component of the signalling complex. Recent work has shed light on the mobile RNA species, the genes involved in the production and transport of the signal. This review discusses the advances in systemic RNAi and presents the current challenges and questions in this rapidly evolving field. Local small RNA generation can silence gene expression over long distances. Recent progress in our understanding of how these mobile RNA species are transported between cells is described.

Circadian clocks synchronise biological processes with the day/night cycle, using molecular mechanisms that include interlocked, transcriptional feedback loops. Recent experiments identified the evening complex (EC) as a repressor that can be essential for gene expression rhythms in plants. Integrating the EC components in this role significantly alters our mechanistic, mathematical model of the clock gene circuit. Negative autoregulation of the EC genes constitutes the clock's evening loop, replacing the hypothetical component Y . The EC explains our earlier conjecture that the morning gene PSEUDO‐RESPONSE REGULATOR 9 was repressed by an evening gene, previously identified with TIMING OF CAB EXPRESSION1 ( TOC1 ). Our computational analysis suggests that TOC1 is a repressor of the morning genes LATE ELONGATED HYPOCOTYL and CIRCADIAN CLOCK ASSOCIATED1 rather than an activator as first conceived. This removes the necessity for the unknown component X (or TOC1mod) from previous clock models. As well as matching timeseries and phase‐response data, the model provides a new conceptual framework for the plant clock that includes a three‐component repressilator circuit in its complex structure. Recent findings are incorporated into a new mathematical model of the plant circadian clock, revealing a complex circuit structure comprised of multiple negative feedback loops, and predicting a repressive role for a key regulator, TOC1, which the authors confirm experimentally. Synopsis Recent findings are incorporated into a new mathematical model of the plant circadian clock, revealing a complex circuit structure comprised of multiple negative feedback loops, and predicting a repressive role for a key regulator, TOC1, which the authors confirm experimentally. The feedback structure of the plant clock's evening loop was reconstructed based on multiple data, and is now represented by the evening complex (ELF3‐ELF4‐LUX), which represses transcription from the ELF4 and LUX promoters. Computational analysis of timeseries data from mutant plants predicts that TOC1 is a repressor of the key morning genes LHY and CCA1 , not an activator. Analysis of LHY and CCA1 expression in TOC1 gain‐ and loss‐of‐function plants confirms this prediction. Light induction of LHY and CCA1 expression is predicted to determine the clock's response to brief light pulses, matching the observed phase‐response curve. The evening complex controls LHY and CCA1 expression by a double‐negative connection, rather than direct activation, forming part of a three‐component repressilator circuit, which is itself only part of the more complex circuit of the clock system.

Polycomb group (PcG) proteins form essential epigenetic memory systems for controlling gene expression during development in plants and animals. However, the mechanism of plant PcG protein functions remains poorly understood. Here, we probed the composition and function of plant Polycomb repressive complex 2 (PRC2). This work established the fact that all known plant PRC2 complexes contain MSI1, a homologue of Drosophila p55. While p55 is not essential for the in vitro enzymatic activity of PRC2, plant MSI1 was required for the functions of the EMBRYONIC FLOWER and the VERNALIZATION PRC2 complexes including trimethylation of histone H3 Lys27 (H3K27) at the target chromatin, as well as gene repression and establishment of competence to flower. We found that MSI1 serves to link PRC2 to LIKE HETEROCHROMATIN PROTEIN 1 (LHP1), a protein that binds H3K27me3 in vitro and in vivo and is required for a functional plant PcG system. The LHP1–MSI1 interaction forms a positive feedback loop to recruit PRC2 to chromatin that carries H3K27me3. Consequently, this can provide a mechanism for the faithful inheritance of local epigenetic information through replication. The Arabidopsis protein MSI1 is an essential component of the Polycomb repressive complex 2, PRC2, and links PRC2 to the polycomb group protein LHP1 to promote the inheritance of H3K27me3 during DNA replication.

The distribution of the phytohormone auxin regulates many aspects of plant development including growth response to gravity. Gravitropic root curvature involves coordinated and asymmetric cell elongation between the lower and upper side of the root, mediated by differential cellular auxin levels. The asymmetry in the auxin distribution is established and maintained by a spatio‐temporal regulation of the PIN‐FORMED (PIN) auxin transporter activity. We provide novel insights into the complex regulation of PIN abundance and activity during root gravitropism. We show that PIN2 turnover is differentially regulated on the upper and lower side of gravistimulated roots by distinct but partially overlapping auxin feedback mechanisms. In addition to regulating transcription and clathrin‐mediated internalization, auxin also controls PIN abundance at the plasma membrane by promoting their vacuolar targeting and degradation. This effect of elevated auxin levels requires the activity of SKP‐Cullin‐F‐box TIR1/AFB (SCF TIR1/AFB )‐dependent pathway. Importantly, also suboptimal auxin levels mediate PIN degradation utilizing the same signalling pathway. These feedback mechanisms are functionally important during gravitropic response and ensure fine‐tuning of auxin fluxes for maintaining as well as terminating asymmetric growth. A gradient of the phytohormone Auxin regulates root gravitropism. Too low or high auxin promotes the vacuolar targeting and degradation of the auxin transporter PIN2 via the SCF TIR1/AFB pathway.

Individual plant cells possess a genetic network, the circadian clock, that times internal processes to the day‐night cycle. Mathematical models of the clock are typically either “whole‐plant” that ignore tissue or cell type‐specific clock behavior, or “phase‐only” that do not include molecular components. To address the complex spatial coordination observed in experiments, here we implemented a clock network model on a template of a seedling. In our model, the sensitivity to light varies across the plant, and cells communicate their timing via local or long‐distance sharing of clock components, causing their rhythms to couple. We found that both varied light sensitivity and long‐distance coupling could generate period differences between organs, while local coupling was required to generate the spatial waves of clock gene expression observed experimentally. We then examined our model under noisy light‐dark cycles and found that local coupling minimized timing errors caused by the noise while allowing each plant region to maintain a different clock phase. Thus, local sensitivity to environmental inputs combined with local coupling enables flexible yet robust circadian timing. Synopsis A spatial molecular model is developed to understand the design principles of plant clock coordination. The model shows that local cell‐to‐cell coupling combined with varied environmental signaling allows robust, yet flexible, timing. A spatial molecular model of the plant circadian clock provides a framework for understanding timing across cellular, organ, and whole‐plant scales. Varied sensing of the environment by cells can explain the period differences observed within plants in experiments. Local cell‐to‐cell communication drives spatial waves of gene expression whereas long‐distance communication can create period differences between organs. Under noisy light‐dark conditions, local cell‐to‐cell communication improves timing accuracy yet allows regional phase differences to persist. Graphical Abstract A spatial molecular model is developed to understand the design principles of plant clock coordination. The model shows that local cell‐to‐cell coupling combined with varied environmental signaling allows robust, yet flexible, timing.