Chromatin-based epigenetic information plays an important role in developmental gene regulation, in response to environment, and in natural variation of gene expression levels. Histone H3 lysine 4 ...di/trimethylation (H3K4me2/3) is abundant in euchromatin and is generally associated with transcriptional activation. Strikingly, however, enzymes catalyzing H3K4me2/3 remain poorly characterized in crops so far.
Here, we investigated the function of the rice SET DOMAIN GROUP 701 (SDG701) gene by molecular and biochemical characterization of the gene product, and by studying effects of its loss or gain of function on plant growth and development.
We demonstrated that SDG701 encodes a methytransferase specifically catalyzing H3K4 methylation. Overexpression and knockdown experiments showed that SDG701 is crucial for proper sporophytic plant development as well as for gametophytic transmission that directly impacts rice grain production. In-depth analysis of plant flowering time revealed that SDG701 promotes rice flowering under either long-day or short-day photoperiods. Consistently, the SDG701 protein was found to bind chromatin to promote H3K4me3 and to enhance expression of the rice Hd3a and RFT1 florigens.
Collectively, our results establish SDG701 as a major rice H3K4-specific methyltransferase and provide important insights into function of H3K4me3 deposition in transcription activation of florigens in promoting plant flowering.
For shade‐intolerant plants, changes in light quality through competition from neighbors trigger shade avoidance syndrome (SAS): a series of morphological and physiological adaptations that are ...ultimately detrimental to plant health and crop yield. Phytochrome‐interacting factor 7 (PIF7) is a major transcriptional regulator of SAS in Arabidopsis; however, how it regulates gene expression is not fully understood. Here, we show that PIF7 directly interacts with the histone chaperone anti‐silencing factor 1 (ASF1). The ASF1‐deprived asf1ab mutant showed defective shade‐induced hypocotyl elongation. Histone regulator homolog A (HIRA), which mediates deposition of the H3.3 variant into chromatin, is also involved in SAS. RNA/ChIP‐sequencing analyses identified the role of ASF1 in the direct regulation of a subset of PIF7 target genes. Furthermore, shade‐elicited gene activation is accompanied by H3.3 enrichment, which is mediated by the PIF7‐ASF1‐HIRA regulatory module. Collectively, our data reveal that PIF7 recruits ASF1‐HIRA to increase H3.3 incorporation into chromatin to promote gene transcription, thus enabling plants to effectively respond to environmental shade.
Synopsis
In Arabidopsis, the transcription factor PIF7 plays a dominant role in ameliorating the impact shade conditions have on fitness. In this study, a PIF7‐ASF1‐HIRA regulatory module is found to mediate H3.3 incorporation at a subset of shade‐responsive loci, leading to shade‐induced gene expression and morphological adaptation.
PIF7 recruits the ASF1‐HIRA complex under shade conditions
ASF1 and HIRA positively regulate shade‐induced hypocotyl elongation and define changes in gene expression
Shade increases ASF1 and H3.3 enrichment in the chromatin of a subset of PIF7 target genes
A PIF7‐ASF1‐HIRA regulatory module is responsible for H3.3 incorporation in the shade
When an Arabidopsis plant grows in shade, the transcription factor PIF7 triggers the adaptive growth response by guiding H3.3 deposition via the histone chaperone ASF1.
Summary
Chromatin modifications play important roles in plant adaptation to abiotic stresses, but the precise function of histone H3 lysine 36 (H3K36) methylation in drought tolerance remains poorly ...evaluated.
Here, we report that SDG708, a specific H3K36 methyltransferase, functions as a positive regulator of drought tolerance in rice. SDG708 promoted abscisic acid (ABA) biosynthesis by directly targeting and activating the crucial ABA biosynthesis genes NINE‐CIS‐EPOXYCAROTENOID DIOXYGENASE 3 (OsNCED3) and NINE‐CIS‐EPOXYCAROTENOID DIOXYGENASE 5 (OsNCED5).
Additionally, SDG708 induced hydrogen peroxide accumulation in the guard cells and promoted stomatal closure to reduce water loss. Overexpression of SDG708 concomitantly enhanced rice drought tolerance and increased grain yield under normal and drought stress conditions.
Thus, SDG708 is potentially useful as an epigenetic regulator in breeding for grain yield improvement.
As a key epigenetic modification, the methylation of histone H3 lysine 36 (H3K36) modulates chromatin structure and is involved in diverse biological processes. To better understand the language of ...H3K36 methylation in rice (Oryza sativa), we chose potential histone methylation enzymes for functional exploration. In particular, we characterized rice SET DOMAIN GROUP 708 (SDG708) as an H3K36‐specific methyltransferase possessing the ability to deposit up to three methyl groups on H3K36. Compared with the wild‐type, SDG708‐knockdown rice mutants displayed a late‐flowering phenotype under both long‐day and short‐day conditions because of the down‐regulation of the key flowering regulatory genes Heading date 3a (Hd3a), RICE FLOWERING LOCUS T1 (RFT1), and Early heading date 1 (Ehd1). Chromatin immunoprecipitation experiments indicated that H3K36me1, H3K36me2, and H3K36me3 levels were reduced at these loci in SDG708‐deficient plants. More importantly, SDG708 was able to directly target and effect H3K36 methylation on specific flowering genes. In fact, knockdown of SDG708 led to misexpression of a set of functional genes and a genome‐wide decrease in H3K36me1/2/3 levels during the early growth stages of rice. SDG708 is a methyltransferase that catalyses genome‐wide deposition of all three methyl groups on H3K36 and is involved in many biological processes in addition to flowering promotion.
Previous studies in Arabidopsis thaliana have identified several histone methylation enzymes, including ARABIDOPSIS TRITHORAX1 (ATX1)/SET DOMAIN GROUP 27 (SDG27), ATX2/SDG30, LSD1-LIKE1 (LDL1), LDL2, ...SDG8, SDG25, and CURLY LEAF (CLF)/SDG1, as regulators of the key flowering repressor FLOWERING LOCUS C (FLC) and the florigen FLOWERING LOCUS T (FT). However, the combinatorial functions of these enzymes remain largely uninvestigated.
Here, we investigated functional interplays of different histone methylation enzymes by studying higher order combinations of their corresponding gene mutants.
We showed that H3K4me2/me3 and H3K36me3 depositions occur largely independently and that SDG8-mediated H3K36me3 overrides ATX1/ATX2-mediated H3K4me2/me3 or LDL1/LDL2-mediated H3K4 demethylation in regulating FLC expression and flowering time. By contrast, a reciprocal inhibition was observed between deposition of the active mark H3K4me2/me3 and/or H3K36me3 and deposition of the repressive mark H3K27me3 at both FLC and FT chromatin; and the double mutants sdg8 clf and sdg25 clf displayed enhanced early-flowering phenotypes of the respective single mutants.
Collectively, our results provide important insights into the interactions of different types of histone methylation and enzymes in the regulation of FLC and FT expression in flowering time control.
Day-length changes represent an important cue for modulating flowering time. In Arabidopsis, the expression of the florigen gene FLOWERING LOCUS T (FT) exhibits a 24-h circadian rhythm under long-day ...(LD) conditions. Here we focus on the chromatin-based mechanism regarding the control of FT expression.
We conducted co-immunoprecipitation assays along with LC-MS/MS analysis and identified HD2C histone deacetylase as the binding protein of the H3K4/H3K36 methylation reader MRG2.
HD2C and MRG1/2 regulate flowering time under LD conditions, but not under short-day conditions. Moreover, HD2C functions as an effective deacetylase in planta, mainly targeting H3K9ac, H3K23ac and H3K27ac. At dusk, HD2C is recruited to FT to deacetylate histones and repress transcription in an MRG1/2-dependent manner. More importantly, HD2C competes with CO for the binding of MRG2, and the accumulation of HD2C at the FT locus occurs at the end of the day.
Our findings not only reveal a histone deacetylation mechanism contributing to prevent FT overexpression and precocious flowering, but also support the model in which the histone methylation readers MRG1/2 provide a platform on chromatin for connecting regulatory factors involved in activating FT expression in response to daylight and decreasing FT expression around dusk under long days.
Most plant organs develop postembryonically from stem cells in the shoot and root meristems 1. In Arabidopsis, Class I KNOTTED-like homeobox (KNOX) transcription factors are specifically expressed in ...shoot meristems and play a primary role in the maintenance of meristem function 2, 3. Although suppression of KNOX was shown to associate with histone H3K27-methylation 4, the molecular mechanism underlying this suppression is not well understood. Here, we provide genetic, molecular, and functional evidence that an Arabidopsis POLYCOMB REPRESSIVE COMPLEX1 (PRC1)-like complex acts in conjunction with PRC2 in KNOX suppression. We identified AtRING1a and AtRING1b as homologs of the animal PRC1 core component RING1. Loss-of-function mutant Atring1a−/−Atring1b−/− shows release of KNOX suppression and ectopic-meristem formation. AtRING1a and AtRING1b proteins are localized in the nucleus. AtRING1a binds to itself and to AtRING1b, to CURLY LEAF (CLF), a PRC2 core component catalyzing H3K27-methylation 4, 5, and to LIKE HETEROCHROMATIN PROTEIN1 (LHP1), a chromodomain protein binding trimethyl-H3K27 6–8. We further show that clf−/− and lhp1−/− enhance Atring1a−/−Atring1b−/− in release of KNOX suppression and mutant phenotypes. We propose a model in which AtRING1a, AtRING1b, and LHP1 form a PRC1-like complex, which binds trimethyl-H3K27 marked by the CLF-containing PRC2, resulting in transcriptional suppression of KNOX.
As sessile organisms, plants are constantly exposed to changing environments frequently under diverse stresses. Invasion by pathogens, including virus, bacterial and fungal infections, can severely ...impede plant growth and development, causing important yield loss and thus challenging food/feed security worldwide. During evolution, plants have adapted complex systems, including coordinated global gene expression networks, to defend against pathogen attacks. In recent years, growing evidences indicate that pathogen infections can trigger local and global epigenetic changes that reprogram the transcription of plant defense genes, which in turn helps plants to fight against pathogens. Here, we summarize up plant defense pathways and epigenetic mechanisms and we review in depth current knowledge’s about histone modifications and chromatin-remodeling factors found in the epigenetic regulation of plant response to biotic stresses. It is anticipated that epigenetic mechanisms may be explorable in the design of tools to generate stress-resistant plant varieties.
Summary
The histone variant H2A.Z plays key functions in transcription and genome stability in all eukaryotes ranging from yeast to human, but the molecular mechanisms by which H2A.Z is incorporated ...into chromatin remain largely obscure.
Here, we characterized the two homologs of yeast Chaperone for H2A.Z‐H2B (Chz1) in Arabidopsis thaliana, AtChz1A and AtChz1B. AtChz1A/AtChz1B were verified to bind to H2A.Z‐H2B and facilitate nucleosome assembly in vitro. Simultaneous knockdown of AtChz1A and AtChz1B, which exhibit redundant functions, led to a genome‐wide reduction in H2A.Z and phenotypes similar to those of the H2A.Z‐deficient mutant hta9‐1hta11‐2, including early flowering and abnormal flower morphologies.
Interestingly, AtChz1A was found to physically interact with ACTIN‐RELATED PROTEIN 6 (ARP6), an evolutionarily conserved subunit of the SWR1 chromatin‐remodeling complex. Genetic interaction analyses showed that atchz1a‐1atchz1b‐1 was hypostatic to arp6‐1. Consistently, genome‐wide profiling analyses revealed partially overlapping genes and fewer misregulated genes and H2A.Z‐reduced chromatin regions in atchz1a‐1atchz1b‐1 compared with arp6‐1.
Together, our results demonstrate that AtChz1A and AtChz1B act as histone chaperones to assist the deposition of H2A.Z into chromatin via interacting with SWR1, thereby playing critical roles in the transcription of genes involved in flowering and many other processes.
The electrochemical reduction of carbon dioxide (CO2) to ethylene creates a carbon‐neutral approach to converting carbon dioxide into intermittent renewable electricity. Exploring efficient ...electrocatalysts with potentially high ethylene selectivity is extremely desirable, but still challenging. In this report, a laboratory‐designed catalyst HKUST‐1@Cu2O/PTFE‐1 is prepared, in which the high specific surface area of the composites with improved CO2 adsorption and the abundance of active sites contribute to the increased electrocatalytic activity. Furthermore, the hydrophobic interface constructed by the hydrophobic material polytetrafluoroethylene (PTFE) effectively inhibits the occurrence of hydrogen evolution reactions, providing a significant improvement in the efficiency of CO2 electroreduction. The distinctive structures result in the remarkable hydrocarbon fuels generation with high Faraday efficiency (FE) of 67.41%, particularly for ethylene with FE of 46.08% (−1.0 V vs RHE). The superior performance of the catalyst is verified by DFT calculation with lower Gibbs free energy of the intermediate interactions with improved proton migration and selectivity to emerge the polycarbon（C2+） product. In this work, a promising and effective strategy is presented to configure MOF‐based materials with tailored hydrophobic interface, high adsorption selectivity and more exposed active sites for enhancing the efficiency of the electroreduction of CO2 to C2+ products with high added value.
Elaborate design of core–shell catalyst HKUST‐1@Cu2O/PTFE‐1 with hydrophobic interface exhibits outstanding electrocatalytic activities for hydrocarbon fuels with high Faraday efficiency of 67.41% in CO2 electroreduction, benefiting from the improved CO2 adsorption, the abundance of synergistic active sites and blocking the supply of protons and electrons to inhibit HER.
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