The complexity of PRC2 catalysts CLF and SWN in plants

2020 ◽  
Vol 48 (6) ◽  
pp. 2779-2789
Author(s):  
Jie Shu ◽  
Chen Chen ◽  
Chenlong Li ◽  
Yuhai Cui
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Molecular Mechanisms ◽  
Histone H3 ◽  
Catalytic Subunits ◽  
Trithorax Group ◽  
Polycomb Repressive Complex 2 ◽  
Plant Life ◽  
Plant Life Cycle ◽  
Curly Leaf

Polycomb repressive complex 2 (PRC2) is an evolutionally conserved multisubunit complex essential for the development of eukaryotes. In Arabidopsis thaliana (Arabidopsis), CURLY LEAF (CLF) and SWINGER (SWN) are PRC2 catalytic subunits that repress gene expression through trimethylating histone H3 at lysine 27 (H3K27me3). CLF and SWN function to safeguard the appropriate expression of key developmental regulators throughout the plant life cycle. Recent researches have advanced our knowledge of the biological roles and the regulation of the activity of CLF and SWN. In this review, we summarize these recent findings and highlight the redundant and differential roles of CLF and SWN in plant development. Further, we discuss the molecular mechanisms underlying CLF and SWN recruitment to specific genomic loci, as well as their interplays with Trithorax-group (TrxG) proteins in plants.

Current understanding of plant Polycomb group proteins and the repressive histone H3 Lysine 27 trimethylation

2020 ◽  
Vol 48 (4) ◽  
pp. 1697-1706
Author(s):  
Huijun Jiao ◽  
Yuanyuan Xie ◽  
Zicong Li
Keyword(s):  
Gene Expression ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Protein Complexes ◽  
Close Association ◽  
Histone H3 ◽  
Polycomb Group ◽  
Dynamic Regulation ◽  
Trithorax Group ◽  
Repressive Mark

Polycomb group (PcG) proteins are highly conserved chromatin-modifying complexes that implement gene silencing in higher eukaryotes. Thousands of genes and multiple developmental processes are regulated by PcG proteins. As the first chromatin modifier been identified in model plant Arabidopsis thaliana, the methyltransferase CURLY LEAF (CLF) and its catalyzed histone H3 Lysine 27 trimethylation (H3K27me3) have already become well-established paradigm in plant epigenetic study. Like in animals, PcG proteins mediate plant development and repress homeotic gene expression by antagonizing with trithorax group proteins. Recent researches have advanced our understanding on plant PcG proteins, including the plant-specific components of these well-conserved protein complexes, the close association with transcription factors and noncoding RNA for the spatial and temporal specificity, the dynamic regulation of the repressive mark H3K27me3 and the PcG-mediated chromatin conformation alterations in gene expression. In this review, we will summarize the molecular mechanisms of PcG-implemented gene repression and the relationship between H3K27me3 and another repressive mark histone H2A Lysine 121 mono-ubiquitination (H2A121ub) will also be discussed.

NUP98-MLL fusion in human acute myeloblastic leukemia

Blood ◽  
2010 ◽  
Vol 116 (13) ◽  
pp. 2332-2335 ◽  
Author(s):  
Sophie Kaltenbach ◽  
Gwendoline Soler ◽  
Carole Barin ◽  
Carine Gervais ◽  
Olivier A. Bernard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fusion Protein ◽  
Histone H3 ◽  
Cellular Transformation ◽  
Human Leukemia ◽  
Trithorax Group ◽  
Group Protein ◽  
Hoxa Genes ◽  
Hoxa Gene Expression ◽  
Methylation Activity

Abstract Posttranscriptional modifications of histones play important roles in the control of chromatin structure and transcription. H3K4 (histone H3 lysine 4) methylation by the SET domain of the trithorax-group protein MLL (mixed-lineage leukemia) is important for the control of homeobox (HOX) gene expression during development. MLL is tethered to the HOXA locus through interaction of its amino-terminus with menin. MLL fusion proteins associated with human leukemia contain the menin interaction peptide and frequently recruit H3K79 (histone H3 lysine 79) methylation activity. This allows sustained expression of HOXA genes important for cellular transformation. We have characterized a novel recurrent chromosomal aberration, inv(11)(p15q23), as an isolated chromosomal abnormality in 2 patients with acute myeloid leukemia. This aberration is predicted to result in the expression of an NUP98 (nucleoporin 98 kDa)–MLL fusion protein that is unable to interact with menin. As expected, low levels of HOXA gene expression were observed in the patients' samples. This fusion protein is predicted to participate in cellular transformation by activating MLL targets other than HOXA genes.

scholarly journals JAZF1-SUZ12 dysregulates PRC2 function and gene expression during cell differentiation

2021 ◽  
Author(s):  
Manuel Tavares ◽  
Garima Khandelwal ◽  
Joanne Mutter ◽  
Keijo Viiri ◽  
Manuel Beltran ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Differentiation ◽  
Target Genes ◽  
Histone H3 ◽  
Endometrial Stromal Sarcoma ◽  
Cell Types ◽  
Polycomb Repressive Complex 2 ◽  
Stromal Sarcoma ◽  
N Terminus ◽  
Undifferentiated Cells

Polycomb repressive complex 2 (PRC2) methylates histone H3 lysine 27 (H3K27me3) to maintain repression of genes specific for other cell types and is essential for cell differentiation. In endometrial stromal sarcoma, the PRC2 subunit SUZ12 is often fused with the NuA4/TIP60 subunit JAZF1. Here, we show that JAZF1-SUZ12 dysregulates PRC2 composition, recruitment, histone modification, gene expression and cell differentiation. The loss of the SUZ12 N-terminus in the fusion protein disrupted interaction with the PRC2 accessory factors JARID2, EPOP and PALI1 and prevented recruitment of PRC2 from RNA to chromatin. In undifferentiated cells, JAZF1-SUZ12 occupied PRC2 target genes but gained a JAZF1-like binding profile during cell differentiation. JAZF1-SUZ12 reduced H3K27me3 and increased H4Kac at PRC2 target genes, and this was associated with disruption in gene expression and cell differentiation programs. These results reveal the defects in chromatin regulation caused by JAZF1-SUZ12, which may underlie its role in oncogenesis.

scholarly journals Molecular mechanisms underlying phytochrome-controlled morphogenesis in plants

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Martina Legris ◽  
Yetkin Çaka Ince ◽  
Christian Fankhauser
Keyword(s):  
Conformational Changes ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Plant Life ◽  
Signaling Mechanisms ◽  
Open Questions ◽  
Whole Plant ◽  
Promoter Usage ◽  
Plant Life Cycle ◽  
Compare And Contrast

AbstractPhytochromes are bilin-binding photosensory receptors which control development over a broad range of environmental conditions and throughout the whole plant life cycle. Light-induced conformational changes enable phytochromes to interact with signaling partners, in particular transcription factors or proteins that regulate them, resulting in large-scale transcriptional reprograming. Phytochromes also regulate promoter usage, mRNA splicing and translation through less defined routes. In this review we summarize our current understanding of plant phytochrome signaling, emphasizing recent work performed in Arabidopsis. We compare and contrast phytochrome responses and signaling mechanisms among land plants and highlight open questions in phytochrome research.

scholarly journals Involvement of Histone Lysine Methylation in p21 Gene Expression in Rat KidneyIn Vivoand Rat Mesangial CellsIn Vitrounder Diabetic Conditions

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Xiangjun Li ◽  
Chaoyuan Li ◽  
Xiaoxia Li ◽  
Peihe Cui ◽  
Qifeng Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Mesangial Cells ◽  
Histone H3 ◽  
Diabetic Rats ◽  
Lysine Methylation ◽  
Histone Lysine Methylation ◽  
Histone Lysine

Diabetic nephropathy (DN), a common complication associated with type 1 and type 2 diabetes mellitus (DM), characterized by glomerular mesangial expansion, inflammation, accumulation of extracellular matrix (ECM) protein, and hypertrophy, is the major cause of end-stage renal disease (ESRD). Increasing evidence suggested that p21-dependent glomerular and mesangial cell (MC) hypertrophy play key roles in the pathogenesis of DN. Recently, posttranscriptional modifications (PTMs) have uncovered novel molecular mechanisms involved in DN. However, precise regulatory mechanism of histone lysine methylation (HKme) mediating p21 related hypertrophy associated with DN is not clear. We evaluated the roles of HKme and histone methyltransferase (HMT) SET7/9 in p21 gene expression in glomeruli of diabetic rats and in high glucose- (HG-) treated rat mesangial cells (RMCs). p21 gene expression was upregulated in diabetic rats glomeruli; chromatin immunoprecipitation (ChIP) assays showed decreased histone H3-lysine9-dimethylation (H3K9me2) accompanied with enhanced histone H3-lysine4-methylation (H3K4me1/3) and SET7/9 occupancies at the p21 promoter. HG-treated RMCs exhibited increased p21 mRNA, H3K4me level, SET7/9 recruitment, and inverse H3K9me, which were reversed by TGF-β1 antibody. These data uncovered key roles of H3Kme and SET7/9 responsible for p21 gene expressionin vivoandin vitrounder diabetic conditions and confirmed preventive effect of TGF-β1 antibody on DN.

scholarly journals EZH2 abnormalities in lymphoid malignancies: underlying mechanisms and therapeutic implications

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Boheng Li ◽  
Wee-Joo Chng
Keyword(s):  
Gene Expression ◽  
Essential Role ◽  
Histone H3 ◽  
Epigenetic Silencing ◽  
Post Translational Modifications ◽  
Therapeutic Implications ◽  
Polycomb Repressive Complex 2 ◽  
Lymphoid Malignancies ◽  
Underlying Mechanisms

AbstractEZH2 is the catalytic subunit of the polycomb repressive complex 2 (PRC2), which along with other PRC2 components mediates gene expression suppression via the methylation of Histone H3 at lysine 27. Recent studies have revealed a dichotomous role of EZH2 in physiology and in the pathogenesis of cancer. While it plays an essential role in the development of the lymphoid system, its deregulation, whether due to genetic or non-genetic causes, promotes B cell- and T cell-related lymphoma or leukemia. These findings triggered a boom in the development of therapeutic EZH2 inhibitors in recent years. Here, we discuss physiologic and pathogenic function of EZH2 in lymphoid context, various internal causes of EZH2 aberrance and how EZH2 modulates lymphomagenesis through epigenetic silencing, post-translational modifications (PTMs), orchestrating with surrounding tumor micro-environment and associating with RNA or viral partners. We also summarize different strategies to directly inhibit PRC2-EZH2 or to intervene EZH2 upstream signaling.

scholarly journals The incorporation loci of H3.3K36M determine its preferential prevalence in chondroblastomas

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yanjun Zhang ◽  
Dong Fang
Keyword(s):  
Gene Expression ◽  
Colony Formation ◽  
Molecular Mechanisms ◽  
Histone H3 ◽  
Mutant Protein ◽  
H3k36 Methylation ◽  
Mutant Proteins ◽  
Histone H3 Variant ◽  
Mutant Cells ◽  
Shed Light

AbstractThe histone H3.3K36M mutation, identified in over 90% of chondroblastoma cases, reprograms the H3K36 methylation landscape and gene expression to promote tumorigenesis. However, it’s still unclear how the H3K36M mutation preferentially occurs in the histone H3 variant H3.3 in chondroblastomas. Here, we report that H3.3K36M-, but not H3.1K36M-, mutant cells showed increased colony formation ability and differentiation defects. H3K36 methylations and enhancers were reprogrammed to different status in H3.3K36M- and H3.1K36M-mutant cells. The reprogramming of H3K36 methylation and enhancers was depended on the specific loci at which H3.3K36M and H3.1K36M were incorporated. Moreover, targeting H3K36M-mutant proteins to the chromatin inhibited the H3K36 methylation locally. Taken together, these results highlight the roles of the chromatic localization of H3.3K36M-mutant protein in the reprogramming of the epigenome and the subsequent induction of tumorigenesis, and shed light on the molecular mechanisms by which the H3K36M mutation mainly occurs in histone H3.3 in chondroblastomas.

scholarly journals Nitrate-regulated growth processes involve activation of gibberellin pathway

2021 ◽  
Author(s):  
Lucie Camut ◽  
Barbora Gallova ◽  
Lucas Jilli ◽  
Mathilde Sirlin-Josserand ◽  
Esther Carrera ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plant Architecture ◽  
Cellular Level ◽  
N Availability ◽  
Growth Processes ◽  
Independent Manner ◽  
Hormone Synthesis ◽  
Plant Life ◽  
Plant Life Cycle ◽  
Metabolism Gene

Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport, to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent and -independent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.

scholarly journals PRC2 activates interferon-stimulated genes indirectly by repressing miRNAs in glioblastoma

2019 ◽  
Author(s):  
Haridha Shivram ◽  
Steven V. Le ◽  
Vishwanath R. Iyer
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Anaplastic Astrocytoma ◽  
Gene Expression Analysis ◽  
Histone H3 ◽  
Chromatin Binding ◽  
Chromosome 14 ◽  
Methyltransferase Activity ◽  
Polycomb Repressive Complex 2 ◽  
Interferon Stimulated Genes

AbstractPolycomb repressive complex 2 (PRC2) is a chromatin binding complex that represses gene expression by methylating histone H3 at K27 to establish repressed chromatin domains. PRC2 can either regulate genes directly through the methyltransferase activity of its component EZH2 or indirectly by regulating other gene regulators. Gene expression analysis of glioblastoma (GBM) cells lacking EZH2 showed that PRC2 regulates hundreds of interferon-stimulated genes (ISGs). We found that PRC2 directly represses several ISGs and also indirectly activates a distinct set of ISGs. Assessment of EZH2 binding proximal to miRNAs showed that PRC2 directly represses miRNAs encoded in the chromosome 14 imprinted DLK1-DIO3 locus. We found that repression of this locus by PRC2 occurs in immortalized GBM-derived cell lines as well as in primary bulk tumors from GBM and anaplastic astrocytoma patients. Through repression of these miRNAs and several other miRNAs, PRC2 activates a set of ISGs that are targeted by these miRNAs. This PRC2-miRNA-ISG network is likely to be important in regulating gene expression programs in GBM.

scholarly journals KAI2 regulates seedling development by mediating light-induced remodelling of auxin transport

2021 ◽  
Author(s):  
Maxime Hamon-Josse ◽  
Jose Villaecija-Aguilar ◽  
Karin Ljung ◽  
Ottoline Leyser ◽  
Caroline Gutjahr ◽  
...  
Keyword(s):  
Gene Expression ◽  
Seedling Growth ◽  
Auxin Transport ◽  
Root Meristem ◽  
Seedling Development ◽  
Protein Abundance ◽  
Plant Life ◽  
Per Se ◽  
Plant Life Cycle ◽  
F Box Protein

The photomorphogenic remodelling of seedling growth upon exposure to light is a key developmental transition in the plant life cycle. The α/β-hydrolase signalling protein KARRIKIN-INSENSITIVE2 (KAI2), a close homologue of the strigolactone receptor DWARF14 (D14), is involved in this process, and kai2 mutants have strongly altered seedling growth as a result. KAI2 and D14 both act through the MAX2 (MORE AXILLARY BRANCHING2) F-box protein to target proteins of the SMAX1-LIKE (SUPPRESSOR OF MAX2 1) (SMXL) family for degradation, but the signalling events downstream of this step are unclear in both pathways. Here, we show that kai2 phenotypes arise because of a failure to downregulate auxin transport from the seedling shoot apex towards the root system, rather than a failure to respond to light per se. We demonstrate that KAI2 controls the light-induced remodelling of the PIN-mediated auxin transport system in seedlings, promoting the reduction of PIN3, PIN4, and PIN7 abundance in older tissues, and the increase of PIN1, PIN2, PIN3, and PIN7 abundance in the root meristem, consistent with transition from elongation-mediated growth in the dark to meristematically-mediated growth in the light. We show that removing PIN3, PIN4 and PIN7 from kai2 mutants, or pharmacological inhibition of auxin transport and synthesis, is sufficient to suppress most kai2 seedling phenotypes. KAI2 is not required for the light-mediated changes in PIN gene expression but is required for the changes in PIN protein abundance at the plasma membrane; we thus propose that KAI2 acts to promote vesicle trafficking, consistent with previous suggestions about D14-mediated signalling in the shoot.

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