scholarly journals Histone acetylation orchestrates wound-induced transcriptional activation and cellular reprogramming in Arabidopsis

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Bart Rymen ◽  
Ayako Kawamura ◽  
Alice Lambolez ◽  
Soichi Inagaki ◽  
Arika Takebayashi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Transcriptional Activation ◽  
Temporal Dynamics ◽  
Callus Formation ◽  
Early Time ◽  
Cellular Reprogramming ◽  
Epigenetic Mechanism ◽  
Transcriptional Responses ◽  
Physiological Processes

Abstract Plant somatic cells reprogram and regenerate new tissues or organs when they are severely damaged. These physiological processes are associated with dynamic transcriptional responses but how chromatin-based regulation contributes to wound-induced gene expression changes and subsequent cellular reprogramming remains unknown. In this study we investigate the temporal dynamics of the histone modifications H3K9/14ac, H3K27ac, H3K4me3, H3K27me3, and H3K36me3, and analyze their correlation with gene expression at early time points after wounding. We show that a majority of the few thousand genes rapidly induced by wounding are marked with H3K9/14ac and H3K27ac before and/or shortly after wounding, and these include key wound-inducible reprogramming genes such as WIND1, ERF113/RAP2.6 L and LBD16. Our data further demonstrate that inhibition of GNAT-MYST-mediated histone acetylation strongly blocks wound-induced transcriptional activation as well as callus formation at wound sites. This study thus uncovered a key epigenetic mechanism that underlies wound-induced cellular reprogramming in plants.

scholarly journals PfGCN5-Mediated Histone H3 Acetylation Plays a Key Role in Gene Expression in Plasmodium falciparum

2007 ◽  
Vol 6 (7) ◽  
pp. 1219-1227 ◽  
Author(s):  
Long Cui ◽  
Jun Miao ◽  
Tetsuya Furuya ◽  
Xinyi Li ◽  
Xin-zhuan Su ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plasmodium Falciparum ◽  
Histone Acetylation ◽  
Transcriptional Activation ◽  
Histone H3 ◽  
Epigenetic Mechanism ◽  
Promoter Regions ◽  
Specific Expression ◽  
Transcriptional Initiation ◽  
Translational Start

ABSTRACT Histone acetylation, regulated by the opposing actions of histone acetyltransferases (HATs) and deacetylases, is an important epigenetic mechanism in eukaryotic transcription. Although an acetyltransferase (PfGCN5) has been shown to preferentially acetylate histone H3 at K9 and K14 in Plasmodium falciparum, the scale of histone acetylation in the parasite genome and its role in transcriptional activation are essentially unknown. Using chromatin immunoprecipitation (ChIP) and DNA microarray, we mapped the global distribution of PfGCN5, histone H3K9 acetylation (H3K9ac) and trimethylation (H3K9m3) in the P. falciparum genome. While the chromosomal distributions of H3K9ac and PfGCN5 were similar, they are radically different from that of H3K9m3. In addition, there was a positive, though weak correlation between relative occupancy of H3K9ac on individual genes and the levels of gene expression, which was inversely proportional to the distance of array elements from the putative translational start codons. In contrast, H3K9m3 was negatively correlated with gene expression. Furthermore, detailed mapping of H3K9ac for selected genes using ChIP and real-time PCR in three erythrocytic stages detected stage-specific peak H3K9ac enrichment at the putative transcriptional initiation sites, corresponding to stage-specific expression of these genes. These data are consistent with H3K9ac and H3K9m3 as epigenetic markers of active and silent genes, respectively. We also showed that treatment with a PfGCN5 inhibitor led to reduced promoter H3K9ac and gene expression. Collectively, these results suggest that PfGCN5 is recruited to the promoter regions of genes to mediate histone acetylation and activate gene expression in P. falciparum.

scholarly journals Phase separation of TAZ compartmentalizes the transcription machinery to promote gene expression

2019 ◽  
Author(s):  
Tiantian Wu ◽  
Yi Lu ◽  
Orit Gutman ◽  
Huasong Lu ◽  
Qiang Zhou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Phase Separation ◽  
Transcriptional Activation ◽  
Target Gene ◽  
Coiled Coil ◽  
Separation Mechanism ◽  
Hippo Signaling ◽  
Transcriptional Responses ◽  
Coiled Coil Domain

AbstractTAZ promotes cell proliferation, development, and tumorigenesis by regulating target gene transcription. However, how TAZ orchestrates the transcriptional responses remains poorly defined. Here we demonstrate that TAZ forms nuclear condensates via liquid-liquid phase separation to compartmentalize its DNA binding co-factor TEAD4, the transcription co-activators BRD4 and MED1 and the transcription elongation factor CDK9 for activation of gene expression. TAZ, but not its paralog YAP, forms phase-separated droplets in vitro and liquid-like nuclear condensates in vivo, and this ability is negatively regulated by Hippo signaling via LATS-mediated phosphorylation and mediated by the coiled-coil domain. Deletion of the TAZ coiled-coil domain or substitution with the YAP coiled-coil domain does not affect the interaction of TAZ with its partners, but prevents its phase separation and more importantly, its ability to induce target gene expression. Thus, our study identifies a novel mechanism for the transcriptional activation by TAZ and demonstrates for the first time that pathway-specific transcription factors also engage the phase separation mechanism for efficient transcription activation.

scholarly journals Genome-wide profiling of transcribed enhancers during macrophage activation

2017 ◽  
Author(s):  
Elena Denisenko ◽  
Reto Guler ◽  
Musa Mhlanga ◽  
Harukazu Suzuki ◽  
Frank Brombacher ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Large Scale ◽  
Transcriptional Control ◽  
Macrophage Activation ◽  
Transcriptional Responses ◽  
Protein Coding ◽  
Genome Wide ◽  
Ifn Γ ◽  
Cap Analysis

AbstractMacrophages are sentinel cells essential for tissue homeostasis and host defence. Owing to their plasticity, macrophages acquire a range of functional phenotypes in response to microenvironmental stimuli, of which M(IFN-γ) and M(IL-4/IL-13) are well-known for their opposing pro- and anti-inflammatory roles. Enhancers have emerged as regulatory DNA elements crucial for transcriptional activation of gene expression. Using cap analysis of gene expression and epigenetic data, we identify on large-scale transcribed enhancers in mouse macrophages, their time kinetics and target protein-coding genes. We observe an increase in target gene expression, concomitant with increasing numbers of associated enhancers and find that genes associated to many enhancers show a shift towards stronger enrichment for macrophage-specific biological processes. We infer enhancers that drive transcriptional responses of genes upon M(IFN-γ) and M(IL-4/IL-13) macrophage activation and demonstrate stimuli-specificity of regulatory associations. Finally, we show that enhancer regions are enriched for binding sites of inflammation-related transcription factors, suggesting a link between stimuli response and enhancer transcriptional control. Our study provides new insights into genome-wide enhancer-mediated transcriptional control of macrophage genes, including those implicated in macrophage activation, and offers a detailed genome-wide catalogue to further elucidate enhancer regulation in macrophages.

scholarly journals 134INCOMPLETE HISTONE ACETYLATION OF SOMATIC CHROMATIN IN BOVINE OOCYTES

2004 ◽  
Vol 16 (2) ◽  
pp. 189
Author(s):  
G. Wee ◽  
S.-H. Kim ◽  
K.P. Kim ◽  
S. Yeo ◽  
D.-B. Koo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Somatic Cell ◽  
Histone Acetylation ◽  
Transcriptional Activation ◽  
Linear Models ◽  
Trichostatin A ◽  
Specific Inhibitor ◽  
Early Embryo ◽  
Image Analyzer ◽  
Cell Nuclei

Histone acetylation as an important regulatory mechanism of chromatin structure preceeding zygotic gene expression in early embryo development. After fertilization, transcriptional activation of the embryo begins during the S/G2 phase of the first cell cycle. However, the precise mechanism underlying activation of zygotic transcription remains to be understood, especially in bovine nuclear transfer (NT) embryos. It is known that acetylation of histone H4 lysine 5 (H4K5) represents hyperacetylation state, which is correlated with gene expression. In this study, the acetylation of H4K5 was observed during pronuclear formation by using immunofluorescence analysis with anti-AcH4K5. Our data were analyzed by the general linear models (GLM) procedure of the SAS. In IVF embryos, acetylation of H4K5 occurred on the paternal chromatin at 8h after fertilization but did not occur on the maternal chromatin until 10h after fertilization. Reconstructed oocytes with deactylated somatic cell nuclei began to show signs of acetylation on chromatin at 3h after fusion. When acetylation intensity was calculated using an image analyzer, IVF embryos presented a higher acetylation signal than NT embryos (P<0.05). To induce hyperacetylation in NT embryos, somatic cells were exposed to trichostatin A (TSA, 1μM for 60h), a specific inhibitor of histone deacetylase (HDAC), prior to NT. Acetylated signals of H4K5 increased significantly in TSA-treated cells as compared with non-treated cells (P<0.05). The reconstructed embryos with TSA-treated cells showed a higher fluorescence intensity than the oocytes with non-treated cells (P<0.05), but weak signals compared to IVF embryos. Thus, the results demonstrated low histone acetylation level of somatic cell nuclei after NT during the zygotic progress. Our findings suggest that developmental failures of NT embryos may be due to incomplete chromatin remodeling of somatic cell nuclei during early embryonic development.

scholarly journals HnRNPA2 is a novel histone acetyltransferase that mediates mitochondrial stress-induced nuclear gene expression

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Manti Guha ◽  
Satish Srinivasan ◽  
Kip Guja ◽  
Edison Mejia ◽  
Miguel Garcia-Diaz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dna ◽  
Transcriptional Activation ◽  
Nuclear Gene ◽  
C2c12 Cells ◽  
Retrograde Signaling ◽  
Epigenetic Mechanism ◽  
Mitochondrial Stress ◽  
Nuclear Gene Expression ◽  
Mitochondrial Dna Copy Number

Abstract Reduced mitochondrial DNA copy number, mitochondrial DNA mutations or disruption of electron transfer chain complexes induce mitochondria-to-nucleus retrograde signaling, which induces global change in nuclear gene expression ultimately contributing to various human pathologies including cancer. Recent studies suggest that these mitochondrial changes cause transcriptional reprogramming of nuclear genes although the mechanism of this cross talk remains unclear. Here, we provide evidence that mitochondria-to-nucleus retrograde signaling regulates chromatin acetylation and alters nuclear gene expression through the heterogeneous ribonucleoprotein A2 (hnRNAP2). These processes are reversed when mitochondrial DNA content is restored to near normal cell levels. We show that the mitochondrial stress-induced transcription coactivator hnRNAP2 acetylates Lys 8 of H4 through an intrinsic histone lysine acetyltransferase (KAT) activity with Arg 48 and Arg 50 of hnRNAP2 being essential for acetyl-CoA binding and acetyltransferase activity. H4K8 acetylation at the mitochondrial stress-responsive promoters by hnRNAP2 is essential for transcriptional activation. We found that the previously described mitochondria-to-nucleus retrograde signaling-mediated transformation of C2C12 cells caused an increased expression of genes involved in various oncogenic processes, which is retarded in hnRNAP2 silenced or hnRNAP2 KAT mutant cells. Taken together, these data show that altered gene expression by mitochondria-to-nucleus retrograde signaling involves a novel hnRNAP2-dependent epigenetic mechanism that may have a role in cancer and other pathologies.

scholarly journals The hepatic innate immune response is lobe-specific in a murine model endotoxemia

2019 ◽  
Vol 25 (2) ◽  
pp. 144-154 ◽  
Author(s):  
Leanna Nguyen ◽  
Jeryl Sandoval ◽  
Robyn De Dios ◽  
Elesa Yihdego ◽  
Miguel Zarate ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Innate Immune Response ◽  
Early Time ◽  
Innate Immune ◽  
Immune Response Gene ◽  
Hepatic Tissue ◽  
Transcriptional Responses ◽  
Time Points ◽  
Lps Challenge

The liver plays a central role in the innate immune response to endotoxemia. While previous studies have demonstrated lobe-specific transcriptional responses to various insults, whether this is true in response to endotoxemia is unknown. We sought to assess whether there were significant intra- and inter-lobe differences in the murine hepatic innate immune transcriptional response to endotoxemia. Adult male ICR mice were exposed to i.p. LPS (5 mg/kg, 30 min, 60 min, 5 h) and primary ( Tnf, Cxcl1, Nfkbia, Tnfiap3) and secondary ( Il6, Nos2) innate immune response gene expression was assessed in the left medial, right medial, left lateral, and right lateral lobes, and the papillary and caudate processes. The expression of all innate immune response genes increased following i.p. LPS challenge. When tested at the early time points (30 and 60 min), the left medial lobe and caudate process consistently demonstrated the highest induction of gene expression. Most inter-lobe differences were attenuated at later time points (5 h). To improve reproducibility of the study of endotoxemia induced by i.p. LPS challenge, inclusion of appropriate methodological details regarding collection of hepatic tissue should be included when reporting scientific results in published manuscripts.

Nuclear Hormone Receptors and Gene Expression

2001 ◽  
Vol 81 (3) ◽  
pp. 1269-1304 ◽  
Author(s):  
Ana Aranda ◽  
Angel Pascual
Keyword(s):  
Gene Expression ◽  
Nuclear Receptors ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Hormone Receptors ◽  
Target Genes ◽  
Specific Interaction ◽  
Nuclear Hormone Receptor ◽  
Transcriptional Responses ◽  
Orphan Receptors

The nuclear hormone receptor superfamily includes receptors for thyroid and steroid hormones, retinoids and vitamin D, as well as different “orphan” receptors of unknown ligand. Ligands for some of these receptors have been recently identified, showing that products of lipid metabolism such as fatty acids, prostaglandins, or cholesterol derivatives can regulate gene expression by binding to nuclear receptors. Nuclear receptors act as ligand-inducible transcription factors by directly interacting as monomers, homodimers, or heterodimers with the retinoid X receptor with DNA response elements of target genes, as well as by “cross-talking” to other signaling pathways. The effects of nuclear receptors on transcription are mediated through recruitment of coregulators. A subset of receptors binds corepressor factors and actively represses target gene expression in the absence of ligand. Corepressors are found within multicomponent complexes that contain histone deacetylase activity. Deacetylation leads to chromatin compactation and transcriptional repression. Upon ligand binding, the receptors undergo a conformational change that allows the recruitment of multiple coactivator complexes. Some of these proteins are chromatin remodeling factors or possess histone acetylase activity, whereas others may interact directly with the basic transcriptional machinery. Recruitment of coactivator complexes to the target promoter causes chromatin decompactation and transcriptional activation. The characterization of corepressor and coactivator complexes, in concert with the identification of the specific interaction motifs in the receptors, has demonstrated the existence of a general molecular mechanism by which different receptors elicit their transcriptional responses in target genes.

scholarly journals Updated Mechanisms of GCN5—The Monkey King of the Plant Kingdom in Plant Development and Resistance to Abiotic Stresses

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 979 ◽  
Author(s):  
Lei Gan ◽  
Zhenzhen Wei ◽  
Zuoren Yang ◽  
Fuguang Li ◽  
Zhi Wang
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Plant Development ◽  
Developmental Stages ◽  
Protein Substrates ◽  
Physiological Processes ◽  
Exogenous Stress ◽  
Interaction Factors ◽  
Monkey King ◽  
Underlying Mechanisms

Histone modifications are the main epigenetic mechanisms that regulate gene expression, chromatin structure, and plant development, among which histone acetylation is one of the most important and studied epigenetic modifications. Histone acetylation is believed to enhance DNA access and promote transcription. GENERAL CONTROL NON-REPRESSIBLE 5 (GCN5), a well-known enzymatic protein responsible for the lysine acetylation of histone H3 and H4, is a universal and crucial histone acetyltransferase involved in gene transcription and plant development. Many studies have found that GCN5 plays important roles in the different development stages of Arabidopsis. In terms of exogenous stress conditions, GCN5 is also involved in the responses to heat stress, cold stress, and nutrient element deficiency by regulating the related gene expression to maintain the homeostasis of some key metabolites (e.g., cellulose) or ions (e.g., phosphate, iron); in addition, GCN5 is involved in the phytohormone pathways such as ethylene, auxin, and salicylic acid to play various roles during the plant lifecycle. Some of the pathways involved by GCN5 also interwind to regulate specific physiological processes or developmental stages. Here, interactions between various developmental events and stress-resistant pathways mediated by GCN5 are comprehensively addressed and the underlying mechanisms are discussed in the plant. Studies with some interacting factors such as ADA2b provided valuable information for the complicated histone acetylation mechanisms. We also suggest the future focuses for GCN5 functions and mechanisms such as functions in seed development/germination stages, exploration of novel interaction factors, identification of more protein substrates, and application of advanced biotechnology-CRISPR in crop genetic improvement, which would be helpful for the complete illumination of roles and mechanisms of GCN5.

scholarly journals Adrenocorticotropic Hormone-Mediated Signaling Cascades Coordinate a Cyclic Pattern of Steroidogenic Factor 1-Dependent Transcriptional Activation

2006 ◽  
Vol 20 (1) ◽  
pp. 147-166 ◽  
Author(s):  
Jonathon N. Winnay ◽  
Gary D. Hammer
Keyword(s):  
Signaling Pathways ◽  
Transcriptional Activation ◽  
Hormone Receptors ◽  
Temporal Dynamics ◽  
Transcriptional Response ◽  
Endocrine Function ◽  
Signaling Cascades ◽  
Orphan Nuclear Receptor ◽  
Transcriptional Responses ◽  
Steroidogenic Factor 1

Abstract Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor that has emerged as a critical mediator of endocrine function at multiple levels of the hypothalamic-pituitary-steroidogenic axis. Within the adrenal cortex, ACTH-dependent transcriptional responses, including transcriptional activation of several key steroidogenic enzymes within the steroid biosynthetic pathway, are largely dependent upon SF-1 action. The absence of a bona fide endogenous eukaryotic ligand for SF-1 suggests that signaling pathway activation downstream of the melanocortin 2 receptor (Mc2r) modulates this transcriptional response. We have used the chromatin immunoprecipitation assay to examine the temporal formation of ACTH-dependent transcription complexes on the Mc2r gene promoter. In parallel, ACTH-dependent signaling events were examined in an attempt to correlate transcriptional events with the upstream activation of signaling pathways. Our results demonstrate that ACTH-dependent signaling cascades modulate the temporal dynamics of SF-1-dependent complex assembly on the Mc2r promoter. Strikingly, the pattern of SF-1 recruitment and the subsequent attainment of active rounds of transcription support a kinetic model of SF-1 transcriptional activation, a model originally established in the context of ligand-dependent transcription by several classical nuclear hormone receptors. An assessment of the major ACTH-dependent signaling pathways highlights pivotal roles for the MAPK as well as the cAMP-dependent protein kinase A pathway in the entrainment of SF-1-mediated transcriptional events. In addition, the current study demonstrates that specific enzymatic activities are capable of regulating distinct facets of a highly ordered transcriptional response.

scholarly journals H2AK121ub in Arabidopsis associates with a less accessible chromatin state at transcriptional regulation hotspots

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xiaochang Yin ◽  
Francisco J. Romero-Campero ◽  
Pedro de Los Reyes ◽  
Peng Yan ◽  
Jing Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Transcriptional Activation ◽  
Chromatin Accessibility ◽  
Polycomb Group ◽  
Gene Repression ◽  
Chromatin State ◽  
Transcriptional Responses ◽  
Histone Marks ◽  
Accessible Chromatin

AbstractAlthough it is well established that the Polycomb Group (PcG) complexes maintain gene repression through the incorporation of H2AK121ub and H3K27me3, little is known about the effect of these modifications on chromatin accessibility, which is fundamental to understand PcG function. Here, by integrating chromatin accessibility, histone marks and expression analyses in different Arabidopsis PcG mutants, we show that PcG function regulates chromatin accessibility. We find that H2AK121ub is associated with a less accessible but still permissive chromatin at transcriptional regulation hotspots. Accessibility is further reduced by EMF1 acting in collaboration with PRC2 activity. Consequently, H2AK121ub/H3K27me3 marks are linked to inaccessible although responsive chromatin. In contrast, only-H3K27me3-marked chromatin is less responsive, indicating that H2AK121ub-marked hotspots are required for transcriptional responses. Nevertheless, despite the loss of PcG activities leads to increased chromatin accessibility, this is not necessarily accompanied by transcriptional activation, indicating that accessible chromatin is not always predictive of gene expression.

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