Genome-wide cooperation by HAT Gcn5, remodeler SWI/SNF, and chaperone Ydj1 in promoter nucleosome eviction and transcriptional activation

Abstract Biosynthesis of secondary metabolites relies on primary metabolic pathways to provide precursors, energy, and cofactors, thus requiring coordinated regulation of primary and secondary metabolic networks. However, to date, it remains largely unknown how this coordination is achieved. Using Petunia hybrida flowers, which emit high levels of phenylpropanoid/benzenoid volatile organic compounds (VOCs), we uncovered genome-wide dynamic deposition of histone H3 lysine 9 acetylation (H3K9ac) during anthesis as an underlying mechanism to coordinate primary and secondary metabolic networks. The observed epigenome reprogramming is accompanied by transcriptional activation at gene loci involved in primary metabolic pathways that provide precursor phenylalanine, as well as secondary metabolic pathways to produce volatile compounds. We also observed transcriptional repression among genes involved in alternative phenylpropanoid branches that compete for metabolic precursors. We show that GNAT family histone acetyltransferase(s) (HATs) are required for the expression of genes involved in VOC biosynthesis and emission, by using chemical inhibitors of HATs, and by knocking down a specific HAT gene, ELP3, through transient RNAi. Together, our study supports that regulatory mechanisms at chromatin level may play an essential role in activating primary and secondary metabolic pathways to regulate VOC synthesis in petunia flowers.

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Genome-Wide Identification and Analysis of the APETALA2 (AP2) Transcription Factor in Dendrobium officinale

International Journal of Molecular Sciences ◽

10.3390/ijms22105221 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5221

Author(s):

Danqi Zeng ◽

Jaime A. Teixeira da Silva ◽

Mingze Zhang ◽

Zhenming Yu ◽

Can Si ◽

...

Keyword(s):

Transcriptional Activation ◽

Flower Development ◽

Regulatory Elements ◽

Negative Control ◽

Dendrobium Officinale ◽

Luciferase Reporter ◽

Pcr Analysis ◽

Luciferase Reporter Gene ◽

Genome Wide ◽

Ap2 Transcription Factor

The APETALA2 (AP2) transcription factors (TFs) play crucial roles in regulating development in plants. However, a comprehensive analysis of the AP2 family members in a valuable Chinese herbal orchid, Dendrobium officinale, or in other orchids, is limited. In this study, the 14 DoAP2 TFs that were identified from the D. officinale genome and named DoAP2-1 to DoAP2-14 were divided into three clades: euAP2, euANT, and basalANT. The promoters of all DoAP2 genes contained cis-regulatory elements related to plant development and also responsive to plant hormones and stress. qRT-PCR analysis showed the abundant expression of DoAP2-2, DoAP2-5, DoAP2-7, DoAP2-8 and DoAP2-12 genes in protocorm-like bodies (PLBs), while DoAP2-3, DoAP2-4, DoAP2-6, DoAP2-9, DoAP2-10 and DoAP2-11 expression was strong in plantlets. In addition, the expression of some DoAP2 genes was down-regulated during flower development. These results suggest that DoAP2 genes may play roles in plant regeneration and flower development in D. officinale. Four DoAP2 genes (DoAP2-1 from euAP2, DoAP2-2 from euANT, and DoAP2-6 and DoAP2-11 from basal ANT) were selected for further analyses. The transcriptional activation of DoAP2-1, DoAP2-2, DoAP2-6 and DoAP2-11 proteins, which were localized in the nucleus of Arabidopsis thaliana mesophyll protoplasts, was further analyzed by a dual-luciferase reporter gene system in Nicotiana benthamiana leaves. Our data showed that pBD-DoAP2-1, pBD-DoAP2-2, pBD-DoAP2-6 and pBD-DoAP2-11 significantly repressed the expression of the LUC reporter compared with the negative control (pBD), suggesting that these DoAP2 proteins may act as transcriptional repressors in the nucleus of plant cells. Our findings on AP2 genes in D. officinale shed light on the function of AP2 genes in this orchid and other plant species.

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H3 K79 dimethylation marks developmental activation of the β-globin gene but is reduced upon LCR-mediated high-level transcription

Blood ◽

10.1182/blood-2007-12-128983 ◽

2008 ◽

Vol 112 (2) ◽

pp. 406-414 ◽

Cited By ~ 11

Author(s):

Tomoyuki Sawado ◽

Jessica Halow ◽

Hogune Im ◽

Tobias Ragoczy ◽

Emery H. Bresnick ◽

...

Keyword(s):

Gene Expression ◽

Transcriptional Activation ◽

Globin Gene ◽

Erythroid Differentiation ◽

Genome Wide ◽

Activation Of Transcription ◽

High Level ◽

The Relationship ◽

Mutant Genes ◽

Gene Expression Levels

Abstract Genome-wide analyses of the relationship between H3 K79 dimethylation and transcription have revealed contradictory results. To clarify this relationship at a single locus, we analyzed expression and H3 K79 modification levels of wild-type (WT) and transcriptionally impaired β-globin mutant genes during erythroid differentiation. Analysis of fractionated erythroid cells derived from WT/Δ locus control region (LCR) heterozygous mice reveals no significant H3 K79 dimethylation of the β-globin gene on either allele prior to activation of transcription. Upon transcriptional activation, H3 K79 di-methylation is observed along both WT and ΔLCR alleles, and both alleles are located in proximity to H3 K79 dimethylation nuclear foci. However, H3 K79 di-methylation is significantly increased along the ΔLCR allele compared with the WT allele. In addition, analysis of a partial LCR deletion mutant reveals that H3 K79 dimethylation is inversely correlated with β-globin gene expression levels. Thus, while our results support a link between H3 K79 dimethylation and gene expression, high levels of this mark are not essential for high level β-globin gene transcription. We propose that H3 K79 dimethylation is destabilized on a highly transcribed template.

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Genome-Wide Analysis Reveals PADI4 Facilitates Transcriptional Activation of a Subset of Elk-1 Target Genes in MCF-7 Cells.

10.1210/endo-meetings.2010.part1.p3.p1-108 ◽

2010 ◽

pp. P1-108-P1-108

Author(s):

XS Zhang ◽

MJ Gamble ◽

S Stadler ◽

BD Cherrington ◽

MS Roberson ◽

...

Keyword(s):

Transcriptional Activation ◽

Target Genes ◽

Genome Wide Analysis ◽

Genome Wide ◽

Mcf 7

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Low temperature triggers genome-wide hypermethylation of transposable elements and centromeres in maize

10.1101/573915 ◽

2019 ◽

Cited By ~ 1

Author(s):

Zeineb Achour ◽

Johann Joets ◽

Martine Leguilloux ◽

Hélène Sellier ◽

Jean-Philippe Pichon ◽

...

Keyword(s):

Dna Methylation ◽

Transposable Elements ◽

Transcriptional Activation ◽

Gene Expression Regulation ◽

Environmental Cues ◽

Specific Response ◽

Genome Wide ◽

A Genome ◽

Response To Stress ◽

Context Specific

ABSTRACTCharacterizing the molecular processes developed by plants to respond to environmental cues is a major task to better understand local adaptation. DNA methylation is a chromatin mark involved in the transcriptional silencing of transposable elements (TEs) and gene expression regulation. While the molecular bases of DNA methylation regulation are now well described, involvement of DNA methylation in plant response to environmental cues remains poorly characterized. Here, using the TE-rich maize genome and analyzing methylome response to prolonged cold at the chromosome and feature scales, we investigate how genomic architecture affects methylome response to stress in a cold-sensitive genotype. Interestingly, we show that cold stress induces a genome-wide methylation increase through the hypermethylation of TE sequences and centromeres. Our work highlights a cytosine context-specific response of TE methylation that depends on TE types, chromosomal location and proximity to genes. The patterns observed can be explained by the parallel transcriptional activation of multiple DNA methylation pathways that methylate TEs in the various chromatin locations where they reside. Our results open new insights into the possible role of genome-wide DNA methylation in phenotypic response to stress.

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Central clock components modulate plant shade avoidance by directly repressing transcriptional activation activity of PIF proteins

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1918317117 ◽

2020 ◽

Vol 117 (6) ◽

pp. 3261-3269 ◽

Cited By ~ 10

Author(s):

Yu Zhang ◽

Anne Pfeiffer ◽

James M. Tepperman ◽

Jutta Dalton-Roesler ◽

Pablo Leivar ◽

...

Keyword(s):

Transcriptional Activation ◽

Target Genes ◽

Direct Action ◽

Published Data ◽

Shade Avoidance ◽

Response Regulators ◽

Genome Wide ◽

Promoter Occupancy ◽

Factor Abundance ◽

Direct Target

Light-environment signals, sensed by plant phytochrome photoreceptors, are transduced to target genes through direct regulation of PHYTOCHROME-INTERACTING FACTOR (PIF) transcription factor abundance and activity. Previous genome-wide DNA-binding and expression analysis has identified a set of genes that are direct targets of PIF transcriptional regulation. However, quantitative analysis of promoter occupancy versus expression level has suggested that unknown “trans factors” modulate the intrinsic transcriptional activation activity of DNA-bound PIF proteins. Here, using computational analysis of published data, we have identified PSEUDO-RESPONSE REGULATORS (PRR5 and PRR7) as displaying a high frequency of colocalization with the PIF proteins at their binding sites in the promoters of PIF Direct Target Genes (DTGs). We show that the PRRs function to suppress PIF-stimulated growth in the light and vegetative shade and that they repress the rapid PIF-induced expression of PIF-DTGs triggered by exposure to shade. The repressive action of the PRRs on both growth and DTG expression requires the PIFs, indicating direct action on PIF activity, rather than a parallel antagonistic pathway. Protein interaction assays indicate that the PRRs exert their repressive activity by binding directly to the PIF proteins in the nucleus. These findings support the conclusion that the PRRs function as direct outputs from the core circadian oscillator to regulate the expression of PIF-DTGs through modulation of PIF transcriptional activation activity, thus expanding the roles of the multifunctional PIF-signaling hub.

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Histone deacetylase 3 preferentially binds and collaborates with the transcription factor RUNX1 to repress AML1–ETO–dependent transcription in t(8;21) AML

Journal of Biological Chemistry ◽

10.1074/jbc.ra119.010707 ◽

2020 ◽

Vol 295 (13) ◽

pp. 4212-4223 ◽

Cited By ~ 1

Author(s):

Chun Guo ◽

Jian Li ◽

Nickolas Steinauer ◽

Madeline Wong ◽

Brent Wu ◽

...

Keyword(s):

Transcription Factor ◽

Fusion Protein ◽

Histone Deacetylase ◽

Transcriptional Activation ◽

Target Genes ◽

Chromosomal Translocation ◽

Histone Deacetylase 3 ◽

Genome Wide ◽

Related Transcription Factor ◽

Almost All

In up to 15% of acute myeloid leukemias (AMLs), a recurring chromosomal translocation, termed t(8;21), generates the AML1–eight–twenty-one (ETO) leukemia fusion protein, which contains the DNA-binding domain of Runt-related transcription factor 1 (RUNX1) and almost all of ETO. RUNX1 and the AML1–ETO fusion protein are coexpressed in t(8;21) AML cells and antagonize each other's gene-regulatory functions. AML1–ETO represses transcription of RUNX1 target genes by competitively displacing RUNX1 and recruiting corepressors such as histone deacetylase 3 (HDAC3). Recent studies have shown that AML1–ETO and RUNX1 co-occupy the binding sites of AML1–ETO–activated genes. How this joined binding allows RUNX1 to antagonize AML1–ETO–mediated transcriptional activation is unclear. Here we show that RUNX1 functions as a bona fide repressor of transcription activated by AML1–ETO. Mechanistically, we show that RUNX1 is a component of the HDAC3 corepressor complex and that HDAC3 preferentially binds to RUNX1 rather than to AML1–ETO in t(8;21) AML cells. Studying the regulation of interleukin-8 (IL8), a newly identified AML1–ETO–activated gene, we demonstrate that RUNX1 and HDAC3 collaboratively repress AML1–ETO–dependent transcription, a finding further supported by results of genome-wide analyses of AML1–ETO–activated genes. These and other results from the genome-wide studies also have important implications for the mechanistic understanding of gene-specific coactivator and corepressor functions across the AML1–ETO/RUNX1 cistrome.

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Listeria monocytogenes σB Modulates PrfA-Mediated Virulence Factor Expression

Infection and Immunity ◽

10.1128/iai.01205-08 ◽

2009 ◽

Vol 77 (5) ◽

pp. 2113-2124 ◽

Cited By ~ 66

Author(s):

Juliane Ollinger ◽

Barbara Bowen ◽

Martin Wiedmann ◽

Kathryn J. Boor ◽

Teresa M. Bergholz

Keyword(s):

Gene Expression ◽

Listeria Monocytogenes ◽

Transcriptional Activation ◽

Virulence Gene ◽

Transcript Profiling ◽

Virulence Gene Expression ◽

Qrt Pcr ◽

Genome Wide

ABSTRACT Listeria monocytogenes σB and positive regulatory factor A (PrfA) are pleiotropic transcriptional regulators that coregulate a subset of virulence genes. A positive regulatory role for σB in prfA transcription has been well established; therefore, observations of increased virulence gene expression and hemolytic activity in a ΔsigB strain initially appeared paradoxical. To test the hypothesis that L. monocytogenes σB contributes to a regulatory network critical for appropriate repression as well as induction of virulence gene expression, genome-wide transcript profiling and follow-up quantitative reverse transcriptase PCR (qRT-PCR), reporter fusion, and phenotypic experiments were conducted using L. monocytogenes prfA*, prfA* ΔsigB, ΔprfA, and ΔprfA ΔsigB strains. Genome-wide transcript profiling and qRT-PCR showed that in the presence of active PrfA (PrfA*), σB is responsible for reduced expression of the PrfA regulon. σB-dependent modulation of PrfA regulon expression reduced the cytotoxic effects of a PrfA* strain in HepG2 cells, highlighting the functional importance of regulatory interactions between PrfA and σB. The emerging model of the role of σB in regulating overall PrfA activity includes a switch from transcriptional activation at the P2 prfA promoter (e.g., in extracellular bacteria when PrfA activity is low) to posttranscriptional downregulation of PrfA regulon expression (e.g., in intracellular bacteria when PrfA activity is high).

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Genome-wide modeling of transcription kinetics reveals patterns of RNA production delays

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1420404112 ◽

2015 ◽

Vol 112 (42) ◽

pp. 13115-13120 ◽

Cited By ~ 47

Author(s):

Antti Honkela ◽

Jaakko Peltonen ◽

Hande Topa ◽

Iryna Charapitsa ◽

Filomena Matarese ◽

...

Keyword(s):

Rna Polymerase Ii ◽

Transcriptional Activation ◽

Time Course ◽

Degradation Rate ◽

High Throughput Sequencing ◽

Intron Retention ◽

Activation Kinetics ◽

Genome Wide ◽

Time Course Data ◽

Production Delay

Genes with similar transcriptional activation kinetics can display very different temporal mRNA profiles because of differences in transcription time, degradation rate, and RNA-processing kinetics. Recent studies have shown that a splicing-associated RNA production delay can be significant. To investigate this issue more generally, it is useful to develop methods applicable to genome-wide datasets. We introduce a joint model of transcriptional activation and mRNA accumulation that can be used for inference of transcription rate, RNA production delay, and degradation rate given data from high-throughput sequencing time course experiments. We combine a mechanistic differential equation model with a nonparametric statistical modeling approach allowing us to capture a broad range of activation kinetics, and we use Bayesian parameter estimation to quantify the uncertainty in estimates of the kinetic parameters. We apply the model to data from estrogen receptor α activation in the MCF-7 breast cancer cell line. We use RNA polymerase II ChIP-Seq time course data to characterize transcriptional activation and mRNA-Seq time course data to quantify mature transcripts. We find that 11% of genes with a good signal in the data display a delay of more than 20 min between completing transcription and mature mRNA production. The genes displaying these long delays are significantly more likely to be short. We also find a statistical association between high delay and late intron retention in pre-mRNA data, indicating significant splicing-associated production delays in many genes.

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