scholarly journals Epigenomic Regulatory Mechanism of Flowering in Apple Demonstrated in Two Varieties with Contrasted Flowering Behaviors

2021 ◽  
Author(s):  
Hua Zhou ◽  
Chenguang Zhang ◽  
Mengxue Wang ◽  
Wei Zhang ◽  
Juanjuan Ma ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Cytosine Methylation ◽  
Floral Induction ◽  
Expression Patterns ◽  
Axillary Bud ◽  
Necessary Condition ◽  
Whole Genome ◽  
Transcriptional Responses ◽  
Flowering Genes

Abstract Background: Flowering is the necessary condition and yield basis for woody fruits in their life cycle. Although there has been considerable interest in the regulatory mechanisms underlying floral induction and flowering, the associated epigenetic modifications remain relatively uncharacterized. Results: We identified the genome-wide of DNA methylation changes and the transcriptional responses in axillary bud of ‘Qinguan’ (QA) and ‘Fuji’ (FA) varieties with contrasted flowering behaviors. The DNA methylations were19.35%, 62.96% and 17.68% for FA, and 19.64%, 62.49% and 17.86% for QA in the CG, CHG and CHH contexts, respectively. Number of hypermethylated or hypomethylated DMRs in different regions were contributed to significantly up/downregulated gene expression. DNA methylation can positively or negatively regulate gene expression based on the CG, CHG and CHH contexts in different regions. Additionally, the huge differences in transcription of MIKCc-Type MADS-box genes, and multiple flowering genes in multiple flowering pathways (i.e., light, age, GA and sugar) by changing DNA methylation, contributed to contrasted flowering behaviors in both QA and FA. Specifically, the floral meristem identify genes (i.e., FT, LEAFY, AP1 and SOC1) were significantly higher expression in QA than FA, but the floral repressor (i.e., SVP, AGL15, and AGL18) had an opposite result. Significant differences in multiple hormone levels were due to DEGs and their DMRs in their synthesis pathways, leading to both contrasted axillary bud outgrowth and flowering behaviors. Conclusions: The whole-genome bisulfite sequencing (BS) libraries of QA and FA with diverse flowering capabilities have been constructed for finding whole-genome cytosine methylation profiles. The RNA sequencing of QA and FA and diverse flowering capabilities have been combined together to identify the gene expression patterns and the correlation with their methylation states so that we can better understand the epigenetic regulation mechanisms of floral induction and formation in apple.

scholarly journals Feasibility of constructing multi-dimensional genomic maps of juvenile idiopathic arthritis

2018 ◽  
Author(s):  
Lisha Zhu ◽  
Kaiyu Jiang ◽  
Laiping Wong ◽  
Michael J. Buck ◽  
Yanmin Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Juvenile Idiopathic Arthritis ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Expression Patterns ◽  
Strong Association ◽  
Disease Diagnosis ◽  
Whole Genome ◽  
Healthy Children

AbstractBackgroundJuvenile idiopathic arthritis (JIA) is one of the most common chronic conditions of childhood. Like many common chronic human illnesses, JIA likely involves complex interactions between genes and the environment, mediated by the epigenome. Such interactions are best understood through multi-dimensional genomic maps that identify critical genetic and epigenetic components of the disease. However, constructing such maps in a cost-effective way is challenging, and this challenge is further complicated by the challenge of obtaining biospecimens from pediatric patients at time of disease diagnosis, prior to therapy, as well as the limited quantity of biospecimen that can be obtained from children,particularly those who are unwell. In this paper, we demonstrate the feasibility and utility of creating multi-dimensional genomic maps for JIA from limited sample numbers.MethodsTo accomplish our aims, we used an approach similar to that used in the ENCODE and Roadmap Epigenomics projects, which used only 2 replicates for each component of the genomic maps. We used genome-wide DNA methylation sequencing, whole genome sequencing on the Illumina 10x platform, RNA sequencing, and chromatin immunoprecipitation-sequencing for informative histone marks (H3K4me1 and H3K27ac) to construct a multi-dimensional map of JIA neutrophils, a cell we have shown to be important in the pathobiology of JIA.ResultsThe epigenomes of JIA neutrophils display numerous differences from those from healthy children. DNA methylation changes, however, had only a weak effect on differential gene expression. In contrast, H3K4me1 and H3K27ac, commonly associated with enhancer functions, strongly correlated with gene expression. Furthermore, although unique/novel enhancer marks were associated with insertion-deletion events (indels) identified on whole genome sequencing, we saw no strong association between epigenetic changes and underlying genetic variation. The initiation of treatment in JIA is associated with a re-ordering of both DNA methylation and histone modifications, demonstrating the plasticity of the epigenome in this setting.ConclusionsThese findings, generated from a small number of patient samples, demonstrate how multidimensional genomic studies may yield new understandings of biology of JIA and provide insight into how therapy alters gene expression patterns.

scholarly journals Gene expression profiling of epigenetic chromatin modification enzymes and histone marks by cigarette smoke: implications for COPD and lung cancer

2016 ◽  
Vol 311 (6) ◽  
pp. L1245-L1258 ◽  
Author(s):  
Isaac K. Sundar ◽  
Irfan Rahman
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Dna Methylation ◽  
Cigarette Smoke ◽  
Histone Modifications ◽  
Expression Patterns ◽  
Chromatin Modification ◽  
Gene Expression Patterns ◽  
Validation Data ◽  
Histone Marks

Chromatin-modifying enzymes mediate DNA methylation and histone modifications on recruitment to specific target gene loci in response to various stimuli. The key enzymes that regulate chromatin accessibility for maintenance of modifications in DNA and histones, and for modulation of gene expression patterns in response to cigarette smoke (CS), are not known. We hypothesize that CS exposure alters the gene expression patterns of chromatin-modifying enzymes, which then affects multiple downstream pathways involved in the response to CS. We have, therefore, analyzed chromatin-modifying enzyme profiles and validated by quantitative real-time PCR (qPCR). We also performed immunoblot analysis of targeted histone marks in C57BL/6J mice exposed to acute and subchronic CS, and of lungs from nonsmokers, smokers, and patients with chronic obstructive pulmonary disease (COPD). We found a significant increase in expression of several chromatin modification enzymes, including DNA methyltransferases, histone acetyltransferases, histone methyltransferases, and SET domain proteins, histone kinases, and ubiquitinases. Our qPCR validation data revealed a significant downregulation of Dnmt1, Dnmt3a, Dnmt3b, Hdac2, Hdac4, Hat1, Prmt1, and Aurkb. We identified targeted chromatin histone marks (H3K56ac and H4K12ac), which are induced by CS. Thus CS-induced genotoxic stress differentially affects the expression of epigenetic modulators that regulate transcription of target genes via DNA methylation and site-specific histone modifications. This may have implications in devising epigenetic-based therapies for COPD and lung cancer.

scholarly journals Transcriptional profiling of the murine airway response to acute ozone exposure

2019 ◽  
Author(s):  
Adelaide Tovar ◽  
Gregory J. Smith ◽  
Joseph M. Thomas ◽  
Jack R. Harkema ◽  
Samir N. P. Kelada
Keyword(s):  
Gene Expression ◽  
Airway Inflammation ◽  
Cellular Proliferation ◽  
Expression Patterns ◽  
Differentially Expressed ◽  
Ozone Exposure ◽  
Matrix Remodeling ◽  
Transcriptional Responses ◽  
Morphological Alterations ◽  
Cell Counts

AbstractExposure to ambient ozone (O3) pollution causes airway inflammation, epithelial injury, and decreased lung function. Long-term exposure is associated with increased mortality and exacerbations of respiratory conditions. While the adverse health effects of O3 exposure have been thoroughly described, less is known about the molecular processes that drive these outcomes. The aim of this study was to describe the cellular and molecular alterations observed in murine airways after exposure to either 1 or 2 ppm O3. After exposing adult, female C57BL/6J mice to filtered air, 1 or 2 ppm O3 for 3 hours, we assessed hallmark responses including airway inflammatory cell counts, epithelial permeability, cytokine secretion, and morphological alterations of the large airways. Further, we performed RNA-seq to profile gene expression in two critical tissues involved in O3 responses: conducting airways (CA) and airway macrophages (AM). We observed a concentration-dependent increase in airway inflammation and injury, and a large number of genes were differentially expressed in both target tissues at both concentrations of O3. Genes that were differentially expressed in CA were generally associated with barrier function, detoxification processes, and cellular proliferation. The differentially expressed genes in AM were associated with innate immune signaling, cytokine production, and extracellular matrix remodeling. Overall, our study has described transcriptional responses to acute O3 exposure, revealing both shared and unique gene expression patterns across multiple concentrations of O3 and in two important O3-responsive tissues. These profiles provide broad mechanistic insight into pulmonary O3 toxicity, and reveal a variety of targets for refined follow-up studies.

scholarly journals An integrative multi-omics approach in Sjögren’s Syndrome identifies novel genetic drivers with regulatory function and disease-specificity

2020 ◽  
Author(s):  
María Teruel ◽  
Guillermo Barturen ◽  
Manuel Martínez-Bueno ◽  
Miguel Barroso ◽  
Olivia Castelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Sjögren’S Syndrome ◽  
Genetic Variants ◽  
Sjögren's Syndrome ◽  
Expression Patterns ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Regulatory Function ◽  
Sjögren‘S Syndrome

ABSTRACTPrimary Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration and damage of exocrine salivary and lacrimal glands. The etiology of SS is complex with environmental triggers and genetic factors involved. By conducting an integrated multi-omics study we identified vast coordinated hypomethylation and overexpression effects, that also exhibit increased variability, in many already known IFN-regulated genes. We report a novel epigenetic signature characterized by increased DNA methylation levels in a large number of novel genes enriched in pathways such as collagen metabolism and extracellular matrix organization. We identified new genetic variants associated with SS that mediate their risk by altering DNA methylation or gene expression patterns, as well as disease-interacting genetic variants that exhibit regulatory function only in the SS population. Our study sheds new light on the interaction between genetics, DNA methylation, gene expression and SS, and contributes to elucidate the genetic architecture of gene regulation in an autoimmune population.

scholarly journals Genome-Wide Systematic Characterization of the NPF Family Genes and Their Transcriptional Responses to Multiple Nutrient Stresses in Allotetraploid Rapeseed

2020 ◽  
Vol 21 (17) ◽  
pp. 5947 ◽  
Author(s):  
Hao Zhang ◽  
Shuang Li ◽  
Mengyao Shi ◽  
Sheliang Wang ◽  
Lei Shi ◽  
...  
Keyword(s):  
N Uptake ◽  
Expression Patterns ◽  
Regulatory Elements ◽  
Peptide Transporter ◽  
Future Research ◽  
Whole Genome ◽  
Transcriptional Responses ◽  
Ammonium Toxicity ◽  
Genome Wide

NITRATE TRANSPORTER 1 (NRT1)/PEPTIDE TRANSPORTER (PTR) family (NPF) proteins can transport various substrates, and play crucial roles in governing plant nitrogen (N) uptake and distribution. However, little is known about the NPF genes in Brassica napus. Here, a comprehensive genome-wide systematic characterization of the NPF family led to the identification of 193 NPF genes in the whole genome of B. napus. The BnaNPF family exhibited high levels of genetic diversity among sub-families but this was conserved within each subfamily. Whole-genome duplication and segmental duplication played a major role in BnaNPF evolution. The expression analysis indicated that a broad range of expression patterns for individual gene occurred in response to multiple nutrient stresses, including N, phosphorus (P) and potassium (K) deficiencies, as well as ammonium toxicity. Furthermore, 10 core BnaNPF genes in response to N stress were identified. These genes contained 6–13 transmembrane domains, located in plasma membrane, that respond discrepantly to N deficiency in different tissues. Robust cis-regulatory elements were identified within the promoter regions of the core genes. Taken together, our results suggest that BnaNPFs are versatile transporters that might evolve new functions in B. napus. Our findings benefit future research on this gene family.

scholarly journals Maternal and Post-weaning High-Fat Diets Produce Distinct DNA Methylation Patterns in Hepatic Metabolic Pathways within Specific Genomic Contexts

2019 ◽  
Vol 20 (13) ◽  
pp. 3229 ◽  
Author(s):  
Moody ◽  
Wang ◽  
Jung ◽  
Chen ◽  
Pan
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Metabolic Pathways ◽  
Expression Patterns ◽  
Sprague Dawley ◽  
High Fat ◽  
Differentially Methylated Genes ◽  
High Fat Diets ◽  
Diet Intake ◽  
Fat Diets

Calorie-dense high-fat diets (HF) are associated with detrimental health outcomes, including obesity, cardiovascular disease, and diabetes. Both pre- and post-natal HF diets have been hypothesized to negatively impact long-term metabolic health via epigenetic mechanisms. To understand how the timing of HF diet intake impacts DNA methylation and metabolism, male Sprague–Dawley rats were exposed to either maternal HF (MHF) or post-weaning HF diet (PHF). At post-natal week 12, PHF rats had similar body weights but greater hepatic lipid accumulation compared to the MHF rats. Genome-wide DNA methylation was evaluated, and analysis revealed 1744 differentially methylation regions (DMRs) between the groups with the majority of the DMR located outside of gene-coding regions. Within differentially methylated genes (DMGs), intragenic DNA methylation closer to the transcription start site was associated with lower gene expression, whereas DNA methylation further downstream was positively correlated with gene expression. The insulin and phosphatidylinositol (PI) signaling pathways were enriched with 25 DMRs that were associated with 20 DMGs, including PI3 kinase (Pi3k), pyruvate kinase (Pklr), and phosphodiesterase 3 (Pde3). Together, these results suggest that the timing of HF diet intake determines DNA methylation and gene expression patterns in hepatic metabolic pathways that target specific genomic contexts.

scholarly journals Silencing of Mutator Elements in Maize Involves Distinct Populations of Small RNAs and Distinct Patterns of DNA Methylation

Genetics ◽  
2020 ◽  
Vol 215 (2) ◽  
pp. 379-391 ◽  
Author(s):  
Diane Burgess ◽  
Hong Li ◽  
Meixia Zhao ◽  
Sang Yeol Kim ◽  
Damon Lisch
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Small Rnas ◽  
Cytosine Methylation ◽  
De Novo ◽  
Epigenetic Silencing ◽  
Inverted Repeats ◽  
Causal Relationships ◽  
Terminal Inverted Repeats ◽  
Silencing Pathways

Transposable elements (TEs) are a ubiquitous feature of plant genomes. Because of the threat they post to genome integrity, most TEs are epigenetically silenced. However, even closely related plant species often have dramatically different populations of TEs, suggesting periodic rounds of activity and silencing. Here, we show that the process of de novo methylation of an active element in maize involves two distinct pathways, one of which is directly implicated in causing epigenetic silencing and one of which is the result of that silencing. Epigenetic changes involve changes in gene expression that can be heritably transmitted to daughter cells in the absence of changes in DNA sequence. Epigenetics has been implicated in phenomena as diverse as development, stress response, and carcinogenesis. A significant challenge facing those interested in investigating epigenetic phenomena is determining causal relationships between DNA methylation, specific classes of small RNAs, and associated changes in gene expression. Because they are the primary targets of epigenetic silencing in plants and, when active, are often targeted for de novo silencing, TEs represent a valuable source of information about these relationships. We use a naturally occurring system in which a single TE can be heritably silenced by a single derivative of that TE. By using this system it is possible to unravel causal relationships between different size classes of small RNAs, patterns of DNA methylation, and heritable silencing. Here, we show that the long terminal inverted repeats within Zea mays MuDR transposons are targeted by distinct classes of small RNAs during epigenetic silencing that are dependent on distinct silencing pathways, only one of which is associated with transcriptional silencing of the transposon. Further, these small RNAs target distinct regions of the terminal inverted repeats, resulting in different patterns of cytosine methylation with different functional consequences with respect to epigenetic silencing and the heritability of that silencing.

scholarly journals Impact of Transposable Elements on Methylation and Gene Expression across Natural Accessions of Brachypodium distachyon

2020 ◽  
Vol 12 (11) ◽  
pp. 1994-2001 ◽  
Author(s):  
Michele Wyler ◽  
Christoph Stritt ◽  
Jean-Claude Walser ◽  
Célia Baroux ◽  
Anne C Roulin
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Transposable Elements ◽  
Brachypodium Distachyon ◽  
Large Fraction ◽  
Expression Patterns ◽  
Specific Gene ◽  
Differential Gene ◽  
The Relationship ◽  
Silent State

Abstract Transposable elements (TEs) constitute a large fraction of plant genomes and are mostly present in a transcriptionally silent state through repressive epigenetic modifications, such as DNA methylation. TE silencing is believed to influence the regulation of adjacent genes, possibly as DNA methylation spreads away from the TE. Whether this is a general principle or a context-dependent phenomenon is still under debate, pressing for studying the relationship between TEs, DNA methylation, and nearby gene expression in additional plant species. Here, we used the grass Brachypodium distachyon as a model and produced DNA methylation and transcriptome profiles for 11 natural accessions. In contrast to what is observed in Arabidopsis thaliana, we found that TEs have a limited impact on methylation spreading and that only few TE families are associated with a low expression of their adjacent genes. Interestingly, we found that a subset of TE insertion polymorphisms is associated with differential gene expression across accessions. Thus, although not having a global impact on gene expression, distinct TE insertions may contribute to specific gene expression patterns in B. distachyon.

scholarly journals Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation

2020 ◽  
Vol 178 (2) ◽  
pp. 325-337
Author(s):  
Matthew de Gannes ◽  
Chia-I Ko ◽  
Xiang Zhang ◽  
Jacek Biesiada ◽  
Liang Niu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Heart Development ◽  
Expression Patterns ◽  
Embryonic Stem Cell Line ◽  
Molecular Networks ◽  
Unknown Etiology ◽  
Postnatal Maturation ◽  
Complex Interactions ◽  
And Function

Abstract Congenital heart disease (CHD), the leading birth defect worldwide, has a largely unknown etiology, likely to result from complex interactions between genetic and environmental factors during heart development, at a time when the heart adapts to diverse physiological and pathophysiological conditions. Crucial among these is the regulation of cardiomyocyte development and postnatal maturation, governed by dynamic changes in DNA methylation. Previous work from our laboratory has shown that exposure to the environmental toxicant tetrachlorodibenzo-p-dioxin (TCDD) disrupts several molecular networks responsible for heart development and function. To test the hypothesis that the disruption caused by TCDD in the heart results from changes in DNA methylation and gene expression patterns of cardiomyocytes, we established a stable mouse embryonic stem cell line expressing a puromycin resistance selectable marker under control of the cardiomyocyte-specific Nkx2-5 promoter. Differentiation of these cells in the presence of puromycin induces the expression of a large suite of cardiomyocyte-specific markers. To assess the consequences of TCDD treatment on gene expression and DNA methylation in these cardiomyocytes, we subjected them to transcriptome and methylome analyses in the presence of TCDD. Unlike control cardiomyocytes maintained in vehicle, the TCDD-treated cardiomyocytes showed extensive gene expression changes, with a significant correlation between differential RNA expression and DNA methylation in 111 genes, many of which are key elements of pathways that regulate cardiovascular development and function. Our findings provide an important clue toward the elucidation of the complex interactions between genetic and epigenetic mechanisms after developmental TCDD exposure that may contribute to CHD.

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