Contribution of Epigenetic Mechanisms in the Regulation of Environmentally-Induced Polyphenism in Insects

Many insect species display a remarkable ability to produce discrete phenotypes in response to changes in environmental conditions. Such phenotypic plasticity is referred to as polyphenism. Seasonal, dispersal and caste polyphenisms correspond to the most-studied examples that are environmentally-induced in insects. Cues that induce such dramatic phenotypic changes are very diverse, ranging from seasonal cues, habitat quality changes or differential larval nutrition. Once these signals are perceived, they are transduced by the neuroendocrine system towards their target tissues where gene expression reprogramming underlying phenotypic changes occur. Epigenetic mechanisms are key regulators that allow for genome expression plasticity associated with such developmental switches. These mechanisms include DNA methylation, chromatin remodelling and histone post-transcriptional modifications (PTMs) as well as non-coding RNAs and have been studied to various extents in insect polyphenism. Differential patterns of DNA methylation between phenotypes are usually correlated with changes in gene expression and alternative splicing events, especially in the cases of dispersal and caste polyphenism. Combinatorial patterns of histone PTMs provide phenotype-specific epigenomic landscape associated with the expression of specific transcriptional programs, as revealed during caste determination in honeybees and ants. Alternative phenotypes are also usually associated with specific non-coding RNA profiles. This review will provide a summary of the current knowledge of the epigenetic changes associated with polyphenism in insects and highlights the potential for these mechanisms to be key regulators of developmental transitions triggered by environmental cues.

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Epigenetic Biomarkers in Head and Neck Cancer

Journal of Cancer Genetics and Biomarkers ◽

10.14302/issn.2572-3030.jcgb-18-2428 ◽

2018 ◽

Vol 1 (2) ◽

pp. 41-50 ◽

Cited By ~ 1

Author(s):

Shilpi Gupta ◽

Prabhat Kumar ◽

Jayant Maini ◽

Harsimrut Kaur

Keyword(s):

Risk Factors ◽

Dna Methylation ◽

Head And Neck ◽

Current Knowledge ◽

Human Papillomaviruses ◽

Epigenetic Mechanisms ◽

Definite Diagnosis ◽

Diagnosis And Prognosis ◽

Epigenetic Biomarkers ◽

Non Coding Rna

Head and neck cancers (HNCs) are the most prevalent and aggressive type of cancers. Genetic, epigenetic, environmental and viral risk-factors are associated with HNC carcinogenesis. Persistent infection of oncogenic human papillomaviruses (HR-HPVs) represent distinct biological, molecular and epigenetic entities in HNCs. There are three main epigenetic mechanisms that regulate transcription, these are DNA methylation, histone modifications and alteration in non-coding RNA networks, which can dissected to identify innovative and accurate epigenetic biomarkers for diagnosis and prognosis of HNC patients. Due to the lacunae of accurate distinctive biomarkers for the definite diagnosis of HNC, the identification of predictive epigenetic markers is necessary that might modify or increase HNC patient’s survival. In this mini review, we briefly summarize the current knowledge of different epigenetic biomarkers in HNC.

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DNA methylation in stress and depression: from biomarker to therapeutics

Acta Neuropsychiatrica ◽

10.1017/neu.2021.18 ◽

2021 ◽

pp. 1-67

Author(s):

Amanda J. Sales ◽

Francisco S. Guimarães ◽

Sâmia R. L. Joca

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Stress Responses ◽

Current Knowledge ◽

Antidepressant Treatment ◽

Epigenetic Mechanisms ◽

Stress Exposure ◽

Future Perspectives ◽

Potential Therapeutic Target ◽

The Brain

Abstract Epigenetic mechanisms such as DNA methylation (DNAm) have been associated with stress responses and increased vulnerability to depression. Abnormal DNAm is observed in stressed animals and depressed individuals. Antidepressant treatment modulates DNAm levels and regulates gene expression in diverse tissues, including the brain and the blood. Therefore, DNAm could be a potential therapeutic target in depression. Here, we reviewed the current knowledge about the involvement of DNAm in the behavioral and molecular changes associated with stress exposure and depression. We also evaluated the possible use of DNAm changes as biomarkers of depression. Finally, we discussed our current knowledge limitations and future perspectives.

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Epigenetics

Oxford Textbook of Cancer Biology ◽

10.1093/med/9780198779452.003.0005 ◽

2019 ◽

pp. 56-70

Author(s):

Edward Hookway ◽

Nicholas Athanasou ◽

Udo Oppermann

Keyword(s):

Gene Expression ◽

Histone Deacetylases ◽

Molecular Mechanisms ◽

Current Knowledge ◽

Tumour Suppressor Genes ◽

Epigenetic Mechanisms ◽

Therapeutic Approaches ◽

Control Of Gene Expression ◽

Non Coding Rnas ◽

Epigenetic Processes

Epigenetics is a term that refers to a collection of diverse mechanisms that are important in both the control of gene expression and the transmission of this information during cell division. Epigenetic processes are deranged in many cancers, leading to a combination of inappropriate silencing of tumour suppressor genes and overexpression of oncogenes. In this chapter, the molecular mechanisms that underpin the major epigenetic processes of DNA methylation, histone modification, and non-coding RNAs will be described in both their normal physiological roles and in the context of cancer. The challenge of understanding the complexity of the interactions between different epigenetic mechanisms and the limitations of our current knowledge will be highlighted. Therapeutic approaches towards targeting deranged epigenetic processes will also be described, such as the use of small molecule inhibitors of histone deacetylases.

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Transcriptome Changes during Major Developmental Transitions Accompanied with Little Alteration of DNA Methylome in Two Pleurotus Species

Genes ◽

10.3390/genes10060465 ◽

2019 ◽

Vol 10 (6) ◽

pp. 465 ◽

Cited By ~ 3

Author(s):

Jiawei Wen ◽

Zhibin Zhang ◽

Lei Gong ◽

Hongwei Xun ◽

Juzuo Li ◽

...

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Fruit Body ◽

Transcriptome Profiling ◽

Small Subset ◽

Mushroom Species ◽

Protein Coding ◽

Developmental Transitions ◽

Interspecific Differences ◽

Transcriptional Regulatory Mechanisms

Pleurotus tuoliensis (Pt) and P. eryngii var. eryngii (Pe) are important edible mushrooms. The epigenetic and gene expression signatures characterizing major developmental transitions in these two mushrooms remain largely unknown. Here, we report global analyses of DNA methylation and gene expression in both mushrooms across three major developmental transitions, from mycelium to primordium and to fruit body, by whole-genome bisulfite sequencing (WGBS) and RNA-seq-based transcriptome profiling. Our results revealed that in both Pt and Pe the landscapes of methylome are largely stable irrespective of genomic features, e.g., in both protein-coding genes and transposable elements (TEs), across the developmental transitions. The repressive impact of DNA methylation on expression of a small subset of genes is likely due to TE-associated effects rather than their own developmental dynamics. Global expression of gene orthologs was also broadly conserved between Pt and Pe, but discernible interspecific differences exist especially at the fruit body formation stage, and which are primarily due to differences in trans-acting factors. The methylome and transcriptome repertories we established for the two mushroom species may facilitate further studies of the epigenetic and transcriptional regulatory mechanisms underpinning gene expression during development in Pleurotus and related genera.

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DNA Methylation Pattern in Overweight Women under an Energy-Restricted Diet Supplemented with Fish Oil

BioMed Research International ◽

10.1155/2014/675021 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 18

Author(s):

Cátia Lira do Amaral ◽

Fermín I. Milagro ◽

Rui Curi ◽

J. Alfredo Martínez

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Weight Loss ◽

Fish Oil ◽

Mononuclear Cells ◽

Energy Restriction ◽

Dietary Factors ◽

Epigenetic Mechanisms ◽

Overweight Women ◽

Fish Oil Supplementation

Dietary factors modulate gene expression and are able to alter epigenetic signatures in peripheral blood mononuclear cells (PBMC). However, there are limited studies about the effects of omega-3 polyunsaturated fatty acids (n-3 PUFA) on the epigenetic mechanisms that regulate gene expression. This research investigates the effects ofn-3-rich fish oil supplementation on DNA methylation profile of several genes whose expression has been reported to be downregulated byn-3 PUFA in PBMC:CD36,FFAR3,CD14,PDK4, andFADS1. Young overweight women were supplemented with fish oil or control in a randomized 8-week intervention trial following a balanced diet with 30% energy restriction. Fatty acid receptorCD36decreased DNA methylation at CpG +477 due to energy restriction. Hypocaloric diet-induced weight loss also reduced the methylation percentages of CpG sites located inCD14,PDK4, andFADS1. The methylation patterns of these genes were only slightly affected by the fish oil supplementation, being the most relevant to the attenuation of the weight loss-induced decrease inCD36methylation after adjusting by baseline body weight. These results suggest that then-3 PUFA-induced changes in the expression of these genes in PBMC are not mediated by DNA methylation, although other epigenetic mechanisms cannot be discarded.

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Architectural Epigenetics: Mitotic Retention of Mammalian Transcriptional Regulatory Information

Molecular and Cellular Biology ◽

10.1128/mcb.00646-10 ◽

2010 ◽

Vol 30 (20) ◽

pp. 4758-4766 ◽

Cited By ~ 36

Author(s):

Sayyed K. Zaidi ◽

Daniel W. Young ◽

Martin Montecino ◽

Jane B. Lian ◽

Janet L. Stein ◽

...

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Transcription Factor ◽

Epigenetic Mechanisms ◽

Cellular Phenotype ◽

Transcriptional Regulatory ◽

Regulatory Information ◽

Cellular Identity ◽

Epigenetic Signatures ◽

Transcription Factor Occupancy

ABSTRACT Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustained cellular identity in progeny cells. We propose that these mitotic epigenetic signatures collectively constitute architectural epigenetics, a novel and essential mechanism that conveys regulatory information to sustain the control of phenotype and proliferation in progeny cells by bookmarking genes for activation or suppression.

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Leveraging brain cortex-derived molecular data to elucidate epigenetic and transcriptomic drivers of neurological function and disease

10.1101/429134 ◽

2018 ◽

Author(s):

Charlie Hatcher ◽

Caroline L. Relton ◽

Tom R. Gaunt ◽

Tom G. Richardson

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Histone Acetylation ◽

Genetic Variants ◽

Large Scale ◽

Genetic Variant ◽

Association Studies ◽

Genome Wide Association Studies ◽

Epigenetic Mechanisms ◽

Trait Variation

AbstractIntegrative approaches which harness large-scale molecular datasets can help develop mechanistic insight into findings from genome-wide association studies (GWAS). We have performed extensive analyses to uncover transcriptional and epigenetic processes which may play a role in neurological trait variation.This was undertaken by applying Bayesian multiple-trait colocalization systematically across the genome to identify genetic variants responsible for influencing intermediate molecular phenotypes as well as neurological traits. In this analysis we leveraged high dimensional quantitative trait loci data derived from prefrontal cortex tissue (concerning gene expression, DNA methylation and histone acetylation) and GWAS findings for 5 neurological traits (Neuroticism, Schizophrenia, Educational Attainment, Insomnia and Alzheimer’s disease).There was evidence of colocalization for 118 associations suggesting that the same underlying genetic variant influenced both nearby gene expression as well as neurological trait variation. Of these, 73 associations provided evidence that the genetic variant also influenced proximal DNA methylation and/or histone acetylation. These findings support previous evidence at loci where epigenetic mechanisms may putatively mediate effects of genetic variants on traits, such as KLC1 and schizophrenia. We also uncovered evidence implicating novel loci in neurological disease susceptibility, including genes expressed predominantly in brain tissue such as MDGA1, KIRREL3 and SLC12A5.An inverse relationship between DNA methylation and gene expression was observed more than can be accounted for by chance, supporting previous findings implicating DNA methylation as a transcriptional repressor. Our study should prove valuable in helping future studies prioritise candidate genes and epigenetic mechanisms for in-depth functional follow-up analyses.

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Regulatory Non-coding RNAs for Death Associated Protein Kinase Family

Frontiers in Molecular Biosciences ◽

10.3389/fmolb.2021.649100 ◽

2021 ◽

Vol 8 ◽

Author(s):

Qingshui Wang ◽

Youyu Lin ◽

Wenting Zhong ◽

Yu Jiang ◽

Yao Lin

Keyword(s):

Gene Expression ◽

Current Knowledge ◽

Regulation Of Gene Expression ◽

Tumor Development ◽

Invasion And Metastasis ◽

Calcium Dependent ◽

Non Coding Rna ◽

Death Associated Protein Kinase ◽

Non Coding Rnas ◽

Long Non Coding Rna

The death associated protein kinases (DAPKs) are a family of calcium dependent serine/threonine kinases initially identified in the regulation of apoptosis. Previous studies showed that DAPK family members, including DAPK1, DAPK2 and DAPK3 play a crucial regulatory role in malignant tumor development, in terms of cell apoptosis, proliferation, invasion and metastasis. Accumulating evidence has demonstrated that non-coding RNAs, including microRNA (miRNA), long non-coding RNA (lncRNA) and circRNA, are involved in the regulation of gene expression and tumorigenesis. Recent studies indicated that non-coding RNAs participate in the regulation of DAPKs. In this review, we summarized the current knowledge of non-coding RNAs, as well as the potential miRNAs, lncRNAs and circRNAs, that are involved in the regulation of DAPKs.

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The Use of Natural Products of Epigenetic Modulators in Anti-Cancer Drug Studies

Proceedings ◽

10.3390/proceedings2019040041 ◽

2019 ◽

Vol 40 (1) ◽

pp. 41

Author(s):

Demokan

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Natural Products ◽

Cancer Treatment ◽

Tumor Cells ◽

Histone Modifications ◽

Regulation Of Gene Expression ◽

Epigenetic Mechanisms ◽

Expression Of Genes ◽

Anti Cancer

The natural products obtained from plants, bacteria, fungi and marine have been used in the treatment of human diseases throughout the centuries. These compounds of them also interfere with the expression of genes by influencing epigenetic mechanisms. Recent researches showed significant outcomes suggesting that epigenetic silencing of the main regulatory genesis a sign of cancer onset and its progression. Epigenetic mechanisms that regulate expression of genes without mutation in the DNA are carried through DNA methylation, histone modification, chromatin remodeling and RNA interference. DNA methylation observed in the promoter regions of genes and prevents binding of the transcription factors by suppressing gene expression or by altering the nucleosome package of DNA, and may also directly inhibit transcription. Plant based products, such as curcumin, flavonoids, genistein, have been shown to exhibit cytostatic and apoptotic activities by influencing DNA methylation-based gene expression regulation in tumor cells. Additionally, natural products such as sulforaphane, retinoic acid, cucurbitacin B, casein Q, parthenolide, folate, cobalamin, pyridoxine and methionine also are used as anti-cancer agents based on DNA methylation. On the other hand, microRNAs (miRNAs) play a particular role in the epigenetic regulation of gene expression in post-transcription and post-translation processes. Quercetin, tryptolide, and honokiol are the natural compounds used in miRNA based agents. Histone modifications, which also affect the chromatin structure, play an important role in the initiation and progression of carcinogenesis as well as regulation of gene expression. As expected particular inhibitors of histone acetyltransferases (HATs) and histone deacetylase (HDAC) enzymes which are responsible of histone modifications have been developed for epigenetic intervention in cancer treatment. Numerous natural compounds are known to affect histone-modifying enzymes; such as romidepsin, epigallocatechingallate (EGCG), daidzein, sulphorafane, glucoraphanin, parthenolide, triptolide, sinapinic acid. Natural epigenetic modulators developed for epigenetic mechanisms enable the destruction of apoptotic, necrotic or autophagic pathways of tumor cells. Beside epigenetic mechanisms, these products exert their effects through influencing the cell cycle, DNA repair, and epigenetic mechanisms which modulate gene expression. More extensive in vitro and in vivo studies are required to investigate the effect of natural product-based epigenetic agents which seems to be very promising for future cancer treatment approaches.

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Stability and Lability of Parental Methylation Imprints in Development and Disease

Genes ◽

10.3390/genes10120999 ◽

2019 ◽

Vol 10 (12) ◽

pp. 999 ◽

Cited By ~ 3

Author(s):

Sabina Farhadova ◽

Melisa Gomez-Velazquez ◽

Robert Feil

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Histone Methylation ◽

Histone Variants ◽

Dna Demethylation ◽

Congenital Disorders ◽

Epigenetic Mechanisms ◽

Allelic Gene ◽

The Stability ◽

Covalent Histone Modifications

DNA methylation plays essential roles in mammals. Of particular interest are parental methylation marks that originate from the oocyte or the sperm, and bring about mono-allelic gene expression at defined chromosomal regions. The remarkable somatic stability of these parental imprints in the pre-implantation embryo—where they resist global waves of DNA demethylation—is not fully understood despite the importance of this phenomenon. After implantation, some methylation imprints persist in the placenta only, a tissue in which many genes are imprinted. Again here, the underlying epigenetic mechanisms are not clear. Mouse studies have pinpointed the involvement of transcription factors, covalent histone modifications, and histone variants. These and other features linked to the stability of methylation imprints are instructive as concerns their conservation in humans, in which different congenital disorders are caused by perturbed parental imprints. Here, we discuss DNA and histone methylation imprints, and why unravelling maintenance mechanisms is important for understanding imprinting disorders in humans.

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