scholarly journals How alcohol drinking affects our genes: an epigenetic point of view

2019 ◽  
Vol 97 (4) ◽  
pp. 345-356 ◽  
Author(s):  
Stefania Ciafrè ◽  
Valentina Carito ◽  
Giampiero Ferraguti ◽  
Antonio Greco ◽  
George N. Chaldakov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Chromatin Remodeling ◽  
Histone Methylation ◽  
Chronic Exposure ◽  
Large Body ◽  
Point Of View ◽  
Epigenetic Mechanisms ◽  
The Brain ◽  
Epigenetic Processes

This work highlights recent studies in epigenetic mechanisms that play a role in alcoholism, which is a complex multifactorial disorder. There is a large body of evidence showing that alcohol can modify gene expression through epigenetic processes, namely DNA methylation and nucleosomal remodeling via histone modifications. In that regard, chronic exposure to ethanol modifies DNA and histone methylation, histone acetylation, and microRNA expression. The alcohol-mediated chromatin remodeling in the brain promotes the transition from use to abuse and addiction. Unravelling the multiplex pattern of molecular modifications induced by ethanol could support the development of new therapies for alcoholism and drug addiction targeting epigenetic processes.

scholarly journals Stability and Lability of Parental Methylation Imprints in Development and Disease

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 999 ◽  
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.

DNA modifications in schizophrenia

2020 ◽  
pp. 177-183
Author(s):  
Ehsan Pishva ◽  
Bart P. F. Rutten
Keyword(s):  
Gene Expression ◽  
Risk Factors ◽  
Dna Methylation ◽  
Alternative Splicing ◽  
Epigenetic Modification ◽  
Control Gene ◽  
Dna Modifications ◽  
Genetic And Environmental Factors ◽  
The Brain ◽  
Epigenetic Processes

Interplay between genetic and environmental factors plays a major role in shaping the neurodevelopmental origins of schizophrenia. Epigenetic processes act to dynamically control gene expression and are known to regulate key neurobiological and cognitive processes in the brain. Along with mediating the effects of environmental risk factors on the development of disease, epigenetic processes play a central role in the differentiation and development of the human brain. Therefore, investigating epigenetic variations associated with schizophrenia may shed new light on our understanding about the developmental and environmental origins of schizophrenia. DNA methylation is the best-characterized epigenetic modification, playing a role in regulating gene expression, alternative splicing and other transcriptional processes such as X-chromosome inactivation and genomic imprinting. This chapter discusses the evidence to support a role for DNA modifications in schizophrenia, and highlights the opportunities and challenges of ongoing studies.

DNA methylation in stress and depression: from biomarker to therapeutics

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.

scholarly journals Epigenetic mechanisms in sexual differentiation of the brain and behaviour

2016 ◽  
Vol 371 (1688) ◽  
pp. 20150114 ◽  
Author(s):  
Nancy G. Forger
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Sexual Differentiation ◽  
Wide Distribution ◽  
Epigenetic Modifications ◽  
Epigenetic Mechanism ◽  
Epigenetic Mechanisms ◽  
Genome Wide ◽  
The Brain

Circumstantial evidence alone argues that the establishment and maintenance of sex differences in the brain depend on epigenetic modifications of chromatin structure. More direct evidence has recently been obtained from two types of studies: those manipulating a particular epigenetic mechanism, and those examining the genome-wide distribution of specific epigenetic marks. The manipulation of histone acetylation or DNA methylation disrupts the development of several neural sex differences in rodents. Taken together, however, the evidence suggests there is unlikely to be a simple formula for masculine or feminine development of the brain and behaviour; instead, underlying epigenetic mechanisms may vary by brain region or even by dependent variable within a region. Whole-genome studies related to sex differences in the brain have only very recently been reported, but suggest that males and females may use different combinations of epigenetic modifications to control gene expression, even in cases where gene expression does not differ between the sexes. Finally, recent findings are discussed that are likely to direct future studies on the role of epigenetic mechanisms in sexual differentiation of the brain and behaviour.

Epigenetics and twin studies

2019 ◽  
pp. 32-50
Author(s):  
Jenny van Dongen ◽  
Dorret I Boomsma
Keyword(s):  
Dna Methylation ◽  
Complex Traits ◽  
Molecular Basis ◽  
Twin Studies ◽  
Epigenetic Mechanisms ◽  
Phenotypic Differences ◽  
Dizygotic Twins ◽  
Time Period ◽  
Dna Sequence Variants ◽  
The Brain

Throughout life, human traits are characterized by variability: they show variation between people and within persons over a time period. Such variation between and within persons can be related to genotype or environment and can be examined in studies of mono- and dizygotic twins. Increasingly, twins are also studied to examine variation at the molecular level, including variation in epigenetic mechanisms, such as DNA methylation. These mechanisms regulate how the DNA code is used in cells and are increasingly recognized as important contributors to phenotypic differences. In the brain, epigenetic mechanisms are crucial to development and synaptic plasticity, and are probably at the molecular basis of processes such as learning and memory. Epigenetic mechanisms represent a biological path through which environment and DNA-sequence variants may exert their effects on complex traits. When studying epigenetic mechanisms in human traits and understanding the sources of epigenetic variation twin-based research offers exceptional opportunities. This chapter describes epigenetic mechanisms and the value of twin research, with a focus on DNA methylation and traits related to cognitive and mental health.

Biopsychosocial pathways to mental health and disease across the lifespan: The emerging role of epigenetics

2020 ◽  
pp. 190-206
Author(s):  
Charlotte A.M. Cecil
Keyword(s):  
Gene Expression ◽  
Mental Health ◽  
Dna Methylation ◽  
Mental Illness ◽  
Psychiatric Disorders ◽  
Regulate Gene Expression ◽  
Health And Disease ◽  
Regulate Gene ◽  
Epigenetic Processes

The biopsychosocial (BPS) model of psychiatry has had a major impact on our modern conceptualization of mental illness as a complex, multi-determined phenomenon. Yet, interdisciplinary BPS work remains the exception, rather than the rule in psychiatry. It has been suggested that this may stem in part from a failure of the BPS model to clearly delineate the mechanisms through which biological, psychological, and social factors co-act in the development of mental illness. This chapter discusses how epigenetic processes that regulate gene expression, such as DNA methylation, are fast emerging as a candidate mechanism for BPS interactions, with potentially widespread implications for the way that psychiatric disorders are understood, assessed, and, perhaps in future, even treated.

Epigenetics

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.

scholarly journals Early life stress induces age-dependent epigenetic changes in p11 gene expression in male mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mi Kyoung Seo ◽  
Jung Goo Lee ◽  
Sung Woo Park
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Histone Acetylation ◽  
Histone Methylation ◽  
Life Stress ◽  
Early Life ◽  
Age Groups ◽  
Early Life Stress ◽  
Epigenetic Modifications ◽  
Age Dependent

AbstractEarly life stress (ELS) causes long-lasting changes in gene expression through epigenetic mechanisms. However, little is known about the effects of ELS in adulthood, specifically across different age groups. In this study, the epigenetic modifications of p11 expression in adult mice subjected to ELS were investigated in different stages of adulthood. Pups experienced maternal separation (MS) for 3 h daily from postnatal day 1 to 21. At young and middle adulthood, behavioral test, hippocampal p11 expression levels, and levels of histone acetylation and methylation and DNA methylation at the hippocampal p11 promoter were measured. Middle-aged, but not young adult, MS mice exhibited increased immobility time in the forced swimming test. Concurrent with reduced hippocampal p11 levels, mice in both age groups showed a decrease in histone acetylation (AcH3) and permissive histone methylation (H3K4me3) at the p11 promoter, as well as an increase in repressive histone methylation (H3K27me3). Moreover, our results showed that the expression, AcH3 and H3Kme3 levels of p11 gene in response to MS were reduced with age. DNA methylation analysis of the p11 promoter revealed increased CpG methylation in middle-aged MS mice only. The results highlight the age-dependent deleterious effects of ELS on the epigenetic modifications of p11 transcription.

scholarly journals Eating Disorders, Heredity and Environmental Activation: Getting Epigenetic Concepts into Practice

2020 ◽  
Vol 9 (5) ◽  
pp. 1332 ◽  
Author(s):  
Howard Steiger ◽  
Linda Booij
Keyword(s):  
Gene Expression ◽  
Eating Disorders ◽  
Eating Disorder ◽  
Empirical Evidence ◽  
Life Experiences ◽  
Epigenetic Mechanisms ◽  
Epigenetic Factors ◽  
Epigenetic Programming ◽  
Gene Environment ◽  
Epigenetic Processes

Epigenetic mechanisms are believed to link environmental exposures to alterations in gene expression, and in so doing, to provide a physical substrate for the activation of hereditary potentials by life experiences. In keeping with this idea, accumulating data suggest that epigenetic processes are implicated in eating-disorder (ED) etiology. This paper reviews literature on putative links between epigenetic factors and EDs, and examines ways in which epigenetic programming of gene expression could account for gene-environment interactions acting in the EDs. The paper also presents evidence suggesting that epigenetic processes link malnutrition and life stresses (gestational, perinatal, childhood, and adult) to risk of ED development. Drawing from empirical evidence and clinical experience, we propose that an epigenetically informed understanding of ED etiology can benefit patients, caregivers, and clinicians alike, in the sense that the perspective can reduce judgmental or blameful attitudes on the part of clinicians and caregivers, and increase self-acceptance and optimism about recovery on the part of those affected.

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

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
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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