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A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 35149

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Prof. Dr. Frédéric Silvestre

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Guest Editor

Research Unit in Environmental and Evolutionary Biology (URBE), Narilis (Namur Research Institute for Lifesciences), University of Namur rue de Bruxelles 61, B-5000 Namur, Belgium
Interests: environmental epigenetics; DNA methylation; toxicology

Dr. Bambarendage Perera

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Guest Editor

Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA
Interests: ncRNA biomarkers; epigenetics; genomic imprinting; toxicology

Special Issue Information

Dear Colleagues,

We are pleased to invite submissions for a Special Issue focusing on environmental epigenetics. Research in epigenetics has dramatically grown during the last decade, including various aspects of environmental biology. Nowadays, many questions are still pending regarding the effects and consequences of environmental stressors on the epigenome, embracing the particular role of epigenetic mechanisms in the adaptation and evolution of organisms in a changing environment. Epigenetics is commonly defined as mitotically and/or meiotically heritable changes in gene function that cannot be explained by changes in gene sequence. It includes DNA methylation and hydroxymethylation, histone modifications, chromatin structure and non-coding RNAs that may, under some circumstances, be inherited across generations. At the interplay between the environment and the genome, epigenetic mechanisms are perfect candidates to extend our understanding of the modes of action of environmental stressors on organisms and to explain the rapid phenomenon of adaptive evolution. Evidences exist showing that environmental cues can affect the epigenome, which can modify gene expression accordingly. These changes may thereafter induce phenotypic modifications at the organism level, being morphological, physiological or behavioral. In the field of evolutionary biology, epigenetic mechanisms have been seen as the "missing link" that could give neo-lamarckian theories a new youth.

It has been assumed that epigenetic modifications, such as genetic changes, can have a critical role in short-term microevolution while contributing to macroevolutionary processes such as speciation and adaptive radiation. However, to correctly evaluate the potential of epigenetics to be a driver of evolution, it is necessary that correlated phenotypic changes affect the fitness. It is also required that we evaluate its autonomy from genetic variation as well as its transgenerational stability. In this special issue, the term "environmental" refers to any change of an organism's surroundings, abiotic or biotic, excluding the exposure to specific pathogens. Examples of environmental parameters are temperature, acidity, oxygen level or other physico-chemical changes, as well as exposure to xenobiotics. Host-pathogen interactions can also be considered in a perspective of co-evolution. Any species can be included, model organisms or wild species. Studies on humans can also be considered if it is not purely biomedical.

Some examples of topics that can be tackled in this Special Issue are (non-exhaustive): the role of epigenetics in evolutionary theories, the effects of environmental stressors on non-model species, the origin of epimutations (genetic, environmental, stochastic), the transgenerational epigenetic inheritance, the modes of action and adverse outcome pathways of xenobiotics, epigenetic changes at the population level, consequences of epigenetic changes on an organism's fitness, early life stress and delayed effects, autonomy of epigenetic variation from genetic variation, epigenome-wide association studies, contribution of epigenetic variation in phenotypic variation, etc. Pure methodological papers are not in the scope of this issue, except if it concerns a specific development in environmental epigenetics. Studies about any epigenetic mechanisms are welcome. We look forward to receiving your manuscripts soon.

Prof. Dr. Frédéric Silvestre
Dr. Bambarendage Perera
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Epigenomes is an international peer-reviewed open access quarterly journal published by MDPI.

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Published Papers (9 papers)

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Editorial

Jump to: Research, Review

3 pages, 192 KiB

Open AccessEditorial

Environmental Epigenomes

by Bambarendage P. U. Perera and Frédéric Silvestre

Epigenomes 2023, 7(3), 21; https://doi.org/10.3390/epigenomes7030021 - 7 Sep 2023

Cited by 3 | Viewed by 1997

Abstract

Research in epigenetics has dramatically risen during the last decade to include aspects of environmental biology. However, many questions remain regarding the effects of environmental stressors on the epigenome, incorporating the particular role of epigenetic mechanisms in the adaptation and evolution of organisms in changing environments. Epigenetics is commonly defined as mitotically and/or meiotically heritable changes in gene function that occur without altering the underlying DNA sequence. It encompasses DNA (hydroxy)methylation, histone modifications, chromatin structure, and non-coding RNAs that may be inherited across generations under certain circumstances. Epigenetic mechanisms are perfect candidates to extend our understanding of the impact of environmental stressors on organisms and to explain the rapid phenomenon of adaptive evolution. Existing evidence shows that environmental cues can affect the epigenome and modify gene expression accordingly. These changes can then induce phenotypic modifications that are morphological, physiological, or behavioral at the organismal level. In this Special Issue focusing on environmental epigenetics, we provide an overview of influences to the epigenome that are driven by various environmental and evolutionary factors, with a particular focus on DNA methylation (DNAm). Five research groups have contributed insightful studies or reviews on (1) DNAm and demethylation events affected by the exposome; (2) DNAm as a potential biomarker to determine cardiometabolic risk early in life; (3) consequences of DNAm across multiple generations; (4) DNAm variation within natural animal populations; and (5) epigenetic mechanisms in genetically uniform organisms. Collectively, the articles from this Special Issue consistently support that environmental changes can induce long-lasting epigenetic effects within a given organism pertaining to individual risk for disease, or multi-generational impacts that ultimately impact evolution. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

Research

Jump to: Editorial, Review

12 pages, 1225 KiB

Open AccessArticle

Epigenetic Features in Newborns Associated with Preadolescence Lung Function and Asthma Acquisition during Adolescence

by Mohammad Nahian Ferdous Abrar, Yu Jiang, Hongmei Zhang, Liang Li and Hasan Arshad

Epigenomes 2024, 8(2), 12; https://doi.org/10.3390/epigenomes8020012 - 22 Mar 2024

Viewed by 1839

Abstract

The association between newborn DNA methylation (DNAm) and asthma acquisition (AA) during adolescence has been suggested. Lung function (LF) has been shown to be associated with asthma risk and its severity. However, the role of LF in the associations between DNAm and AA is unclear, and it is also unknown whether the association between DNAm and AA is consistent with that between DNAm and LF. We address this question through assessing newborn epigenetic features of preadolescence LF and of AA during adolescence, along with their biological pathways and processes. Our study’s primary medical significance lies in advancing the understanding of asthma’s early life origins. By investigating epigenetic markers in newborns and their association with lung function in preadolescence, we aim to uncover potential early biomarkers of asthma risk. This could facilitate earlier detection and intervention strategies. Additionally, exploring biological pathways linking early lung function to later asthma development can offer insights into the disease’s pathogenesis, potentially leading to novel therapeutic targets. Methods: The study was based on the Isle of Wight Birth cohort (IOWBC). Female subjects with DNAm data at birth and with no asthma at age 10 years were included (n = 249). The R package ttScreening was applied to identify CpGs potentially associated with AA from 10 to 18 years and with LF at age 10 (FEV1, FVC, and FEV1/FVC), respectively. Agreement in identified CpGs between AA and LF was examined, along with their biological pathways and processes via the R function gometh. We tested the findings in an independent cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC), to examine overall replicability. Results: In IOWBC, 292 CpGs were detected with DNAm associated with AA and 1517 unique CpGs for LF (514 for FEV1, 436 for FVC, 408 for FEV1/FVC), with one overlapping CpG, cg23642632 (NCKAP1) between AA and LF. Among the IOWBC-identified CpGs, we further tested in ALSPAC and observed the highest agreement between the two cohorts in FVC with respect to the direction of association and statistical significance. Epigenetic enrichment analyses indicated non-specific connections in the biological pathways and processes between AA and LF. Conclusions: The present study suggests that FEV1, FVC, and FEV1/FVC (as objective measures of LF) and AA (incidence of asthma) are likely to have their own specific epigenetic features and biological pathways at birth. More replications are desirable to fully understand the complexity between DNAm, lung function, and asthma acquisition. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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17 pages, 551 KiB

Open AccessArticle

DNA Methylation Is a Potential Biomarker for Cardiometabolic Health in Mexican Children and Adolescents

by Abeer A. Aljahdali, Jaclyn M. Goodrich, Dana C. Dolinoy, Hyungjin M. Kim, Edward A. Ruiz-Narváez, Ana Baylin, Alejandra Cantoral, Libni A. Torres-Olascoaga, Martha M. Téllez-Rojo and Karen E. Peterson

Epigenomes 2023, 7(1), 4; https://doi.org/10.3390/epigenomes7010004 - 3 Feb 2023

Cited by 1 | Viewed by 2845

Abstract

DNA methylation (DNAm) is a plausible mechanism underlying cardiometabolic abnormalities, but evidence is limited among youth. This analysis included 410 offspring of the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) birth cohort followed up to two time points in late childhood/adolescence. At Time 1, DNAm was quantified in blood leukocytes at long interspersed nuclear elements (LINE-1), H19, and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and at Time 2 in peroxisome proliferator-activated receptor alpha (PPAR-α). At each time point, cardiometabolic risk factors were assessed including lipid profiles, glucose, blood pressure, and anthropometry. Linear mixed effects models were used for LINE-1, H19, and 11β-HSD-2 to account for the repeated-measure outcomes. Linear regression models were conducted for the cross-sectional association between PPAR-α with the outcomes. DNAm at LINE-1 was associated with log glucose at site 1 [β = −0.029, p = 0.0006] and with log high-density lipoprotein cholesterol at site 3 [β = 0.063, p = 0.0072]. 11β-HSD-2 DNAm at site 4 was associated with log glucose (β = −0.018, p = 0.0018). DNAm at LINE-1 and 11β-HSD-2 was associated with few cardiometabolic risk factors among youth in a locus-specific manner. These findings underscore the potential for epigenetic biomarkers to increase our understanding of cardiometabolic risk earlier in life. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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13 pages, 1407 KiB

Open AccessArticle

Modulation of DNA Methylation/Demethylation Reactions Induced by Nutraceuticals and Pollutants of Exposome Can Promote a C > T Mutation in the Breast Cancer Predisposing Gene PALB2

by Florestan Courant, Gwenola Bougras-Cartron, Caroline Abadie, Jean-Sébastien Frenel and Pierre-François Cartron

Epigenomes 2022, 6(4), 32; https://doi.org/10.3390/epigenomes6040032 - 30 Sep 2022

Viewed by 2976

Abstract

Background: Deregulation of DNA methylation/demethylation reactions may be the source of C > T mutation via active deamination of 5-methylcytosine to thymine. Exposome, that is to say, the totality of exposures to which an individual is subjected during their life, can deregulate these reactions. Thus, one may wonder whether the exposome can induce C > T mutations in the breast cancer-predisposing gene PALB2. Methods: Our work is based on the exposure of MCF10A mammary epithelial cells to seven compounds of our exposome (folate, Diuron, glyphosate, PFOA, iron, zinc, and ascorbic acid) alone or in cocktail. The qMSRE and RMS techniques were used to study the impact of these exposures on the level of methylation and mutation of the PALB2 gene. Results: Here, we have found that exposome compounds (nutriments, ions, pollutants) promoting the cytosine methylation and the 5-methylcytosine deamination have the ability to promote a specific C > T mutation in the PALB2 gene. Interestingly, we also noted that the addition of exposome compounds promoting the TET-mediated conversion of 5-methylcytosine (Ascorbic acid and iron) abrogates the presence of C > T mutation in the PALB2 gene. Conclusions: Our study provides a proof of concept supporting the idea that exposomes can generate genetic mutation by affecting DNA methylation/demethylation. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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Review

Jump to: Editorial, Research

20 pages, 2826 KiB

Open AccessReview

Pathogenesis of PM_2.5-Related Disorders in Different Age Groups: Children, Adults, and the Elderly

by Teerachai Amnuaylojaroen and Nichapa Parasin

Epigenomes 2024, 8(2), 13; https://doi.org/10.3390/epigenomes8020013 - 31 Mar 2024

Cited by 7 | Viewed by 3317

Abstract

The effects of PM_2.5 on human health fluctuate greatly among various age groups, influenced by a range of physiological and immunological reactions. This paper compares the pathogenesis of the disease caused by PM_2.5 in people of different ages, focusing on how children, adults, and the elderly are each susceptible to it because of differences in their bodies. Regarding children, exposure to PM_2.5 is linked to many negative consequences. These factors consist of inflammation, oxidative stress, and respiratory problems, which might worsen pre-existing conditions and potentially cause neurotoxicity and developmental issues. Epigenetic changes can affect the immune system and make people more likely to get respiratory diseases. On the other hand, exposures during pregnancy can change how the cardiovascular and central nervous systems develop. In adults, the inhalation of PM_2.5 is associated with a wide range of health problems. These include respiratory difficulties, reduced pulmonary function, and an increased susceptibility to illnesses such as asthma, chronic obstructive pulmonary disease (COPD), and lung cancer. In addition, exposure to PM_2.5 induces systemic inflammation, cardiovascular diseases, insulin resistance, and neurotoxic consequences. Evident disturbances in the immune system and cognitive function demonstrate the broad impact of PM_2.5. The elderly population is prone to developing respiratory and cardiovascular difficulties, which worsen their pre-existing health issues and raise the risk of cognitive decline and neurological illnesses. Having additional medical conditions, such as peptic ulcer disease, significantly increases the likelihood of being admitted to hospital. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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12 pages, 307 KiB

Open AccessReview

World Trade Center Exposure, DNA Methylation Changes, and Cancer: A Review of Current Evidence

by Stephanie Tuminello, Emelie Nguyen, Nedim Durmus, Ramazan Alptekin, Muhammed Yilmaz, Maria Cecilia Crisanti, Matija Snuderl, Yu Chen, Yongzhao Shao, Joan Reibman, Emanuela Taioli and Alan A. Arslan

Epigenomes 2023, 7(4), 31; https://doi.org/10.3390/epigenomes7040031 - 8 Dec 2023

Cited by 3 | Viewed by 3099

Abstract

Introduction: Known carcinogens in the dust and fumes from the destruction of the World Trade Center (WTC) towers on 9 November 2001 included metals, asbestos, and organic pollutants, which have been shown to modify epigenetic status. Epigenome-wide association analyses (EWAS) using uniform (Illumina) methodology have identified novel epigenetic profiles of WTC exposure. Methods: We reviewed all published data, comparing differentially methylated gene profiles identified in the prior EWAS studies of WTC exposure. This included DNA methylation changes in blood-derived DNA from cases of cancer-free “Survivors” and those with breast cancer, as well as tissue-derived DNA from “Responders” with prostate cancer. Emerging molecular pathways related to the observed DNA methylation changes in WTC-exposed groups were explored and summarized. Results: WTC dust exposure appears to be associated with DNA methylation changes across the genome. Notably, WTC dust exposure appears to be associated with increased global DNA methylation; direct dysregulation of cancer genes and pathways, including inflammation and immune system dysregulation; and endocrine system disruption, as well as disruption of cholesterol homeostasis and lipid metabolism. Conclusion: WTC dust exposure appears to be associated with biologically meaningful DNA methylation changes, with implications for carcinogenesis and development of other chronic diseases. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

29 pages, 21798 KiB

Open AccessReview

Environmental Adaptation of Genetically Uniform Organisms with the Help of Epigenetic Mechanisms—An Insightful Perspective on Ecoepigenetics

by Günter Vogt

Epigenomes 2023, 7(1), 1; https://doi.org/10.3390/epigenomes7010001 - 26 Dec 2022

Cited by 10 | Viewed by 5578

Abstract

Organisms adapt to different environments by selection of the most suitable phenotypes from the standing genetic variation or by phenotypic plasticity, the ability of single genotypes to produce different phenotypes in different environments. Because of near genetic identity, asexually reproducing populations are particularly suitable for the investigation of the potential and molecular underpinning of the latter alternative in depth. Recent analyses on the whole-genome scale of differently adapted clonal animals and plants demonstrated that epigenetic mechanisms such as DNA methylation, histone modifications and non-coding RNAs are among the molecular pathways supporting phenotypic plasticity and that epigenetic variation is used to stably adapt to different environments. Case studies revealed habitat-specific epigenetic fingerprints that were maintained over subsequent years pointing at the existence of epigenetic ecotypes. Environmentally induced epimutations and corresponding gene expression changes provide an ideal means for fast and directional adaptation to changing or new conditions, because they can synchronously alter phenotypes in many population members. Because microorganisms inclusive of human pathogens also exploit epigenetically mediated phenotypic variation for environmental adaptation, this phenomenon is considered a universal biological principle. The production of different phenotypes from the same DNA sequence in response to environmental cues by epigenetic mechanisms also provides a mechanistic explanation for the “general-purpose genotype hypothesis” and the “genetic paradox of invasions”. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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15 pages, 1214 KiB

Open AccessReview

The Mutagenic Consequences of DNA Methylation within and across Generations

by Haley E. Hanson and Andrea L. Liebl

Epigenomes 2022, 6(4), 33; https://doi.org/10.3390/epigenomes6040033 - 4 Oct 2022

Cited by 9 | Viewed by 5385

Abstract

DNA methylation is an epigenetic modification with wide-ranging consequences across the life of an organism. This modification can be stable, persisting through development despite changing environmental conditions. However, in other contexts, DNA methylation can also be flexible, underlying organismal phenotypic plasticity. One underappreciated aspect of DNA methylation is that it is a potent mutagen; methylated cytosines mutate at a much faster rate than other genetic motifs. This mutagenic property of DNA methylation has been largely ignored in eco-evolutionary literature, despite its prevalence. Here, we explore how DNA methylation induced by environmental and other factors could promote mutation and lead to evolutionary change at a more rapid rate and in a more directed manner than through stochastic genetic mutations alone. We argue for future research on the evolutionary implications of DNA methylation driven mutations both within the lifetime of organisms, as well as across timescales. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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25 pages, 1313 KiB

Open AccessReview

Population Epigenetics: The Extent of DNA Methylation Variation in Wild Animal Populations

by Valentine Chapelle and Frédéric Silvestre

Epigenomes 2022, 6(4), 31; https://doi.org/10.3390/epigenomes6040031 - 28 Sep 2022

Cited by 19 | Viewed by 6605

Abstract

Population epigenetics explores the extent of epigenetic variation and its dynamics in natural populations encountering changing environmental conditions. In contrast to population genetics, the basic concepts of this field are still in their early stages, especially in animal populations. Epigenetic variation may play a crucial role in phenotypic plasticity and local adaptation as it can be affected by the environment, it is likely to have higher spontaneous mutation rate than nucleotide sequences do, and it may be inherited via non-mendelian processes. In this review, we aim to bring together natural animal population epigenetic studies to generate new insights into ecological epigenetics and its evolutionary implications. We first provide an overview of the extent of DNA methylation variation and its autonomy from genetic variation in wild animal population. Second, we discuss DNA methylation dynamics which create observed epigenetic population structures by including basic population genetics processes. Then, we highlight the relevance of DNA methylation variation as an evolutionary mechanism in the extended evolutionary synthesis. Finally, we suggest new research directions by highlighting gaps in the knowledge of the population epigenetics field. As for our results, DNA methylation diversity was found to reveal parameters that can be used to characterize natural animal populations. Some concepts of population genetics dynamics can be applied to explain the observed epigenetic structure in natural animal populations. The set of recent advancements in ecological epigenetics, especially in transgenerational epigenetic inheritance in wild animal population, might reshape the way ecologists generate predictive models of the capacity of organisms to adapt to changing environments. Full article

(This article belongs to the Special Issue Environmental Epigenomes)

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