Environmental Epigenetics最新文献

{"title":"Marion Julia Lamb (29 July 1939–12 December 2021)","authors":"E. Jablonka","doi":"10.1093/eep/dvac009","DOIUrl":"https://doi.org/10.1093/eep/dvac009","url":null,"abstract":"Marion Julia Lamb, a pioneer in the field of evolutionary epigenetics, died in London on the 12th of December 2021 at the age of 82 of lung cancer. Marion was an original and accomplished scientist and her intellectual brilliance was combined with deep political and intellectual courage, a fascination with the natural world and an almost fanatical studiousness. Coming from a natureand bookloving working-class family, she roamed, as a child, the coasts and estuaries of East Anglia, watching birds, investigating rock pools, turning every rotten log, developing the naturalist’s ardent and focused competence. She was always grateful to her parents for the freedom they gave her and for their one demand—that she ‘does her best’—whatever ‘best’ may be. And indeed she did—from decorating her flat to gardening, sailing, teaching and researching. Her intellect was clear and powerful and she excelled in everything she ever put it to—as a 16-year-old lab assistant in Max Perutz’s lab in Cambridge during her high-school vacations, as a brilliant university student (she shared with Robin Weiss the Francis Perch Bedford Prize for the best first degree in University College London), as an inspiring teacher and as a ground-breaking scientist. Marion loved the elegant beauty of genetics, and when John Maynard Smith, her genetics teacher in University College London (UCL) suggested that she does a PhD with him, she was delighted. Her thesis on ‘Radiation and Ageing in Drosophila’ was awarded a PhD in 1965. Her laboratory research was conducted in UCL, Harwell and Birkbeck College (where she became a senior lecturer) and was concerned mainly with various aspects of the biology and genetics of ageing, using Drosophila as a research tool. Her large body of experimental work on ageing, radiation biology and mutagenesis, 25 papers altogether, stood the test of time, and she wrote a highly acclaimed, crystal-clear and concise book ‘The Biology of Ageing’ (published by Blackie, 1), on which several advanced courses in the biology of ageing around the world were based. Evolutionary biology was Marion’s passion and guide since she was a high-school student and read Huxley’s Evolution: The Modern Synthesis. She told me that the first tutorial she ever attended as a first-year student in UCL was on Waddington’s The Strategy of the Genes and that it blew her mind. Our first conversation, in 1973, also happened to be about Waddington (I discovered Waddington, independently, through reading Arthur Koestler’s Ghost in the Machine, well before I knew any genetics). I was a first-year student, and she was my genetics teacher in Birkbeck College, where I spent a year. I asked her if she knowsWaddington and she looked at me with a wry smile and suggested that I learn to walk before I start running. I ended up doing a PhD in genetics. Long before we started writing papers together, Marion sent me evolutionary biology books to Israel, and when we met we discussed the many hot topics of","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42918750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Epigenetics 2022 update","authors":"M. Skinner","doi":"10.1093/eep/dvac008","DOIUrl":"https://doi.org/10.1093/eep/dvac008","url":null,"abstract":"An Oxford University Press publication, ‘Environmental Epigenetics’, just initiated its eighth year of operations with this Volume 8 Issue 1. We are a 100% open access journal listed in PubMed Central, along with numerous other access sites. Environmental Epigenetics is in review to obtain an impact factor in 2022. Special issues have occurred each year, and we encourage requests for special issues in environmental epigenetics. Our Special Issues in 2021–22 were on Epigenetic Transgenerational Inheritance, Generational Toxicology, and Environmental Epigenetics and Evolution (https://academic.oup.com/eep/pages/special_issues). The amount and diversity of our published studies are increasing as the field of environmental epigenetics grows and expands. We are looking forward to another productive year and encourage you to consider submissions to ‘Environmental Epigenetics’.","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44305879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Geospatiotemporal and causal inference study of cannabis and other drugs as risk factors for female breast cancer USA 2003-2017.","authors":"Albert Stuart Reece, Gary Kenneth Hulse","doi":"10.1093/eep/dvac006","DOIUrl":"10.1093/eep/dvac006","url":null,"abstract":"<p><p>Breast cancer (BC) is the commonest human cancer and its incidence (BC incidence, BCI) is rising worldwide. Whilst both tobacco and alcohol have been linked to BCI genotoxic cannabinoids have not been investigated. Age-adjusted state-based BCI 2003-2017 was taken from the Surveillance Epidemiology and End Results database of the Centers for Disease Control. Drug use from the National Survey of Drug Use and Health, response rate 74.1%. Median age, median household income and ethnicity were from US census. Inverse probability weighted (ipw) multivariable regression conducted in R. In bivariate analysis BCI was shown to be significantly linked with rising cannabis exposure {β-est. = 3.93 [95% confidence interval 2.99, 4.87], <i>P</i> = 1.10 × 10^-15}. At 8 years lag cigarettes:cannabis [β-est. = 2660 (2150.4, 3169.3), <i>P</i> = 4.60 × 10^-22] and cannabis:alcoholism [β-est. = 7010 (5461.6, 8558.4), <i>P</i> = 1.80 × 10^-17] were significant in ipw-panel regression. Terms including cannabidiol [CBD; β-est. = 16.16 (0.39, 31.93), <i>P</i> = 0.446] and cannabigerol [CBG; β-est. = 6.23 (2.06, 10.39), <i>P</i> = 0.0034] were significant in spatiotemporal models lagged 1:2 years, respectively. Cannabis-liberal paradigms had higher BCI [67.50 ± 0.26 v. 65.19 ± 0.21/100 000 (mean ± SEM), <i>P</i> = 1.87 × 10^-11; β-est. = 2.31 (1.65, 2.96), <i>P</i> = 9.09 × 10^-12]. 55/58 expected values >1.25 and 13/58 >100. Abortion was independently and causally significant in space-time models. Data show that exposure to cannabis and the cannabinoids Δ9-tetrahydrocannabinol, CBD, CBG and alcoholism fulfil quantitative causal criteria for BCI across space and time. Findings are robust to adjustment for age and several known sociodemographic, socio-economic and hormonal risk factors and establish cannabinoids as an additional risk factor class for breast carcinogenesis. BCI is higher under cannabis-liberal legal paradigms.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac006"},"PeriodicalIF":4.8,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8978645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60653128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paternal grandmother’s smoking in pregnancy is associated with extreme aversion to bitter taste in their grandchildren","authors":"J. Golding, M. Pembrey, Steven Gregory, M. Suderman, Yasmin Iles-Caven, K. Northstone","doi":"10.1093/eep/dvac003","DOIUrl":"https://doi.org/10.1093/eep/dvac003","url":null,"abstract":"Abstract Although there are many examples in the experimental literature of an environmental exposure in one generation impacting the phenotypes of subsequent generations, there are few studies that can assess whether such associations occur in humans. The Avon Longitudinal Study of Parents and Children (ALSPAC) has, however, been able to determine whether there are associations between grandparental exposures and their grandchildren’s development. Several of our studies, including sensitivity to loud noise, have shown associations between a grandmother smoking in pregnancy and the phenotype of the grandchild. These results were mostly specific to the sex of the grandchild and to whether the prenatal (i.e. during pregnancy) smoking occurred in the maternal or paternal grandmother. Here, we have used ancestral data on prenatal smoking among the grandmothers of the ALSPAC index children to examine possible effects on the grandchild’s ability to detect the bitter taste of PROP (6 n-propylthiouracil), distinguishing between the 10% deemed ‘extreme tasters’, and the rest of the population (total N = 4656 children). We showed that grandchildren whose paternal (but not maternal) grandmothers had smoked in pregnancy were more likely than those of non-smoking grandmothers to be extreme tasters [odds ratio (OR) 1.28; 95% confidence interval (CI) 1.03, 1.59] and that this was more likely in granddaughters (OR 1.42; 95% CI 1.03, 1.95) than grandsons (OR 1.18; 95% CI 0.88, 1.60). This pattern of association between paternal foetal exposure and the granddaughter’s development has been found with several other outcomes, suggesting that investigations should be undertaken to investigate possible mechanisms.","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2022-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43455915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perfluoroalkyl substances influence DNA methylation in school-age children highly exposed through drinking water contaminated from firefighting foam: a cohort study in Ronneby, Sweden","authors":"Yiyi Xu, C. Lindh, T. Fletcher, K. Jakobsson, Karin Engström","doi":"10.1093/eep/dvac004","DOIUrl":"https://doi.org/10.1093/eep/dvac004","url":null,"abstract":"Abstract Perfluoroalkyl substances (PFASs) are widespread synthetic substances with various adverse health effects. A potential mechanism of toxicity for PFASs is via epigenetic changes, such as DNA methylation. Previous studies have evaluated associations between PFAS exposure and DNA methylation among newborns and adults. However, no study has evaluated how PFASs influence DNA methylation among children of school age. In this exploratory study with school-age children exposed to PFASs through drinking water highly contaminated from firefighting foams, we aimed to investigate whether exposure to PFASs was associated with alteration in DNA methylation and epigenetic age acceleration. Sixty-three children aged 7–11 years from the Ronneby Biomarker Cohort (Sweden) were included. The children were either controls with only background exposure (n = 32; perfluorooctane sulfonic acid: median 2.8 and range 1–5 ng/ml) or those exposed to very high levels of PFASs (n = 31; perfluorooctane sulfonic acid: median 295 and range 190–464 ng/ml). These two groups were matched on sex, age, and body mass index. Genome-wide methylation of whole-blood DNA was analyzed using the Infinium MethylationEPIC BeadChip kit. Epigenetic age acceleration was derived from the DNA methylation data. Twelve differentially methylated positions and seven differentially methylated regions were found when comparing the high-exposure group to the control group. There were no differences in epigenetic age acceleration between these two groups (P = 0.66). We found that PFAS exposure was associated with DNA methylation at specific genomic positions and regions in children at school age, which may indicate a possible mechanism for linking PFAS exposure to health effects.","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2022-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44821357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenotypic plasticity as a facilitator of microbial evolution.","authors":"Emerson Santiago,&nbsp;David F Moreno,&nbsp;Murat Acar","doi":"10.1093/eep/dvac020","DOIUrl":"https://doi.org/10.1093/eep/dvac020","url":null,"abstract":"<p><p>Tossed about by the tides of history, the inheritance of acquired characteristics has found a safe harbor at last in the rapidly expanding field of epigenetics. The slow pace of genetic variation and high opportunity cost associated with maintaining a diverse genetic pool are well-matched by the flexibility of epigenetic traits, which can enable low-cost exploration of phenotypic space and reactive tuning to environmental pressures. Aiding in the generation of a phenotypically plastic population, epigenetic mechanisms often provide a hotbed of innovation for countering environmental pressures, while the potential for genetic fixation can lead to strong epigenetic-genetic evolutionary synergy. At the level of cells and cellular populations, we begin this review by exploring the breadth of mechanisms for the storage and intergenerational transmission of epigenetic information, followed by a brief review of common and exotic epigenetically regulated phenotypes. We conclude by offering an in-depth coverage of recent papers centered around two critical issues: the evolvability of epigenetic traits through Baldwinian adaptive phenotypic plasticity and the potential for synergy between epigenetic and genetic evolution.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac020"},"PeriodicalIF":3.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8b/52/dvac020.PMC9709823.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9549153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic and epigenetic interplay allows rapid transgenerational adaptation to metal pollution in zebrafish.","authors":"Fabien Pierron,&nbsp;Débora Heroin,&nbsp;Guillemine Daffe,&nbsp;Flore Daramy,&nbsp;Aurélien Barré,&nbsp;Olivier Bouchez,&nbsp;Alicia Romero-Ramirez,&nbsp;Patrice Gonzalez,&nbsp;Macha Nikolski","doi":"10.1093/eep/dvac022","DOIUrl":"https://doi.org/10.1093/eep/dvac022","url":null,"abstract":"<p><p>Despite still being a matter of debate, there is growing evidence that pollutant-induced epigenetic changes can be propagated across generations. Whereas such modifications could have long-lasting effects on organisms and even on population, environmentally relevant data from long-term exposure combined with follow-up through multiple generations remain scarce for non-mammalian species. We performed a transgenerational experiment comprising four successive generations of zebrafish. Only fish from the first generation were exposed to an environmentally realistic concentration of cadmium (Cd). Using a whole methylome analysis, we first identified the DNA regions that were differentially methylated in response to Cd exposure and common to fish of the first two generations. Among them, we then focused our investigations on the exon 3 (ex3) of the <i>cep19</i> gene. We indeed recorded transgenerational growth disorders in Cd-exposed fish, and a mutation in this exon is known to cause morbid obesity in mammals. Its methylation level was thus determined in zebrafish from all the four generations by means of a targeted and base resolution method. We observed a transgenerational inheritance of Cd-induced DNA methylation changes up to the fourth generation. However, these changes were closely associated with genetic variations, mainly a single nucleotide polymorphism. This single nucleotide polymorphism was itself at the origin of the creation or deletion of a methylation site and deeply impacted the methylation level of neighboring methylation sites. Cd-induced epigenetic changes were associated with different mRNA transcripts and an improved condition of Cd fish. Our results emphasize a tight relationship between genetic and epigenetic mechanisms and suggest that their interplay and pre-existing diversity can allow rapid adaptation to anthropogenic environmental changes.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac022"},"PeriodicalIF":3.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/39/f6/dvac022.PMC9716877.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10737960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of omics analysis for low-dose radiotoxicology and health risk assessment: the case of uranium.","authors":"Stéphane Grison,&nbsp;Maâmar Souidi","doi":"10.1093/eep/dvac025","DOIUrl":"https://doi.org/10.1093/eep/dvac025","url":null,"abstract":"<p><p>Exposure to environmental pollution and the increase in the incidence of multifactorial diseases in the population have become health problems for industrialized countries. In this context, the question of the health impact of exposure to these pollutants is not clearly identified in the low-dose range. This article looks at this problem using the example of preclinical studies of the effects of chronic low-dose exposure to uranium in rats. These studies demonstrate the value of molecular screening analyses (omics) and multimodal integrative approaches, of which the extreme sensitivity and breadth of observation spectrum make it possible to observe all the biological processes affected and the mechanisms of action triggered at the molecular level by exposure to low doses. They also show the value of these analytical approaches for finding diagnostic biomarkers or indicators of prognosis, which can be necessary to evaluate a risk. Finally, the results of these studies raise the question of the health risk caused by epigenomic deregulations occurring during critical developmental phases and their potential contribution to the development of chronic diseases that are metabolic in origin or to the development of certain cancer liable in the long term to affect the exposed adult and possibly its progeny.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac025"},"PeriodicalIF":3.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/02/1a/dvac025.PMC9743459.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10731081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Inheritance: Impact for Biology and Society-recent progress, current questions and future challenges.","authors":"Rodrigo G Arzate-Mejía,&nbsp;Isabelle M Mansuy","doi":"10.1093/eep/dvac021","DOIUrl":"https://doi.org/10.1093/eep/dvac021","url":null,"abstract":"<p><p>Epigenetic inheritance has emerged as a new research discipline that aims to study the mechanisms underlying the transmission of acquired traits across generations. Such transmission is well established in plants and invertebrates but remains not well characterized and understood in mammals. Important questions are how life experiences and environmental factors induce phenotypic changes that are passed to the offspring of exposed individuals, sometimes across several successive generations, what is the contribution of germ cells and what are the consequences for health and disease. These questions were recently discussed at the symposium Epigenetic Inheritance: Impact for Biology and Society organized every 2 years in Zürich, Switzerland. This review provides a summary of the research presented during the symposium and discusses current important questions, perspectives and challenges for the field in the future.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac021"},"PeriodicalIF":3.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9790978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10816902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental toxicant exposures and sex-specific effects on epigenetic programming and cardiovascular health across generations.","authors":"Laurie K Svoboda,&nbsp;Tomoko Ishikawa,&nbsp;Dana C Dolinoy","doi":"10.1093/eep/dvac017","DOIUrl":"https://doi.org/10.1093/eep/dvac017","url":null,"abstract":"<p><p>Despite substantial strides in diagnosis and treatment, cardiovascular diseases (CVDs) continue to represent the leading cause of death in the USA and around the world, resulting in significant morbidity and loss of productive years of life. It is increasingly evident that environmental exposures during early development can influence CVD risk across the life course. CVDs exhibit marked sexual dimorphism, but how sex interacts with environmental exposures to affect cardiovascular health is a critical and understudied area of environmental health. Emerging evidence suggests that developmental exposures may have multi- and transgenerational effects on cardiovascular health, with potential sex differences; however, further research in this important area is urgently needed. Lead (Pb), phthalate plasticizers, and perfluoroalkyl substances (PFAS) are ubiquitous environmental contaminants with numerous adverse human health effects. Notably, recent evidence suggests that developmental exposure to each of these toxicants has sex-specific effects on cardiovascular outcomes, but the underlying mechanisms, and their effects on future generations, require further investigation. This review article will highlight the role for the developmental environment in influencing cardiovascular health across generations, with a particular emphasis on sex differences and epigenetic mechanisms. In particular, we will focus on the current evidence for adverse multi and transgenerational effects of developmental exposures to Pb, phthalates, and PFAS and highlight areas where further research is needed.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"8 1","pages":"dvac017"},"PeriodicalIF":3.8,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9600458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9486304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}