Field Of Environmental Epigenetics Research Articles

To live or let die? Epigenetic adaptations to climate change-a review.

Anthropogenic activities are responsible for a wide array of environmental disturbances that threaten biodiversity. Climate change, encompassing temperature increases, ocean acidification, increased salinity, droughts, and floods caused by frequent extreme weather events, represents one of the most significant environmental alterations. These drastic challenges pose ecological constraints, with over a million species expected to disappear in the coming years. Therefore, organisms must adapt or face potential extinctions. Adaptations can occur not only through genetic changes but also through non-genetic mechanisms, which often confer faster acclimatization and wider variability ranges than their genetic counterparts. Among these non-genetic mechanisms are epigenetics defined as the study of molecules and mechanisms that can perpetuate alternative gene activity states in the context of the same DNA sequence. Epigenetics has received increased attention in the past decades, as epigenetic mechanisms are sensitive to a wide array of environmental cues, and epimutations spread faster through populations than genetic mutations. Epimutations can be neutral, deleterious, or adaptative and can be transmitted to subsequent generations, making them crucial factors in both long- and short-term responses to environmental fluctuations, such as climate change. In this review, we compile existing evidence of epigenetic involvement in acclimatization and adaptation to climate change and discuss derived perspectives and remaining challenges in the field of environmental epigenetics. Graphical Abstract.

The use of race terms in epigenetics research: considerations moving forward.

The field of environmental epigenetics is uniquely suited to investigate biologic mechanisms that have the potential to link stressors to health disparities. However, it is common practice in basic epigenetic research to treat race as a covariable in large data analyses in a way that can perpetuate harmful biases without providing any biologic insight. In this article, we i) propose that epigenetic researchers open a dialogue about how and why race is employed in study designs and think critically about how this might perpetuate harmful biases; ii) call for interdisciplinary conversation and collaboration between epigeneticists and social scientists to promote the collection of more detailed social metrics, particularly institutional and structural metrics such as levels of discrimination that could improve our understanding of individual health outcomes; iii) encourage the development of standards and practices that promote full transparency about data collection methods, particularly with regard to race; and iv) encourage the field of epigenetics to continue to investigate how social structures contribute to biological health disparities, with a particular focus on the influence that structural racism may have in driving these health disparities.

The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants

People are exposed to wide range of redox-active environmental pollutants. Air pollution, heavy metals, pesticides, and endocrine disrupting chemicals can disrupt cellular redox status. Redox-active pollutants in our environment all trigger their own sets of specific cellular responses, but they also activate a common set of general stress responses that buffer the cell against homeostatic insults. These cellular defense system (CDS) pathways include the heat shock response, the oxidative stress response, the hypoxia response, the unfolded protein response, the DNA damage response, and the general stress response mediated by the stress-activated p38 mitogen-activated protein kinase. Over the past two decades, the field of environmental epigenetics has investigated epigenetic responses to environmental pollutants, including redox-active pollutants. Studies of these responses highlight the role of chromatin modifications in controlling the transcriptional response to pollutants and the role of transcriptional memory, often referred to as “epigenetic reprogramming”, in predisposing previously exposed individuals to more potent transcriptional responses on secondary challenge. My central thesis in this review is that high dose or chronic exposure to redox-active pollutants leads to transcriptional memories at CDS target genes that influence the cell's ability to mount protective responses. To support this thesis, I will: (1) summarize the known chromatin features required for inducible gene activation; (2) review the known forms of transcriptional memory; (3) discuss the roles of inducible chromatin and transcriptional memory in CDS responses that are activated by redox-active environmental pollutants; and (4) propose a conceptual framework for CDS pathway responsiveness as a readout of total cellular exposure to redox-active pollutants.

DNA Methylation-Based Biomarkers of Environmental Exposures for Human Population Studies.

This manuscript orients the reader to the underlying motivations of environmental biomarker development for human population studies and provides the foundation for applying these novel biomarkers in future research. In this review, we focus our attention on the DNA methylation-based biomarkers of (i) smoking, among adults and pregnant women, (ii) lifetime cannabis use, (iii) alcohol consumption, and (iv) cumulative exposure to lead. Prior environmental exposures and lifestyle modulate DNA methylation levels. Exposure-related DNA methylation changes can either be persistent or reversible once the exposure is no longer present, and this combination of both persistent and reversible changes has essential value for biomarker development. Here, we present available biomarkers representing past and cumulative exposures using individual DNA methylation profiles. In the present work, we describe how the field of environmental epigenetics can leverage machine learning algorithms to develop exposure biomarkers and reduce problems of misreporting exposures or limited access technology. We emphasize the crucial role of the individual DNA methylation profiles in those predictions, providing a summary of each biomarker, and highlighting their advantages, and limitations. Future research can cautiously leverage these DNA methylation-based biomarkers to understand the onset and progression of diseases.

Downregulation of long noncoding RNA UCA1 is involved in Het-1A cells malignant transformation induced by N-nitrosamines combined microcystin-LR

Here, we review the fast-changing state-of-the-art and future perspectives for environmental epigenetics where the model organism for environment, Daphnia, is in focus. First, we describe why we believe the genus Daphnia possesses such remarkable characteristics for usage in epigenetic studies and especially in environmental epigenetics. Further, we consider current epigenetic research that employ these animals, followed by a discourse on the methods used and hint at other methods available. As part of this exercise, we identify the gaps in current knowledge and offer some questions that require attention. Finally, we offer our perspective on how, we think, this particular model organism could be exploited in the future in the field of environmental epigenetics.

Environmental epigenetics: a role in endocrine disease?

Endocrine disrupting chemicals that are structurally similar to steroid or amine hormones have the potential to mimic endocrine endpoints at the receptor level. However, more recently, epigenetic-induced alteration in gene expression has emerged as an alternative way in which environmental compounds may exert endocrine effects. We review concepts related to environmental epigenetics and relevance for endocrinology through three broad examples: 1) effect of early-life nutritional exposures on future obesity and insulin resistance, 2) effect of lifetime environmental exposures such as ionizing radiation on endocrine cancer risk, and 3) potential for compounds previously classified as endocrine disrupting to additionally or alternatively exert effects through epigenetic mechanisms. The field of environmental epigenetics is still nascent, and additional studies are needed to confirm and reinforce data derived from animal models and preliminary human studies. Current evidence suggests that environmental exposures may significantly impact expression of endocrine-related genes and thereby affect clinical endocrine outcomes.

Environmental Influences on Epigenetic Profiles

Studies of environmental challenges, such as hazardous air pollutants, nonmutagenic toxins, diet choice, and maternal behavioral patterns, reveal changes in gene expression patterns, DNA methylation, and histone modifications that are in causal association with exogenous exposures. In this article we summarize some of the recent advances in the field of environmental epigenetics and highlight seminal studies that implicate in utero exposures as causative agents in altering not only the epigenome of the exposed gestation, but that of subsequent generations. Current studies of the effects of maternal behavior, exposure to environmental toxins, and exposure to maternal diet and an altered gestational milieu are summarized.