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This research topic focuses on epigenetic components of PTSD. Epigenetic mechanisms are a class of molecular mechanisms by which environmental influences, including stress, can interact with the genome to have long-term consequences for brain plasticity and behavior. Articles herein include empirical reports and reviews that link stress and trauma with epigenetic alterations in humans and animal models of early- or later-life stress. Themes present throughout the collection include: DNA methylation is a useful biomarker of stress and treatment outcome in humans; epigenetic programming of stress-sensitive physiological systems early in development confers an enhanced risk on disease development upon re-exposure to trauma or stress; and, long-lived fear memories are associated with epigenetic alterations in fear memory and extinction brain circuitry.
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Studies have shown that alterations of epigenetics and microRNAs (miRNAs) play critical roles in the initiation and progression of human cancer. Epigenetic silencing of tumor suppressor genes in cancer cells is generally mediated by DNA hypermethylation of CpG island promoter and histone modification such as methylation of histone H3 lysine 9 (H3K9) and tri-methylation of H3K27. MiRNAs are small non-coding RNAs that regulate expression of various target genes. Specific miRNAs are aberrantly expressed and play roles as tumor suppressors or oncogenes during carcinogenesis. Important tumor suppressor miRNAs are silenced by epigenetic alterations, resulting in activation of target oncogenes in human malignancies. Stem cells have the ability to perpetuate themselves through self-renewal and to generate mature cells of various tissues through differentiation. Accumulating evidence suggests that a subpopulation of cancer cells with distinct stem-like properties is responsible for tumor initiation, invasive growth, and metastasis formation, which is defined as cancer stem cells. Cancer stem cells are considered to be resistant to conventional chemotherapy and radiation therapy, suggesting that these cells are important targets of cancer therapy. DNA methylation, histone modification and miRNAs may be deeply involved in stem-like properties in cancer cells. Restoring the expression of tumor suppressor genes and miRNAs by chromatin modifying drugs may be a promising therapeutic approach for cancer stem cells. In this Research Topic, we discuss about alterations of epigenetics and miRNAs in cancer and cancer stem cell and understand the molecular mechanism underlying the formation of cancer stem cell, which may provide a novel insight for treatment of refractory cancer.
epigenetics --- MicroRNAs --- Cancer --- cancer stem cells --- Methylation
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DNA methylation, a modification found in most species, regulates chromatin functions in conjunction with other epigenome modifications, such as histone post-translational modifications and non-coding RNAs. In mammals, DNA methylation has an essential role in development by orchestrating the generation and maintenance of the phenotypic diversity of human cell types. Recent years have brought spectacular advances in our understanding of the mechanism, function and regulation of DNA methyltransferases through their interaction with other epigenome modifications, chromatin factors and post-translational modifications, which are described in this Special Issue of Genes. Manuscripts are specifically addressing describing the targeting and regulation of DNA methyltransferases by interacting factors and their roles in cellular differentiation and the development of diseases. Prof. Dr. Albert Jeltsch and Prof. Dr. Humaira Gowher, Guest Editors
DNA methylation --- DNA methyltransferase --- histone modification --- molecular epigenetics --- DNA methylation --- DNMT1 --- UHRF1 --- USP7 --- ubiquitination --- epigenetics --- DNA methylation --- DNA methyltransferases --- DNMT1 --- DNMT3A --- DNA methyltransferase --- maintenance DNA methylation --- de novo DNA methylation --- allosteric regulation --- autoinhibition --- cell identity --- DNA methylation --- DNMT1 --- epigenetics --- gene expression --- UHRF1 --- DNA methylation --- DNA methyltransferase --- DNMT --- DNMT3B --- epigenetics --- DNA methylation --- embryogenesis --- germ cells --- DNMTs --- TETs --- ADCA-DN --- HSAN1E --- TBRS --- dwarfism --- DNMT3A --- DNMT1 --- rare diseases --- PCC/PGL --- DNA methylation --- n/a --- DNA methyltransferase function --- DNA methyltransferase mechanism --- DNA methyltransferase regulation --- DNA methyltransferase structure --- DNMT1 --- DNMT3A --- DNMT3B --- DNA Methylation
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Epigenetics is a new field that explains gene expression at the chromatin structure and organization level. Three principal epigenetic mechanisms are known and hundreds of combinations among them can develop different phenotypic characteristics. DNA methylation, histone modifications and small RNAs have been identified, and their functions are being studied in order to understand the mechanisms of interaction and regulation among the different biological processes in plants. Although, fundamental epigenetic mechanisms in crop plants are beginning to be elucidated, the comprehension of the different epigenetic mechanisms, by which plant gene regulation and phenotype are modified, is a major topic to develop in the near future in order to increase crop productivity. Thus, the importance of epigenetics in improving crop productivity is undoubtedly growing. Current research on epigenetics suggest that DNA methylation, histone modifications and small RNAs are involved in almost every aspect of plant life including agronomically important traits such as flowering time, fruit development, responses to environmental factors, defense response and plant growth. The aim of this Research Topic is to explore the recent advances concerning the role of epigenetics in crop biotechnology, as well as to enhance and promote interactions among high quality researchers from different disciplines such as genetics, cell biology, pathology, microbiology, and evolutionary biology in order to join forces and decipher the epigenetic mechanisms in crop productivity.
crop --- epigenetics --- Biotechnology --- DNA Methylation --- Histone posttranslational modifications --- small non-coding RNAs
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Symbiosis is an intimate relationship between different living entities and is widespread in virtually all organisms. It was critical for the origin and diversification of Eukaryotes and represents a major driving force in evolution. Indeed, symbiosis may support a wide range of biological processes, including those underlying the physiology, development, reproduction, health, behavior, ecology and evolution of the organisms involved in the relationship. Although often confused with mutualism, when both organisms benefit from the association, symbiosis actually encompasses several and variable relationships. Among them is parasitism, when one organism benefits but the other is harmed, and commensalism, when one organism benefits and the other remains unaffected. Even if many symbiotic lifestyles do exist in nature, in many cases the intimacy between the partners is so deep that the “symbiont” (sensu strictu) resides into the tissues and/or cells of the other partner. Since the partners frequently belong to different kingdoms, e.g. bacteria, fungi, protists and viruses living in association with animal and plant hosts, their shared “language” should be a basic and ancient form of communication able to effectively blur the boundaries between extremely different living entities. In recent years studies on the role of epigenetics in shaping host-symbiont interactions have been flourishing. Epigenetic changes include, but are not limited to, DNA methylation, remodelling of chromatin structure through histone chemical modifications and RNA interference. In this E-book we present a series of papers exploring the fascinating developmental and evolutionary relationship between symbionts and hosts, by focusing on the mediating epigenetic processes that enable the communication to be effective and robust at both the individual, the ecological and the evolutionary time scales. In particular, the papers consider the role of epigenetic factors and mechanisms in the interactions among different species, comprising the holobiont and host-parasite relationships. On the whole, since epigenetics is fast-acting and reversible, enabling dynamic developmental communication between hosts and symbionts at several different time scale, we argue that it could account for the enormous plasticity that characterizes the interactions between all the organisms living symbiotically on our planet.
chromatin re-modeling --- DNA Methylation --- epigenetics --- genome immunity --- Histone Modifications --- holobiont --- host-symbiont crosstalk --- pathogen --- symbiosis
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Folate, vitamin B12, vitamin B6 and riboflavin play a key role as coenzymes in one-carbon metabolism which, in turn, is essential for a broad range of fundamental physiological processes, including RNA and DNA synthesis, cell division, tissue growth and methylation. Deficiencies or imbalance of B-vitamins, as well as genetic polymorphisms and environmental factors, are shown to disturb the normal function of one-carbon metabolism with adverse effects on human health. Although a vast volume of research has already been conducted in this area, there are still significant gaps in our knowledge that require further investigations. This Special Issue of Nutrients invited submission of manuscripts, original research or reviews of the scientific literature, focused on novel findings in relation to B-vitamins and one-carbon metabolism in terms of: metabolic roles and molecular mechanisms; gene–nutrient interactions; fetal growth and programing; risk of disease (birth defects and pregnancy related conditions, cancer, cardiovascular disease and hypertension, neuropsychiatric disease, osteoporosis); health effects of B-vitamin supplementation and food fortification.
B-vitamins --- One-carbon metabolism --- B-vitamins and risk of disease --- B-vitamins and DNA methylation
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Alterations in gene expression are essential during growth and development phases and when plants are exposed to environmental challenges. Stress conditions induce gene expression modifications, which are associated with changes in the biochemical and physiological processes that help plants to avoid or reduce potential damage resulting from these stresses.After exposure to stress, surviving plants tend to flower earlier than normal and therefore transfer the accumulated epigenetic information to their progenies, given that seeds, where this information is stored, are formed at a later stage of plant development.DNA methylation is correlated with expression repression. Likewise, miRNA produced in the cell can reduce the transcript abundance or even prevent translation of mRNA. However, histone modulation, such as histone acetylation, methylation, and ubiquitination, can show distinct effects on gene expression. These alterations can be inherited, especially if the plants are consistently exposed to a particular environmental stress. Retrotransposons and retroviruses are foreign movable DNA elements that play an important role in plant evolution. Recent studies have shown that epigenetic alterations control the movement and the expression of genes harbored within these elements. These epigenetic modifications have an impact on the morphology, and biotic and abiotic tolerance in the subsequent generations because they can be inherited through the transgenerational memory in plants. Therefore, epigenetic modifications, including DNA methylation, histone modifications, and small RNA interference, serve not only to alter gene expression but also may enhance the evolutionary process in eukaryotes.In this E-book, original research and review articles that cover issues related to the role of DNA methylation, histone modifications, and small RNA in plant transgenerational epigenetic memory were published.The knowledge published on this topic may add new insight on the involvement of epigenetic factors in natural selection and environmental adaptation. This information may also help to generate a modeling system to study the epigenetic role in evolution.
transgeneration memory --- DNA methylation --- epigenetics --- chromatin --- environmental stresses --- evolution --- histones --- replication
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Women drinking during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which may feature variable neurodevelopmental deficits, facial dysmorphology, growth retardation, and learning disabilities. Research suggests the human brain is precisely formed through an intrinsic, genetic-cellular expression that is carefully orchestrated by an epigenetic program. This program can be influenced by environmental inputs such as alcohol. Current research suggests the genetic and epigenetic elements of FASD are heavily intertwined and highly dependent on one another. As such, now is the time for investigators to combine genetic, genomic and epigenetic components of alcohol research into a centralized, accessible platform for discussion. Genetic analyses inform gene sets which may be vulnerable to alcohol exposure during early neurulation. Prenatal alcohol exposure indeed alters expression of gene subsets, including genes involved in neural specification, hematopoiesis, methylation, chromatin remodeling, histone variants, eye and heart development. Recently, quantitative genomic mapping has revealed loci (QTLs) that mediate alcohol-induced phenotypes identified between two alcohol-drinking mouse strains. One question to consider is (besides the role of dose and stage of alcohol exposure) why only 5% of drinking women deliver newborns diagnosed with FAS (Fetal Alcohol Syndrome)? Studies are ongoing to answer this question by characterizing genome-wide expression, allele-specific expression (ASE), gene polymorphisms (SNPs) and maternal genetic factors that influence alcohol vulnerability. Alcohol exposure during pregnancy, which can lead to FASD, has been used as a model to resolve the epigenetic pathway between environment and phenotype. Epigenetic mechanisms modify genetic outputs through alteration of 3D chromatin structure and accessibility of transcriptional machinery. Several laboratories have reported altered epigenetics, including DNA methylation and histone modification, in multiple models of FASD. During development DNA methylation is dynamic yet orchestrated in a precise spatiotemporal manner during neurulation and coincidental with neural differentiation. Alcohol can directly influence epigenetics through alterations of the methionine pathway and subsequent DNA or histone methylation/acetylation. Alcohol also alters noncoding RNA including miRNA and transposable elements (TEs). Evidence suggests that miRNA expression may mediate ethanol teratology, and TEs may be affected by alcohol through the alteration of DNA methylation at its regulatory region. In this manner, the epigenetic and genetic components of FASD are revealing themselves to be mechanistically intertwined. Can alcohol-induced epigenomic alterations be passed across generations? Early epidemiological studies have revealed infants with FASD-like features in the absence of maternal alcohol, where the fathers were alcoholics. Novel mechanisms for alcohol-induced phenotypes include altered sperm DNA methylation, hypomethylated paternal allele and heritable epimutations. These studies predict the heritability of alcohol-induced epigenetic abnormalities and gene functionality across generations. We opened a forum to researchers and investigators the field of FASD to discuss their insights, hypotheses, fresh data, past research, and future research themes embedded in this rising field of the genetics and epigenetics of FASD. This eBook is a product of the collective sharing and debate among researchers who have contributed or reviewed each subject.
FASD --- Pregnancy drinking --- Genomics --- DNA Methylation --- histone modification --- Alcoholism --- transgenerational --- Fetal Alcohol Syndrome --- Gene environmental interaction --- Epigenetic medicine
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Epigenetics is defined as the study of modifications of the genome, heritable during cell division that does not involve changes in DNA sequences. Up to date, epigenetic modifications involve at least three general mechanisms regulating gene expression: histone modifications, DNA methylation, and non-coding RNAs (ncRNAs). For the past two decades, an explosion in our interest and understanding of epigenetic mechanisms has been seen. This mainly based on the influence that epigenetic alterations have on an amazing number of biological processes, such as gene expression, imprinting, programmed DNA rearrangements, germ line silencing, developmentally cued stem cell division, and overall chromosomal stability and identity. It has become also evident that the constant exposure of living organisms to environment factors affects their genomes through epigenetic mechanisms. Viruses infecting animal cells are thought to play central roles in shaping the epigenetic scenario of infected cells. In this context it has become obvious that knowing the impact that viral infections have on the epigenetic control of their host cells will certainly lead to a better understanding of the interplay viruses have with animal cells. In fact, DNA viruses use host transcription factors as well as epigenetic regulators in such a way that they affect epigenetic control of gene expression that extends to host gene expression. At the same time, animal cells employ mechanisms controlling transcription factors and epigenetic processes, in order to eliminate viral infections. In summary, epigenetic mechanisms are involved in most virus-cell interactions. We now know that some viruses exhibit epigenetic immune evasion mechanisms to survive and propagate in their host; however, there is still much ambiguity over these epigenetic mechanisms of viral immune evasion, and most of the discovered mechanisms are still incomplete. Other animal viruses associated to cancer often deregulate cellular epigenetic mechanisms, silencing cellular tumor-suppressor genes and/or activating either viral or host cell oncogenes. In addition, in several cancers the down-regulation of tumor suppressor protein-coding genes and ncRNAs with growth inhibitory functions, such as miRNAs, have been closely linked to the presence of cell CpG island promoter hypermethylation. The goal of the aforementioned Research Topic is to bring together the key experimental and theoretical research, linking state-of-the-art knowledge about the epigenetic mechanisms involved in animal virus-cell interactions.
epigenetic --- DNA Methylation --- Interference RNA --- histone modification --- Methyltransferases --- Immune System --- DNase I hypersensitive sites --- virus --- Oncolytic Virotherapy --- NGS technology
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Interest in the study of life in hot environments, both with respect to the inhabiting microorganisms and the enzymes they produce, is currently very high. The biological mechanisms responsible for the resistance to high temperatures are not yet fully understood, whereas thermostability is a highly required feature for industrial applications. In this e-book, the invited authors provide diverse evidence contributing to the understanding of such mechanisms and the unlocking of the biotechnological potential of thermophiles and thermozymes.
Brevibacillus sp. OA30 --- thermophilic --- hot spring --- Algeria --- protease --- characterization --- Vallitalea guaymasensis --- hydrothermal vent --- syntrophy --- whole-genome sequence --- cellulases --- thermophiles --- metagenomics --- biotechnology --- Thermostable --- xylanase --- Geobacillus --- lignocellulosic biomass --- ethanol --- thermophilic proteins --- protein engineering --- protein stability --- evolvability --- Candida rugosa --- lipase --- kinetic --- interfacial activation --- inhibition --- dimerization --- structure --- molecular tunnels --- enzyme structure --- enzyme activity --- temperature --- thermophile --- thermophily --- enzyme thermostability --- archaea --- methylation --- pseudouridine --- RNA modification --- tRNA methyltransferase --- tRNA modification --- insertion sequence --- transposons --- transposases --- HGT --- Thermus --- thermophiles --- mobilome --- n/a
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