Endocrine Disrupting Chemicals, Obesogens, and the Obesity Epidemic
Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss in Nutrition and Cardiometabolic Health, 2017
Recent studies performed in animal models have revealed that ancestral perinatal exposure to obesogens leads to obesity in subsequent generations (Chamorro-Garcia et al. 2013, Manikkam et al. 2013). The transgenerational transmission of diseases implies that the germ line genome has been modified in nucleotide sequence (mutations) in epigenomic marks (epimutations) or both. As discussed more extensively in Chapter 28, the mechanisms involved in the modification of the epigenomic profile include covalent modifications of the DNA (e.g., methylation and hydroxymethylation of cytosines) and histones (e.g., methylation of lysines), and the presence of noncoding RNAs (Xin, Susiarjo, and Bartolomei 2015). By modifying the epigenomic profile of the cell, it is possible to modulate the functional output of the information stored in the genome sequence. During early stages of the development, the primordial germ cells go through a genome-wide demethylation/remethylation cycle before implantation. At this stage, the genome is extremely sensitive to the exposure of agents that may permanently change the original methylation pattern (Heard and Martienssen 2014). Thus, any changes in the epigenomic profile in the germ line at these developmental stages and the biological traits associated with them may be transmitted to subsequent generations, although, the precise mechanisms remain to be elucidated.
Candidate Genes, Gene × Environment Interactions, and Epigenetics
Gail S. Anderson in Biological Influences on Criminal Behavior, 2019
Although all our cells contain the same DNA, different genes in different cells are turned on and off, as we discussed in Chapter 4. So, although every cell carries the entire genome, only certain genes within it will act within the cell. A human being has trillions and trillions of cells, each with different genes turned on or off. The epigenome is a large array of chemicals and proteins that tells the genome how to function—which cells to turn on and off and when—so the epigenome controls the production of proteins and their subsequent functions.52 When an epigenomic chemical or protein attaches to the DNA and changes the function or expression of a gene, it does not change the actual DNA sequence but does change the manner in which the cell interprets the instructions from the genome; in other words, it changes the gene’s expression. These changes can be passed on when the cell replicates and even from generation to generation and so are heritable.52 When the epigenome modifies DNA, it is referred to as marking the genome. There are two main types of marks or markers, DNA methylation and histone modification,52 although other types of epigenetic mechanisms exist, such as non-coding RNAs, positive-effect variegation, parental imprinting, paramutation, and X-chromosome inactivation.48
Embryo/fetal–maternal cross talk
Carlos Simón, Linda C. Giudice in The Endometrial Factor, 2017
From the results obtained to date, it follows that many efforts have been made to elucidate the molecular nature of inherited epigenetic marks responsible for phenotypic transmission of chronic adult disease. However, most studies investigating this question have focused mainly on DNA methylation, thus only scratching the surface of the complete landscape of epigenomic variation. Fortunately, thanks to next-generation global DNA sequencing techniques, there are numerous advances in revealing the complete epigenomic map. Thus, it is now possible to engineer site-specific modifications in the epigenome in a targeted and reproducible manner, opening the door to the establishment of a causal relationship between transgenerational transmission of diseases and specific epigenetic marks (125).
Advancements of next generation sequencing in the field of Rheumatoid Arthritis
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Ankita Pati, Dattatreya Kar, Jyoti Ranjan Parida, Ananya Kuanar
Epigenetic control has been demonstrated to take place at certain levels like the covalent modification of the proteins associated with DNA (histones), the direct chemical alterations in the DNA and modifications in the accessibility of chromatin as well at the higher-order structures. Furthermore, the terminology Epigenomics indicates a genome-wide mould of DNA modifications and accessibility of chromatin. Such patterns of epigenetics are plastic at the time of inflammatory processes [38]. In this context epigenetic modulations are seen to be important in disease states as well as inflammation; thus, it is crucial to understand the changes in epigenetics that may lead to rheumatic diseases has made the study of chromatin landscape and histone modifications easier by an in-depth analysis of these areas. In this context, the analyses of accessibility of chromatin as well as histone modifications are at the near stage, despite the changes in epigenetics within the disease-causing genes that have been identified in RA [39].
Exceptionalism, Information Categories and the Relevance of Gender
Published in The American Journal of Bioethics, 2021
Dupras and Bunnik (2021) take on the particular privacy risks of multi-omics, in particular via a contrast and comparison of genomics and epigenomics, followed by a consideration of the issues in relation to the microbiome. They set out a number of goals including moving away from genomic exceptionalism, recognizing the blurred lines between -omics types, and providing pan-omic guidance. A further sub-goal is to explore the significance of the difference between methylation and histone modification within epigenomics. Dupras and Bunnik further say that they are not examining the privacy debate itself, as it has been widely discussed elsewhere: their particular concern is to examine the ways in which bringing different “omics” together can increase privacy risks. They also provide a formula for assessing privacy risks and offer a tabular form of this which is very useful. This is a timely and important contribution.
Developments in predictive biomarkers for hepatocellular carcinoma therapy
Published in Expert Review of Anticancer Therapy, 2020
Andrea Casadei-Gardini, Orsi Giulia, Caputo Francesco, Ercolani Giorgio
With the epigenomics technique it is possible to study the modifications, such as methylation and acetylation, of DNA and/or DNA-binding histone proteins, which are the processes that regulate gene expression and cellular phenotypes. Up to 50% of HCCs had epigenetic alterations [170], globally the HCC is hypomethylate but had specific locus-specific hypermethylation and hyperexpression of the DNA methyltransferases (DNMT1, DNMT3a and DNMT3b) [171]. A recent paper of the group of Pamplona highlighted a significant correlation between the overexpression of G9a, DNMT1, and UHRF1 and the poor outcome of the patients [172]. Interestingly, the same authors highlighted that the dual targeting of G9a and DNMT1 by CM-272 inhibited HCC cell growth with the potential of new target therapy.
Related Knowledge Centers
- DNA Methylation
- Epigenetics
- Epigenome
- Genomics
- Phenotypic Plasticity
- Protein
- Proteomics
- Rna
- Carcinogenesis
- Central Dogma of Molecular Biology