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Relevant bibliographies by topics / Epigenetic biology

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Academic literature on the topic 'Epigenetic biology'

Author: Grafiati

Published: 10 March 2023

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Journal articles on the topic "Epigenetic biology"

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McGowan, Patrick O., and Tania L. Roth. "Epigenetic pathways through which experiences become linked with biology." Development and Psychopathology 27, no. 2 (May 2015): 637–48. http://dx.doi.org/10.1017/s0954579415000206.

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AbstractThis article highlights the defining principles, progress, and future directions in epigenetics research in relation to this Special Issue. Exciting studies in the fields of neuroscience, psychology, and psychiatry have provided new insights into the epigenetic factors (e.g., DNA methylation) that are responsive to environmental input and serve as biological pathways in behavioral development. Here we highlight the experimental evidence, mainly from animal models, that factors such as psychosocial stress and environmental adversity can become encoded within epigenetic factors with functional consequences for brain plasticity and behavior. We also highlight evidence that epigenetic marking of genes in one generation can have consequences for future generations (i.e., inherited), and work with humans linking epigenetics, cognitive dysfunction, and psychiatric disorder. Though epigenetics has offered more of a beginning than an answer to the centuries-old nature–nurture debate, continued research is certain to yield substantial information regarding biological determinants of central nervous system changes and behavior with relevance for the study of developmental psychopathology.

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Ganesan, A. "Epigenetics: the first 25 centuries." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1748 (April 23, 2018): 20170067. http://dx.doi.org/10.1098/rstb.2017.0067.

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Epigenetics is a natural progression of genetics as it aims to understand how genes and other heritable elements are regulated in eukaryotic organisms. The history of epigenetics is briefly reviewed, together with the key issues in the field today. This themed issue brings together a diverse collection of interdisciplinary reviews and research articles that showcase the tremendous recent advances in epigenetic chemical biology and translational research into epigenetic drug discovery. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.

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Ivanova, Elitsa, Sandrine Le Guillou, Cathy Hue-Beauvais, and Fabienne Le Provost. "Epigenetics: New Insights into Mammary Gland Biology." Genes 12, no. 2 (February 5, 2021): 231. http://dx.doi.org/10.3390/genes12020231.

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The mammary gland undergoes important anatomical and physiological changes from embryogenesis through puberty, pregnancy, lactation and involution. These steps are under the control of a complex network of molecular factors, in which epigenetic mechanisms play a role that is increasingly well described. Recently, studies investigating epigenetic modifications and their impacts on gene expression in the mammary gland have been performed at different physiological stages and in different mammary cell types. This has led to the establishment of a role for epigenetic marks in milk component biosynthesis. This review aims to summarize the available knowledge regarding the involvement of the four main molecular mechanisms in epigenetics: DNA methylation, histone modifications, polycomb protein activity and non-coding RNA functions.

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Linquist, Stefan, and Brady Fullerton. "Transposon dynamics and the epigenetic switch hypothesis." Theoretical Medicine and Bioethics 42, no. 3-4 (August 2021): 137–54. http://dx.doi.org/10.1007/s11017-021-09548-x.

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AbstractThe recent explosion of interest in epigenetics is often portrayed as the dawning of a scientific revolution that promises to transform biomedical science along with developmental and evolutionary biology. Much of this enthusiasm surrounds what we call the epigenetic switch hypothesis, which regards certain examples of epigenetic inheritance as an adaptive organismal response to environmental change. This interpretation overlooks an alternative explanation in terms of coevolutionary dynamics between parasitic transposons and the host genome. This raises a question about whether epigenetics researchers tend to overlook transposon dynamics more generally. To address this question, we surveyed a large sample of scientific publications on the topics of epigenetics and transposons over the past fifty years. We found that enthusiasm for epigenetics is often inversely related to interest in transposon dynamics across the four disciplines we examined. Most surprising was a declining interest in transposons within biomedical science and cellular and molecular biology over the past two decades. Also notable was a delayed and relatively muted enthusiasm for epigenetics within evolutionary biology. An analysis of scientific abstracts from the past twenty-five years further reveals systematic differences among disciplines in their uses of the term epigenetic, especially with respect to heritability commitments and functional interpretations. Taken together, these results paint a nuanced picture of the rise of epigenetics and the possible neglect of transposon dynamics, especially among biomedical scientists.

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de Lima Camillo, Lucas Paulo, and Robert B. A. Quinlan. "A ride through the epigenetic landscape: aging reversal by reprogramming." GeroScience 43, no. 2 (April 2021): 463–85. http://dx.doi.org/10.1007/s11357-021-00358-6.

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AbstractAging has become one of the fastest-growing research topics in biology. However, exactly how the aging process occurs remains unknown. Epigenetics plays a significant role, and several epigenetic interventions can modulate lifespan. This review will explore the interplay between epigenetics and aging, and how epigenetic reprogramming can be harnessed for age reversal. In vivo partial reprogramming holds great promise as a possible therapy, but several limitations remain. Rejuvenation by reprogramming is a young but rapidly expanding subfield in the biology of aging.

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Riddiough, G. "MOLECULAR BIOLOGY: Epigenetic Origins." Science 305, no. 5682 (July 16, 2004): 311b. http://dx.doi.org/10.1126/science.305.5682.311b.

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Mir, Snober Shabnam, Uzma Afaq, Adria Hasan, Suroor Fatima Rizvi, and Sana Parveen. "Novel Insights into Epigenetic Control of Autophagy in Cancer." OBM Genetics 06, no. 04 (November 8, 2022): 1–45. http://dx.doi.org/10.21926/obm.genet.2204170.

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The autophagy mechanism recycles the damaged and long-standing macromolecular substrates and thus maintains cellular homeostatic and proteostatic conditions. Autophagy can be an unavoidable target in cancer therapy because its deregulation leads to cancer formation and progression. Cancer can be controlled by regulating autophagy at different genetic, epigenetic, and post-translational levels. Epigenetics refers to the heritable phenotypic changes that affect gene activity without changing the sequence. Modern biology employs epigenetic alterations as molecular tools to detect and treat a wide range of disorders, including cancer. However, modulating autophagy at the epigenetic level may inhibit cancer growth and progression. Epigenetics-targeting drugs involved in preclinical and clinical trials may trigger antitumor immunity. Here, we have reviewed some experimental evidence in which epigenetics have been used to control deregulated autophagy in cancerous diseases. Furthermore, we also reviewed some current clinical trials of epigenetic therapy against cancer. We hope that this information can be utilized in the near future to treat and overcome cancer.

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Sen, Rwik, and Christopher Barnes. "Do Transgenerational Epigenetic Inheritance and Immune System Development Share Common Epigenetic Processes?" Journal of Developmental Biology 9, no. 2 (May 12, 2021): 20. http://dx.doi.org/10.3390/jdb9020020.

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Epigenetic modifications regulate gene expression for development, immune response, disease, and other processes. A major role of epigenetics is to control the dynamics of chromatin structure, i.e., the condensed packaging of DNA around histone proteins in eukaryotic nuclei. Key epigenetic factors include enzymes for histone modifications and DNA methylation, non-coding RNAs, and prions. Epigenetic modifications are heritable but during embryonic development, most parental epigenetic marks are erased and reset. Interestingly, some epigenetic modifications, that may be resulting from immune response to stimuli, can escape remodeling and transmit to subsequent generations who are not exposed to those stimuli. This phenomenon is called transgenerational epigenetic inheritance if the epigenetic phenotype persists beyond the third generation in female germlines and second generation in male germlines. Although its primary function is likely immune response for survival, its role in the development and functioning of the immune system is not extensively explored, despite studies reporting transgenerational inheritance of stress-induced epigenetic modifications resulting in immune disorders. Hence, this review draws from studies on transgenerational epigenetic inheritance, immune system development and function, high-throughput epigenetics tools to study those phenomena, and relevant clinical trials, to focus on their significance and deeper understanding for future research, therapeutic developments, and various applications.

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Peixoto, Paul, Pierre-François Cartron, Aurélien A. Serandour, and Eric Hervouet. "From 1957 to Nowadays: A Brief History of Epigenetics." International Journal of Molecular Sciences 21, no. 20 (October 14, 2020): 7571. http://dx.doi.org/10.3390/ijms21207571.

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Due to the spectacular number of studies focusing on epigenetics in the last few decades, and particularly for the last few years, the availability of a chronology of epigenetics appears essential. Indeed, our review places epigenetic events and the identification of the main epigenetic writers, readers and erasers on a historic scale. This review helps to understand the increasing knowledge in molecular and cellular biology, the development of new biochemical techniques and advances in epigenetics and, more importantly, the roles played by epigenetics in many physiological and pathological situations.

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Pacini, Clare, and Magdalena J. Koziol. "Bioinformatics challenges and perspectives when studying the effect of epigenetic modifications on alternative splicing." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1748 (April 23, 2018): 20170073. http://dx.doi.org/10.1098/rstb.2017.0073.

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It is widely known that epigenetic modifications are important in regulating transcription, but several have also been reported in alternative splicing. The regulation of pre-mRNA splicing is important to explain proteomic diversity and the misregulation of splicing has been implicated in many diseases. Here, we give a brief overview of the role of epigenetics in alternative splicing and disease. We then discuss the bioinformatics methods that can be used to model interactions between epigenetic marks and regulators of splicing. These models can be used to identify alternative splicing and epigenetic changes across different phenotypes. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.

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Dissertations / Theses on the topic "Epigenetic biology"

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Kizaki, Seiichiro. "Chemical Biology Study on DNA Epigenetic Modifications." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225420.

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Rosselló, Tortella Margalida. "Epigenetic Regulation of tRNA Biology in Cancer." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673026.

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Transfer RNAs (tRNAs) are essential molecules that allow the translation of the genetic code into amino acids. Extensive research during the last 50 years have revealed that, despite their apparently simple structure and function, tRNAs are more than simple adaptors in protein synthesis –they are of high importance in normal cell functions. Reinforcing this, tRNA levels are tightly regulated to match the codon usage patterns of a given cell type or cellular status to meet the cellular specific needs and adapt to stress. Moreover, tRNA nucleoside modifications are critical for their function at multiple levels, such as translation efficiency and fidelity, wobbling and fragmentation. The relevance of tRNA regulation in cell physiology is emphasized by the recent discovery that these molecules and their derived fragments are deregulated in cancer. Not only tRNA biology imbalance is associated to malignant transformation, but it also actively participates in it. These alterations occur at multiple levels of tRNA biology, such as expression, nucleoside modification and fragmentation, but many open questions remain unanswered. Cancer- specific tRNA deregulation is a very new and still unexplored discipline, and further studies are required to fully understand the molecular mechanisms that account for these alterations and their relevance in tumor biology. Because alterations in DNA methylation constitute a frequent mechanism by which transformed cells acquire their malignant characteristics, the cornerstone of this thesis is the description of epigenetic lesions that support the cancer-associated tRNA deregulation. To this end, we have designed and performed two independent studies to unveil the epigenetic regulation of tRNA biology in cancer. In the first study, we highlighted the tumor-specific epigenetic silencing of TYW2 as a mechanism to induce tRNAPhe hypomodification at position 37, a phenomenon that was observed for the first time more than forty years ago but whose cause and consequences have remained obscure. Our results established the connection between this epigenetic defect and a phenotype that enhances -1 ribosome frameshifting events to ultimately confer increased migratory capacities and mesenchymal features to the transformed colon cells. In the second study, we established a founded connection between cancer-associated DNA methylation defects with alterations in the expression of specific tRNAs. Our analyses also revealed that the oncogenic tRNA-Arg-TCT-4-1 overexpression in endometrial cancer was guided by DNA hypomethylation. Most importantly from the clinical perspective, the epigenetic alterations identified in both studies can anticipate the patients’ outcome, for which they may serve as biomarkers to allow the identification of high-risk patients that may benefit from a more comprehensive surveillance or complementary therapeutic strategies.
Els ARN de transferència (tRNAs) són d’una importància clau en la regulació de la síntesi proteica i l’expressió gènica. La seva rellevància en la fisiologia cel·lular es veu reforçada pel descobriment que aquestes molècules i els seus derivats estan alterats en patologies com el càncer, on contribueixen activament. Les alteracions dels tRNAs en càncer suposen una nova disciplina d’estudi on encara moltes preguntes romanen obertes per tal d’arribar a comprendre quines són les causes d’aquestes defectes i quin impacte tenen sobre la malaltia. Aquesta tesi té com objectiu identificar i caracteritzar alteracions en la metilació de l’ADN subjacents als desequilibris en la biologia dels tRNAs de les cèl·lules tumorals. En el primer estudi, hem descobert el silenciament epigenètic de l’enzim TYW2 en càncer colorectal com a causa de la hipomodificació del tRNAPhe, un fenomen que va ser descrit per primer cop fa més de quaranta anys però les causes i conseqüències del qual no van ser mai estudiades. Els nostres resultats estableixen una clara connexió entre aquest defecte epigenètic i un fenotip que és propens a potencial el frameshift dels ribosomes, cosa que augmenta la capacitat migratòria de les cèl·lules de càncer de colon. El segon estudi ha servit per caracteritzar la relació entre els canvis en la metilació de l’ADN i les alteracions en l’expressió dels tRNAs en càncer. Els nostres resultats han revelat que l’expressió de tRNA-Arg-TCT-4-1 augmenta en càncer d’endometri arrel de la hipometilació del seu gen. Més enllà d’aquests dos mecanismes epigenètics per modular la biologia dels tRNAs, els nostres estudis estableixen una connexió entre aquestes lesions epigenètiques i la prognosi dels pacients amb certs tipus de tumor, per la qual cosa podrien proposar-se com biomarcadors per identificar pacients de risc.

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Weaver, Ian Cassford Gordon. "Epigenetic programming by maternal behaviour." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102231.

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Individual differences in gene expression and behaviour are the result of an interaction between a given set of genes and a variety of environmental conditions. The study of epigenetics focuses on the nature of this interaction. The early developmental period in the life of a mammal is exquisitely sensitive to environmental cues. One critical question is how is the genome capable of adapting to these developmental or environmental signals? Building on an established rodent model, in which the effects of maternal care have been demonstrated to regulate the development and expression of neurobiological and behavioural measures in offspring as adults, the current project concerns how events during the first week of life can have sustained effects on gene expression, which persist throughout the life of the organism.
The research presented in this thesis demonstrates how one facet of mothering style leads to a cascade of molecular and cellular changes, resulting in life-long alterations in the nature of stress responses and neuron survival. Frequent licking/grooming by rat mothers alters DNA methylation of the hippocampal glucocorticoid receptor (GR) gene and acetylation of histones early in life, providing a mechanism for these permanent changes in stress responses. Through postnatal cross-fostering studies, I was able to directly study how an identical gene within the same rat strain is expressed and regulated under the different developmental environments and how such effects on gene expression persist through life. I have also examined the potential for reversibility of the long-term consequences of postnatal environment and have demonstrated that both GR levels and the nature of stress responses exhibit a high degree of plasticity in adulthood in response to both pharmacological intervention and dietary amino-acid supplementation. These results demonstrate that the epigenomic marks established early in life through a behavioural mode of programming, are dynamically maintained and potentially reversible in the adult brain. These results contrast with the very dogmatic view that the genome is rendered fixed and immutable. I next questioned the global effects of early-in-life experience on the hippocampal transcriptome and anxiety-mediated behaviours in adulthood. Microarray analysis revealed > 900 different maternal care-responsive mRNA transcripts. These results suggest that effects of early life experience have a stable and broad effect on the hippocampal transcriptome, which may play a role in the development of anxiety-mediated behaviours through life. Finally, both in vivo and in vitro studies show that maternal behaviour increases GR expression in the offspring via increased hippocampal serotonergic tone accompanied by increased histone acetylase transferase activity, histone acetylation and DNA demethylation mediated by the transcription factor NGFI-A.
In summary, this research demonstrates that an epigenetic state of a gene can be established through early-in-life experience, and is potentially reversible in adulthood. We predict that epigenetic modifications of targeted regulatory sequences in response to variations in environmental conditions might serve as a major source of variation in biological and behavioural phenotypes. In the case of GR, the resulting individual differences in behavioural and physiological responses to stress are thought to be a major risk factor for the development of psychiatric and physical illness. Thus, in addition to contributing to our understanding of how gene-environment interactions shape development, our work provides a mechanism that can be targeted for therapeutic intervention to potentially reduce the prevalence of these disorders.

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Magnell, Albert T. (Albert Thomas). "Epigenetic Memory of Mouse Intestinal Inflammation." Thesis, Massachusetts Institute of Technology, 2021. https://hdl.handle.net/1721.1/130670.

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Thesis: S.M., Massachusetts Institute of Technology, Department of Biology, 2021
Cataloged from the official PDF version of thesis.
Includes bibliographical references (pages 29-31).
The gut, encompassing one of the largest epithelial surfaces in the body, interacts with both biological and non-biological agents that can cause regular injury. Fortunately, the small intestinal epithelium has a remarkable capacity to repair itself after severe injury, due to the abundance of highly replicative stem cells housed in the intestinal crypt regions. Much remains to be understood about the activation processes of the repair mechanisms and to what extent the stem cells themselves can adapt to certain forms of damage, including molecular mechanisms related to gene regulation. Here, I show that in response to acute inflammation, chromatin in intestinal stem cells has increased accessibility around specific loci and that this state is maintained in some regions even after the epithelium has recovered from damage, suggesting the possibility of memory. Such epigenetic memory may confer some adaptive resiliency to subsequent damage.
by Albert T. Magnell.
S.M.
S.M. Massachusetts Institute of Technology, Department of Biology

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Lezcano, Magda. "The Control of the Epigenome." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7190.

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The genetic information required for the existence of a living cell of any kind is encoded in the sequence information scripted in the double helix DNA. A modern trend in biology struggles to come to grip with the amazing fact that there are so many different cell types in our body and that they are directed from the same genomic blueprint. It is clear, that the key to this feature is provided by epigenetic information that dictates how, where and when genes should be expressed. Epigenetic states “dress up” the genome by packaging it in chromatin conformations that differentially regulate accessibility for key nuclear factors and in coordination with differential localizations within the nucleus will dictate the ultimate task, expression. In the imprinted Igf2/H19 domain, this feature is determined by the interaction between the chromatin insulator protein CTCF and the unmethylated H19 imprinting control region. Here I show that CTCF interacts with many sites genome-wide and that these sites are generally protected from DNA methylation, suggesting that CTCF function has been recruited to manifest novel imprinted states during mammalian development. This thesis also describes the discovery of an epigenetically regulated network of intra and interchromosomal complexes, identified by the invented 4C method. Importantly, the disruption of CTCF binding sites at the H19 imprinting control region not only disconnects this network, but also leads to significant changes in expression patterns in the interacting partners. Interestingly, CTCF plays an important role in the regulation of the replication timing not only of the Igf2 gene, but also of all other sequences binding this factor potentially by a cell cycle-specific relocation of CTCF-DNA complexes to subnuclear compartments. Finally, I show that epigenetic marks signifying active or inactive states can be gained and lost, respectively, upon exposure to stress. As many genes belonging to the apoptotic pathway are upregulated we propose that stress-induced epigenetic lesions represent a surveillance system marking the affected cells for death to the benefit of the individual. This important observation opens our minds to the view of new intrinsic mechanisms that the cell has in order to maintain proper gene expression, and in the case of misleads there are several check points that direct the cell to towards important survival decisions.

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Vadnal, Jonathan. "Epigenetic Mechanisms in Neurodegenerative Disease." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1353955013.

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Tavoosidana, Gholamreza. "Epigenetic Regulation of Genomic Imprinting and Higher Order Chromatin Conformation." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7435.

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The genetic information encoded by the DNA sequence, can be expressed in different ways. Genomic imprinting is an epigenetic phenomenon that results in monoallelic expression of imprinted genes in a parent of origin-dependent manner. Imprinted genes are frequently found in clusters and can share common regulatory elements. Most of the imprinted genes are regulated by Imprinting Control Regions (ICRs). H19/Igf2 region is a well known imprinted cluster, which is regulated by insulator function of ICR located upstream of the H19 gene. It has been proposed that the epigenetic control of the insulator function of H19 ICR involves organization of higher order chromatin interactions. In this study we have investigated the role of post-translational modification in regulating insulator protein CTCF (CCCTC-binding factor). The results indicated novel links between poly(ADP-ribosyl)ation and CTCF, which are essential for regulating insulators function. We also studied the higher order chromatin conformation of Igf2/H19 region. The results indicated there are different chromatin structures on the parental alleles. We identified CTCF-dependent loop on the maternal allele which is different from the paternal chromatin and is essential for proper imprinting of Igf2 and H19 genes. The interaction of H19 ICR with Differentially Methylated Regions (DMRs) of Igf2 in a parent-specific manner maintains differential epigenetic marks on maternal and paternal alleles. The results indicate that CTCF occupies specific sites on highly condensed mitotic chromosomes. CTCF-dependent long-range key interaction on the maternal allele is maintained during mitosis, suggesting the possible epigenetic memory of dividing cells. In this study, we developed a new method called Circular Chromosome Conformation Capture (4C) to screen genome-wide interactions with H19 ICR. The results indicated there are wide intra- and inter-chromosomal interactions which are mostly dependent on CTCF-binding site at H19 ICR. These observations suggest new aspects of epigenetic regulation of the H19/Igf2 imprinted region and higher order chromatin structure.

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Huang, Chieh-Ting. "Epigenetic involvement of GluR2 regulation in Epileptogenesis." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106297.

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Epilepsy is one of the most common neurological disorders characterized by recurrent seizures. Currently, the underlying mechanisms are not well understood and therapies only serve to relieve the symptoms. A single episode of seizure can trigger epileptogenesis, a process in which the brain undergoes network reorganization including neurodegeneration and sprouting of axons. The mechanisms linking the first seizure to development of epilepsy are currently unknown. Interestingly, changes in neuronal circuitry in epilepsy are accompanied by chronic alterations in the normal brain gene expression profile. Epigenetic mechanisms, including DNA methylation and covalent histone modifications stably program the genome during gestation. However, recent studies suggest also that epigenetic mechanisms might be involved in modifying genome function in response to environmental stimuli. We therefore hypothesize that a single seizure can disrupt normal epigenetic programming in the brain, which results in altered gene expression profiles that drive the network reorganization events. In this study, we used in vitro and in vivo models of temporal lobe epilepsy (TLE) by kainic acid treatment to test whether DNA methylation changes are associated with epileptogenesis. DNA methylation is a covalent modification of DNA by adding a methyl group on the 5' position of cytosine by DNA methyltransferases. We focused our analysis on DNA methylation because of its importance role in gene regulation. Indeed there is an overall inverse correlation between DNA methylation of regulatory regions of genes and gene expression. We closely examined the DNA methylation changes associated with the promoters of the GriA2 gene (codes for glutamate receptor ionotropic AMPA 2 subunit), which has been demonstrated to be down-regulated in epilepsy and to be highly implicated in hyper-excitable neuronal circuitries. We detected rapid hypermethylation in GriA2 after a 2-hour period of epileptiform activity in the in vitro model. Similar changes in GriA2 DNA methylation were also observed in our in vivo model 10 weeks post-kainic acid injection. We also observed a significant positive correlation between the number of seizures recorded by video-EEG and severity assessed by Racine scale and the average GriA2 DNA methylation. Epileptogenic insults induced by kainic acid treatment led to rapid DNA methylation changes in GriA2 gene. This result suggests that alterations in DNA methylation may serve as a molecular memory of the insult, which can lead to the progressive changes in gene expressions, thus contributing to the development of epilepsy as well as the maintenance of an epileptic neuronal circuitry.
L'épilepsie est l'une des maladies neurologiques les plus fréquentes, caractérisée par des crises épileptiques répétées et chroniques. Les mécanismes sous-tendant les troubles neurologiques associés à la maladie sont encore mal compris et seuls des traitements symptomatiques sont actuellement disponibles. Une seule crise épileptique peut induire un processus d'épileptogenèse durant lequel une réorganisation des circuits neuronaux s'effectue, incluant une neurodégénérescence et un bourgeonnement anormal des axones. Les mécanismes conduisant au développement de la maladie épileptique en tant que telle à partir d'un premier épisode épileptique sont encore inconnus. De façon intéressante, les réarrangements des circuits neuronaux observés dans l'épilepsie sont accompagnés de changements stables de schémas d'expression de gènes. Les mécanismes épigénétiques, incluant la méthylation de l'ADN ou les modifications covalentes des histones, permettent une régulation stable des schémas d'expression des gènes se mettant en place durant la gestation. Cependant, de récentes études suggèrent que ces mécanismes épigénétiques permettent également une réorganisation des schémas d'expression de gènes en réponse à des stimuli environnementaux. Nous avons alors émis l'hypothèse qu'un seul épisode épileptique peut perturber les profils épigénétiques cérébraux normaux, aboutissant à des schémas d'expression de gènes altérés et aux réorganisations cérébrales caractéristiques de l'épilepsie. Lors de cette étude, nous avons utilisés des modèles in vitro et in vivo de l'épilepsie du lobe temporal (TLE), par traitements au kaïnate, afin de tester si des changements de méthylation de l'ADN sont associés au processus d'épileptogenèse. La méthylation de l'ADN est un processus épigénétique dans lequel les bases cytosines peuvent être modifiées par l'addition d'un groupement méthyle lors d'une réaction catalysée par des ADN méthyltransférases. Nous avons focalisé notre étude sur l'étude des changements de méthylation de l'ADN en raison de son rôle important dans la régulation de l'expression des gènes. En effet, le niveau de méthylation de régions régulatrices de l'ADN telles que les promoteurs est corrélé négativement au niveau d'expression génique. Nous avons en particulier mesuré les modifications des niveaux de méthylation des promoteurs du gène GriA2 (codant pour la sous-unité 2 du récepteur gutamatergique ionotropique AMPA), qui est sous-exprimé dans l'épilepsie et dont la protéine est fortement impliquée dans l'hyperexcitabilité neuronale observée dans les crises épileptiques. Nous avons mesuré une hyperméthylation du gène GriA2 à la suite d'une période de 2 heures d'activité épileptiforme dans le modèle in vitro. Des modifications similaires ont également été observées dans le modèle in vivo, 10 semaines après une injection intracérébrale de kaïnate. Nous avons également observé une corrélation positive significative entre le nombre de crises épileptiques, détectées par Electro-Encéphalogramme Vidéo, la sévérité des crises, évaluée grâce à l'échelle Racine, et le niveau moyen de méthylation du gène GriA2.Les crises épileptiques, induites par un traitement au kaïnate, conduisent à des changements rapides des niveaux de méthylation du gène GriA2. Ce résultat suggère que des modifications des schémas de méthylation de l'ADN pourraient être un mécanisme moléculaire de mémorisation des crises épileptiques, conduisant à des changements progressifs d'expression de gènes et contribuant au développement de l'épilepsie et au maintien de circuits neuronaux anormaux.

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Khan, Maria Mohammad. "Computational Biology in the Analysis of Epigenetic Nuclear Self-Organization." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146042.

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The function of the nucleus is central to the survival of cells and thus life as a whole. Among other processes, it is the site of gene expression, DNA repair, and genome stability. These functions are carried in the context of a complex nuclear architecture. The nucleus is compartmentalized both spatially and functionally. These compartments are proteinaceous nuclear bodies or chromatin domains, both of which are not segregated from other compartments by membranes-as are the organelles of cells. Specifically, proteinaceous nuclear bodies are characterized as regions within the nucleus with distinct sets of inhabitant proteins. Examples of such proteinaceous nuclear bodies include the nucleolus, splicing factor compartments, and the Cajal body. The nucleolus is the location of the transcription and processing of ribosomal RNA and the Cajal body is the site of snRNP assembly, while the splicing factor compartments are a storage and assembly site for spliceosomal components.

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Nuthikattu, Saivageethi. "Diverse mechanisms of Athila retrotransposon epigenetic silencing in Arabidopsis thaliana." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417685369.

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Books on the topic "Epigenetic biology"

1

Epigenetic principles of evolution. London: Elsevier, 2012.

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Cabej, Nelson R. Epigenetic Principles of Evolution. Burlington: Elsevier Science, 2011.

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Torday, John, and William Miller. Cellular-Molecular Mechanisms in Epigenetic Evolutionary Biology. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38133-2.

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C, Goodwin Brian, and Saunders P. T. 1939-, eds. Theoretical biology: Epigenetic and evolutionary order from complex systems. Baltimore: Johns Hopkins University Press, 1992.

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Hurd, Paul J., Adele Murrell, and Ian C. Wood. Epigenetic mechanisms in development and disease. London: Portland Press Limited, 2013.

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J, Lamb Marion, ed. Epigenetic inheritance and evolution: The Lamarckian dimension. Oxford: Oxford University Press, 1995.

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Evolution in four dimensions: Genetic, epigenetic, behavioral, and symbolic variation in the history of life. Cambridge, MA: MIT Press, 2004.

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1925-, Johnen A. G., and Albers B. 1953-, eds. The epigenetic nature of early chordate development: Inductive interaction and competence. Cambridge [Cambridgeshire]: Cambridge University Press, 1985.

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Epigenomics, from chromatin biology to therapeutics. Cambridge: Cambridge University Press, 2012.

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Manel, Esteller, ed. Epigenetics in biology and medicine. Boca Raton: Taylor & Francis, 2008.

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Book chapters on the topic "Epigenetic biology"

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Soltani, Jalal. "Fungal Epigenetic Engineering." In Fungal Biology, 1–15. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41870-0_1.

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Walters, Kevin. "Epigenetic Variation." In Methods in Molecular Biology, 185–97. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-416-6_14.

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Huang, Yufei. "Epigenetic Regulation." In Encyclopedia of Systems Biology, 665. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_817.

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Verma, Mukesh, and Hirendra Nath Banerjee. "Epigenetic Inhibitors." In Methods in Molecular Biology, 469–85. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1804-1_24.

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Puduvalli, Vinay K. "Epigenetic Changes in Gliomas." In Glioma Cell Biology, 23–45. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1431-5_2.

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Brennan, Kevin, and James M. Flanagan. "Epigenetic Epidemiology for Cancer Risk: Harnessing Germline Epigenetic Variation." In Methods in Molecular Biology, 439–65. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-612-8_27.

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Rosen, Evan D. "Epigenetic Approaches to Adipose Biology." In Research and Perspectives in Endocrine Interactions, 101–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13517-0_10.

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Hu, Li-Fang. "Epigenetic Regulation of Autophagy." In Autophagy: Biology and Diseases, 221–36. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0602-4_11.

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Tollefsbol, Trygve O. "Advances in Epigenetic Technology." In Methods in Molecular Biology, 1–10. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-316-5_1.

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Heil, Sandra G. "Epigenetic Techniques in Pharmacogenetics." In Methods in Molecular Biology, 179–88. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-435-7_11.

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Conference papers on the topic "Epigenetic biology"

1

Tekutskaya, E., I. Raybova, and Lyubov Ramazanovna Gusaruk. "THE DEGREE OF OXIDATIVE DAMAGE TO DNA IN VITRO AS A MOLECULAR PREDICTOR OF DISORDERS CAUSED BY EPIGENETIC AND EXOGENOUS FACTORS." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.49.

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In this work, we studied the mechanisms of oxidative damage to DNA molecules isolated from whole blood of healthy donors and patients with epigenetic disease (epidermolysis bullosa) when exposed to an alternating magnetic field of low frequency in vitro, associated with the formation of reactive oxygen species.

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Zhang, Wei. "Epigenetic regulation of effector gene expression in fungal plant pathogen." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1372292.

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"Epigenetic landscape in human aneuploid embryos." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-255.

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Weiss, Trevor. "Dissecting epigenetic and chromatin influences on CRISPR/Cas9 geme editing and DNA repair." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1374639.

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Aier, Imlimaong, and Utkarsh Raj. "Exploring the role of EZH2 (PRC2) as epigenetic target." In 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552131.

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"Functional annotation of lncRNAs involved in epigenetic regulation." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-042.

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Campos Bermudez, Valeria Alina. "G-quadruplex: Potential epigenetic memory involved in priming induced by Trichoderma in maize plants." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.561509.

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Polyak, Kornelia. "Abstract IA28: Epigenetic heterogeneity in breast cancer." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-ia28.

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Liang, S., Yue Lu, J. Jelinek, M. Estecio, Hao Li, and J. P. Issa. "Analysis of epigenetic modifications by next generation sequencing." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5332853.

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Lawrence, Aamna, Rahul Shukla, Utkarsh Raj, and Pritish Kumar Varadwaj. "Estimating percentage epigenetic modifications in human genome using NGS data." In 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552141.

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