Relevant bibliographies by topics / Epigenetic memory

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Epigenetic memory'

Author: Grafiati
Published: 9 March 2023

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Journal articles on the topic "Epigenetic memory"

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Rusk, Nicole. "Synthetic epigenetic memory." Nature Methods 14, no. 8 (August 2017): 764. http://dx.doi.org/10.1038/nmeth.4382.

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Rusk, Nicole. "Creating epigenetic memory." Nature Methods 16, no. 2 (January 30, 2019): 141. http://dx.doi.org/10.1038/s41592-019-0312-3.

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D’Urso, Agustina, and Jason H. Brickner. "Epigenetic transcriptional memory." Current Genetics 63, no. 3 (November 2, 2016): 435–39. http://dx.doi.org/10.1007/s00294-016-0661-8.

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Mladenov, Velimir, Vasileios Fotopoulos, Eirini Kaiserli, Erna Karalija, Stephane Maury, Miroslav Baranek, Na'ama Segal, et al. "Deciphering the Epigenetic Alphabet Involved in Transgenerational Stress Memory in Crops." International Journal of Molecular Sciences 22, no. 13 (July 1, 2021): 7118. http://dx.doi.org/10.3390/ijms22137118.

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Although epigenetic modifications have been intensely investigated over the last decade due to their role in crop adaptation to rapid climate change, it is unclear which epigenetic changes are heritable and therefore transmitted to their progeny. The identification of epigenetic marks that are transmitted to the next generations is of primary importance for their use in breeding and for the development of new cultivars with a broad-spectrum of tolerance/resistance to abiotic and biotic stresses. In this review, we discuss general aspects of plant responses to environmental stresses and provide an overview of recent findings on the role of transgenerational epigenetic modifications in crops. In addition, we take the opportunity to describe the aims of EPI-CATCH, an international COST action consortium composed by researchers from 28 countries. The aim of this COST action launched in 2020 is: (1) to define standardized pipelines and methods used in the study of epigenetic mechanisms in plants, (2) update, share, and exchange findings in epigenetic responses to environmental stresses in plants, (3) develop new concepts and frontiers in plant epigenetics and epigenomics, (4) enhance dissemination, communication, and transfer of knowledge in plant epigenetics and epigenomics.
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Lubin, Farah D., Swati Gupta, R. Ryley Parrish, Nicola M. Grissom, and Robin L. Davis. "Epigenetic Mechanisms." Neuroscientist 17, no. 6 (April 1, 2011): 616–32. http://dx.doi.org/10.1177/1073858410386967.

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Recent advances in chromatin biology have identified a role for epigenetic mechanisms in the regulation of neuronal gene expression changes, a necessary process for proper synaptic plasticity and memory formation. Experimental evidence for dynamic chromatin remodeling influencing gene transcription in postmitotic neurons grew from initial reports describing posttranslational modifications of histones, including phosphorylation and acetylation occurring in various brain regions during memory consolidation. An accumulation of recent studies, however, has also highlighted the importance of other epigenetic modifications, such as DNA methylation and histone methylation, as playing a role in memory formation. This present review examines learning-induced gene transcription by chromatin remodeling underlying long-lasting changes in neurons, with direct implications for the study of epigenetic mechanisms in long-term memory formation and behavior. Furthermore, the study of epigenetic gene regulation, in conjunction with transcription factor activation, can provide complementary lines of evidence to further understanding transcriptional mechanisms subserving memory storage.
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Roth, Tania L., Eric D. Roth, and J. David Sweatt. "Epigenetic regulation of genes in learning and memory." Essays in Biochemistry 48 (September 20, 2010): 263–74. http://dx.doi.org/10.1042/bse0480263.

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Rapid advances in the field of epigenetics are revealing a new way to understand how we can form and store strong memories of significant events in our lives. Epigenetic modifications of chromatin, namely the post-translational modifications of nuclear proteins and covalent modification of DNA that regulate gene activity in the CNS (central nervous system), continue to be recognized for their pivotal role in synaptic plasticity and memory formation. At the same time, studies are correlating aberrant epigenetic regulation of gene activity with cognitive dysfunction prevalent in CNS disorders and disease. Epigenetic research, then, offers not only a novel approach to understanding the molecular transcriptional mechanisms underlying experience-induced changes in neural function and behaviour, but potential therapeutic treatments aimed at alleviating cognitive dysfunction. In this chapter, we discuss data regarding epigenetic marking of genes in adult learning and memory formation and impairment thereof, as well as data showcasing the promise for manipulating the epigenome in restoring memory capacity.
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Hörmanseder, Eva. "Epigenetic memory in reprogramming." Current Opinion in Genetics & Development 70 (October 2021): 24–31. http://dx.doi.org/10.1016/j.gde.2021.04.007.

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Iwasaki, Mayumi, and Jerzy Paszkowski. "Epigenetic memory in plants." EMBO Journal 33, no. 18 (August 7, 2014): 1987–98. http://dx.doi.org/10.15252/embj.201488883.

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Dean, Caroline. "What holds epigenetic memory?" Nature Reviews Molecular Cell Biology 18, no. 3 (March 2017): 140. http://dx.doi.org/10.1038/nrm.2017.15.

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D’Urso, Agustina, and Jason H. Brickner. "Mechanisms of epigenetic memory." Trends in Genetics 30, no. 6 (June 2014): 230–36. http://dx.doi.org/10.1016/j.tig.2014.04.004.

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Dissertations / Theses on the topic "Epigenetic memory"

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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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Chandramohan, Yalini. "Epigenetic mechanisms underlying stress-related learning and memory." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492580.

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An organism exposed to a stressful situation will undergo a complex array of physiological and behavioural changes aimed at the preservation of the organism during the stressful event as well as at stimulating adaptive and mnemonic processes in case the event would reoccur in the future. It is well-known that the hippocampus is highly involved in these processes. It has become clear in recent years that the processing of environmental stimuli in the hippocampus could be via changes in epigenetic state that lead to changes in neural function.
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Gookin, Dylon Kyle. "Epigenetic Mechanisms for Long-Term Memory Acquisition and Maintenance." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579049.

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In this review, we will explore the evidence that supports an epigenetic foundation for learning and memory. Through this, we will first review the basics of both learning and memory before delving into the foundational mechanisms for epigenetics. Understanding this, we will examine the evidence that suggest a link between epigenetics and long-term memory by observing two distinct directionalities: 1) the procession of learning into consolidation of a memory, and how this affects an organisms genetic code, and 2) the manifestation of change in behavior as a result of the aforementioned epigenetic changes to an organism's DNA. Beyond this, lapses in our current understanding will be discussed, and suggestions for future work will be outlined.
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Cherubini, A. "MYC-DRIVEN EPIGENETIC MEMORY MAINTAINS EMBRYONIC STEM CELL IDENTITY." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/356044.

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Stem cells balance their self-renewal and differentiation potential by integrating environmental signals with the Transcriptional Regulatory Network (TRN). Moreover, the integration between extrinsic and intrinsic signals affects the maintenance of their epigenetic state, establishing an accurate cells identity. Although c-Myc transcription factors plays a major role in stem cells self-renewal and pluripotency, their mechanisms of actions and their ability to establish an epigenetic memory remains poorly defined. We addressed this point by profiling the epigenetic pattern and gene expression in Embryonic Stem (ES) cells, whose growth depends on conditional c-Myc activity. Here we show that c-Myc potentiates the Wnt/β- Catenin signaling pathway, which cooperates with the transcriptional regulatory network in sustaining ES cells self-renewal. c-Myc activation results in the transcriptional repression of Wnt antagonists Dkk1 and Sfrp1 through the direct recruitment of PRC2 on these targets. We found that, through these molecular mechanisms, c-Myc promotes pluripotency and self-renewal of ES cells by activating an alternative epigenetic program. Finally our data suggest that the consequent potentiation of the autocrine Wnt/β-Catenin signaling induces the transcriptional activation of the endogenous Myc family members, which in turn activates a Myc-driven self-reinforcing circuit. Thus, our data unravel a Myc-dependent selfpropagating epigenetic memory in the maintenance of ES cell identity.
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Kłosin, Adam 1985. "Mechanism and dynamics of transgenerational epigenetic memory in Caenorhabditis elegans." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/482206.

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Desde Darwin y Lamarck, a los biólogos les ha intrigado la posibilidad de que rasgos adquiridos debido al ambiente pudieran ser heredados. Se han descrito muchos ejemplos de este tipo debidos a perturbaciones del ambiente y transmitidos durante generaciones en numerosas especies, aunque por el momento no se conoce su regulación a nivel molecular. Usando C. elegans como modelo demostramos que el aumento de la expresión de un transgén artificial en células somáticas inducido por altas temperaturas es conservado durante múltiples generaciones. Esta memoria epigenética está regulada por la transmisión entre generaciones de dos memorias epigenéticas: el principal regulador de los niveles de expresión en la siguiente generación es la transmisión en cis de la modificación de la histona H3K9me3, mientras que los represores RNA pequeños (dsRNA) se heredan en trans y actúan de mediadores en la restitución del estado reprimido de la cromatina. Además, la puesta a cero epigenética es reforzada por la comunicación desde células somáticas a germinales regulada por el canal de dsRNA SID-1. También demostramos finalmente que un estrés en la replicación del DNA durante el desarrollo embrionario interfiere con la transmisión epigenética del estado reprimido de la cromatina. Estos resultados contribuyen a aumentar el conocimiento que tenemos de la herencia epigenética y la posible puesta a cero de los rasgos adquiridos debidos a cambios en el ambiente.
Since Darwin and Lamarck, biologists have been intrigued by the possibility of the inheritance of environmentally-acquired traits. Examples of inter-generational transmission of traits induced by an environmental perturbation have been reported in multiple species, but the molecular mechanisms governing these responses remain obscure. Using C. elegans as a model system we demonstrate that high temperature-induced increase in expression from a somatically expressed transgene array persists for multiple generations. This epigenetic memory is governed by transgenerational transmission of two conflicting epigenetic memories: H3K9me3 histone marks are inherited in cis and act as the major determinant of expression levels in the next generation, whereas repressive small RNAs are inherited in trans and mediate restoration of the repressed state. In addition, epigenetic resetting is reinforced by soma to germline communication mediated by the dsRNA channel SID-1. Finally, we discovered that replication stress during early embryonic development interferes with epigenetic inheritance of a repressed state. These findings contribute to our understanding of the epigenetic inheritance and eventual resetting of environmentally acquired traits.
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Boudadi, Elsa. "Histone modification, gene regulation and epigenetic memory in embryonic stem cells." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3160/.

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Histone modifications are thought to act as a layer of epigenetic information, because of their strong association with gene expression, and their potential role in transcriptional memory. However, although specific histone modifications correlate with transcriptional status, whether they play a causative role or act in the long term inheritance of gene expression patterns is unclear. In order to explore this, the histone deacetylase inhibitor valproic acid (VPA) was used to induce hyperacetylation of histones in embryonic stem cells. Surprisingly, although global levels of acetyl marks were highly increased by VPA treatment (up to 16-fold), only 10% of genes showed transcriptional changes. Interestingly, these global changes in histone modification were not reflected in the changes at individual genes where increases in acetylation were rarely greater than 2-fold. Furthermore, changes in acetylation levels did not correlate with transcriptional effects. Wash-out experiments showed that transient VPA treatment could not induce long term effects on transcription, even during ES cell differentiation when histone modifications play a crucial role. Finally, the role of polycomb silencing in the response to VPA treatment was assessed using an ES cell line in which the polycomb components Eed and Ring1b had been knocked out. Target genes showed small up-regulation in knockout cells but VPA did not further induce transcription. It was concluded that histone acetylation plays an important role in transcription but additional signals are required for transcriptional induction and cellular memory. My results suggest the existence of protective mechanisms against hyperacetylation and highlight the complexity of epigenetic regulation, potentially involving many layers of control.
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Ng, Kit. "Epigenetic memory of donor cell differentiation status in Xenopus nuclear transplant embryos." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615284.

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VIGORELLI, VERA. "CD34+ stem cells and epigenetic memory: key players and pharmacological targets in diabetic cardiovascular complication." Doctoral thesis, Università degli studi di Pavia, 2020. http://hdl.handle.net/11571/1371994.

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Seaborne, R. A. "The role of DNA methylation in the regulation of skeletal muscle atrophy, hypertrophy and epigenetic 'memory'." Thesis, Liverpool John Moores University, 2018. http://researchonline.ljmu.ac.uk/9473/.

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Skeletal muscle mass is vitally important for the maintenance of health and quality of life into old age, with a plethora of disorders and diseases linked to the loss of this tissue. As a consequence, molecular biologists have extensively investigated both atrophying and hypertrophying skeletal muscle, in order to understand the molecular pathways that are induced to evoke both loss and growth of skeletal muscle. Despite huge progressions in the field, a full understanding of the molecular mechanisms that orchestrate growth and loss in skeletal muscle, remain elusive. In this regard, epigenetics, referring to alterations in gene expression via structural modifications of DNA without fundamental alterations of the DNA code, have recently become a promising area of research, specifically for its role in modulating genetic expression. However, the field of skeletal muscle epigenetics is in its infancy, and as such, there is currently a distinct paucity of research investigating this biological phenomenon. Herein, a genomic approach was utilised to examine the role DNA methylation plays in modulating the response, at both a genetic and phenotypic level, of mammalian skeletal muscle. The methodological and analytical approaches utilised in this thesis identify a number of important, novel and impactful findings. Firstly, it is identified that DNA methylation displays a distinct inverse relationship with gene expression during both muscular atrophy and hypertrophy, these findings are furthered by work identifying that DNA methylation alterations may precede functional changes in gene expression during skeletal muscle hypertrophy. This thesis also elucidated that skeletal muscle possesses an epigenetic memory that creates an enhanced adaptive response to resistance load induced hypertrophy, when the same stimulus was previously encountered. Finally, in human subjects, a number of novel and previously unstudied gene transcripts were identified that display significantly positive correlations with changes in skeletal muscle mass, as evoked by resistance training. The data in this thesis demonstrates an important role for DNA methylation in regulating skeletal muscle mass during periods of both muscle atrophy and hypertrophy, respectively. The work presented here may allow for further work to be conducted, expanding our understanding of epigenetics in skeletal muscle and best facilitating the development of therapeutics that may alleviate the detrimental effects observed during periods of skeletal muscle atrophy.
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Wendeln, Ann-Christin [Verfasser]. "Long-lasting epigenetic microglial memory of peripheral inflammation modulates hallmarks of Alzheimer's disease pathology / Ann-Christin Wendeln." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1217249214/34.

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Books on the topic "Epigenetic memory"

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Grafi, Gideon, and Nir Ohad, eds. Epigenetic Memory and Control in Plants. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0.

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Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer London, Limited, 2013.

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Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2013.

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Epigenetic Memory And Control In Plants. Springer-Verlag Berlin and Heidelberg GmbH &, 2013.

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Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2015.

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Johnston, Michael V. Coffin-Lowry Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0057.

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Coffin-Lowry syndrome (CLS) is a relatively rare (1:50,000-100,000 incidence) sex-linked neurodevelopmental disorder that includes severe intellectual disability, dysmorphic features including facial and digital abnormalities, growth retardation, and skeletal changes. Most cases are sporadic with only 20% to 30% of cases having an additional family member. CLS is caused by variable loss of function mutations in the RPS6KA3 gene that maps to Xp22.2 and codes for the hRSK2 S6 kinase that phosphorylates the transcription factor CREB (cAMP response element binding protein) as well as other nuclear transcription factors. Phosphorylated CREB (pCREB) plays a major role in memory formation in fruit flies and mammals by activating specific genes through epigenetic histone acetylation.
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Post, Robert M. Depression as a Recurrent, Progressive Illness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0003.

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Clinical Highlights and summary of Chapter• Episodes of depression and bipolar illness progress in two ways:faster recurrences as a function of number of prior episodes, andgreater autonomy (decreased need for precipitation by stressors(Episode Sensitization)• Recurrent stressors result in increased reactivity to subsequent stressors(Stress sensitization) and bouts of stimulant abuse increase in severity with repetition(Stimulant-induced behavioral sensitization)• Each type of sensitization cross-sensitizes to the others and drives illness progression• Each type of sensitization involves specific memory-like epigenetic processes as well as nonspecific cellular toxicities• Childhood onset depression and bipolar illness have a more adverse course than adult onset illness and are increasing in incidence via a cohort (year of birth) effect• As opposed to genetic vulnerability, each type of sensitization can be prevented with appropriate clinical intervention and prevention, which should lessen illness severity and progression• Seeing depression and bipolar disorder as progressive illnesses changes the therapeutic emphasis away from acute treatment and instead to long term prophylaxis• Preventing recurrent depressions will likely protect the brain, the body, and the personWord count with Named refs = 6,417>Depression and bipolar disorder are illnesses which tend to progress with each new recurrence. Stressors, mood episodes, and bouts of substance abuse each sensitize (show increased reactivity) upon their repetition and cross-sensitization to the others. These sensitization processes appear to have a memory-like and epigenetic basis, in some instances conveying lifelong increased vulnerability to illness recurrence and progression. Greater numbers of episodes are associated with faster recurrences, lesser need for stress precipitation, cognitive dysfunction, pathological changes in brain, treatment refractoriness, and loss of many years of life expectancy, predominantly from cardiovascular disease. Such a perspective emphasizes the need for greater awareness of higher incidence of psychiatric and medical comorbidities in the United States compared to many European countries, and the need for earlier intervention and more sustained long term prophylaxis to prevent illness progression and its adverse consequences on brain and body.
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Rosner, Elizabeth. Survivor Café: The Legacy of Trauma and the Labyrinth of Memory. Counterpoint Press, 2017.

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Miu, Andrei C., Judith R. Homberg, and Klaus-Peter Lesch, eds. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.

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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.
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Survivor Café: The Legacy of Trauma and the Labyrinth of Memory. Counterpoint Press, 2018.

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Book chapters on the topic "Epigenetic memory"

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Sarkies, Peter. "Molecular Mechanisms of Transgenerational Epigenetic Inheritance." In Cultural Memory, 47–60. New York: Routledge, 2022. http://dx.doi.org/10.4324/9781003205135-5.

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Estevez, Marcel A., and Ted Abel. "Epigenetic Mechanisms of Memory Consolidation." In Brain, Behavior and Epigenetics, 267–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17426-1_13.

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Reul, Johannes M. H. M., Andrew Collins, and María Gutièrrez-Mecinas. "Epigenetic Mechanisms in Memory Formation." In Brain, Behavior and Epigenetics, 287–300. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17426-1_14.

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Dong, Jun, Hyun-Dong Chang, and Andreas Radbruch. "Epigenetic Imprinting of Immunological Memory." In Epigenetics - A Different Way of Looking at Genetics, 53–67. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27186-6_4.

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Sano, Hiroshi, and Hyun-Jung Kim. "Transgenerational Epigenetic Inheritance in Plants." In Epigenetic Memory and Control in Plants, 233–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_11.

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Saijo, Yusuke, and Eva-Maria Reimer-Michalski. "Epigenetic Control of Plant Immunity." In Epigenetic Memory and Control in Plants, 57–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_4.

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Zografou, Theo, and Franziska Turck. "Epigenetic Control of Flowering Time." In Epigenetic Memory and Control in Plants, 77–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_5.

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Houben, Andreas, Dmitri Demidov, and Raheleh Karimi-Ashtiyani. "Epigenetic Control of Cell Division." In Epigenetic Memory and Control in Plants, 155–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_8.

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Rothenberg, Ellen V., and Jingli A. Zhang. "T-Cell Identity and Epigenetic Memory." In Current Topics in Microbiology and Immunology, 117–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/82_2011_168.

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Grafi, Gideon, and Nir Ohad. "Plant Epigenetics: A Historical Perspective." In Epigenetic Memory and Control in Plants, 1–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_1.

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Conference papers on the topic "Epigenetic memory"

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Pratama, Ferdian, Fulvio Mastrogiovanni, and Nak Young Chong. "An integrated epigenetic robot architecture via context-influenced long-term memory." In 2014 Joint IEEE International Conferences on Development and Learning and Epigenetic Robotics (ICDL-Epirob). IEEE, 2014. http://dx.doi.org/10.1109/devlrn.2014.6982956.

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Alcalá-Vida, R., C. Lotz, J. Seguin, C. Decraene, B. Brulé, A. Awada, A. Bombardier, et al. "A02 Altered epigenetic and transcriptional regulation during striatum-dependent memory in HD mice." In EHDN 2022 Plenary Meeting, Bologna, Italy, Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jnnp-2022-ehdn.2.

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Thiagalingam, Sam, Arthur W. Lambert, Sait Ozturk, Hamid M. Abdolmaleky, and Panagiotis Papageorgis. "Abstract 187: Epigenetic memory during breast cancer progression is sustained by Smad signaling pathway." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-187.

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Pratama, Ferdian, Fulvio Mastrogiovanni, Sungmoon Jeong, and Nak Young Chong. "Long-term knowledge acquisition in a memory-based epigenetic robot architecture for verbal interaction." In 2015 24th IEEE International Symposium on Robot and Human Interactive Communication (RO-MAN). IEEE, 2015. http://dx.doi.org/10.1109/roman.2015.7333563.

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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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Bhat, Ajaz Ahmad, Vishwanathan Mohan, Francesco Rea, Giulio Sandini, and Pietro Morasso. "“Connecting experiences”: Towards a biologically inspired memory for developmental robots." In 2014 Joint IEEE International Conferences on Development and Learning and Epigenetic Robotics (ICDL-Epirob). IEEE, 2014. http://dx.doi.org/10.1109/devlrn.2014.6983007.

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Falvo, David J., and Rohit Chandwani. "Abstract A12: The establishment, maintenance, and maladaptive role of epigenetic memory in mediating pancreatic tumorigenesis." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-a12.

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Sandamirskaya, Yulia, and Tobias Storck. "Neural-dynamic architecture for looking: Shift from visual to motor target representation for memory saccades." In 2014 Joint IEEE International Conferences on Development and Learning and Epigenetic Robotics (ICDL-Epirob). IEEE, 2014. http://dx.doi.org/10.1109/devlrn.2014.6982951.

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Woods, David M., Karrune Woan, Fengdong Cheng, Hong Wei Wang, Eva Sahakian, John Powers, Jennifer Rock-Klotz, Alejandro Villagra, Javier Pinilla-Ibarz, and Eduardo Sotomayor. "Abstract 692: Histone deacetylase 11 is an epigenetic regulator of CD8+ T-cell effector function and memory formation." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-692.

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Sodre, Andressa L., David M. Woods, Amod Sarnaik, Brian C. Betts, and Jeffrey S. Weber. "Abstract B109: Epigenetic reprogramming of T-cells from metastatic melanoma patients enhances central memory and decreases Th2/Treg phenotypes." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b109.

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Reports on the topic "Epigenetic memory"

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Meiri, Noam, Michael D. Denbow, and Cynthia J. Denbow. Epigenetic Adaptation: The Regulatory Mechanisms of Hypothalamic Plasticity that Determine Stress-Response Set Point. United States Department of Agriculture, November 2013. http://dx.doi.org/10.32747/2013.7593396.bard.

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Our hypothesis was that postnatal stress exposure or sensory input alters brain activity, which induces acetylation and/or methylation on lysine residues of histone 3 and alters methylation levels in the promoter regions of stress-related genes, ultimately resulting in long-lasting changes in the stress-response set point. Therefore, the objectives of the proposal were: 1. To identify the levels of total histone 3 acetylation and different levels of methylation on lysine 9 and/or 14 during both heat and feed stress and challenge. 2. To evaluate the methylation and acetylation levels of histone 3 lysine 9 and/or 14 at the Bdnfpromoter during both heat and feed stress and challenge. 3. To evaluate the levels of the relevant methyltransferases and transmethylases during infliction of stress. 4. To identify the specific localization of the cells which respond to both specific histone modification and the enzyme involved by applying each of the stressors in the hypothalamus. 5. To evaluate the physiological effects of antisense knockdown of Ezh2 on the stress responses. 6. To measure the level of CpG methylation in the promoter region of BDNF in thermal treatments and free-fed, 12-hour fasted, and re-fed chicks during post-natal day 3, which is the critical period for feed-control establishment, and 10 days later to evaluate longterm effects. 7. The phenotypic effect of antisense “knock down” of the transmethylaseDNMT 3a. Background: The growing demand for improvements in poultry production requires an understanding of the mechanisms governing stress responses. Two of the major stressors affecting animal welfare and hence, the poultry industry in both the U.S. and Israel, are feed intake and thermal responses. Recently, it has been shown that the regulation of energy intake and expenditure, including feed intake and thermal regulation, resides in the hypothalamus and develops during a critical post-hatch period. However, little is known about the regulatory steps involved. The hypothesis to be tested in this proposal is that epigenetic changes in the hypothalamus during post-hatch early development determine the stress-response set point for both feed and thermal stressors. The ambitious goals that were set for this proposal were met. It was established that both stressors i.e. feed and thermal stress, can be manipulated during the critical period of development at day 3 to induce resilience to stress later in life. Specifically it was established that unfavorable nutritional conditions during early developmental periods or heat exposure influences subsequent adaptability to those same stressful conditions. Furthermore it was demonstrated that epigenetic marks on the promoter of genes involved in stress memory are altered both during stress, and as a result, later in life. Specifically it was demonstrated that fasting and heat had an effect on methylation and acetylation of histone 3 at various lysine residues in the hypothalamus during exposure to stress on day 3 and during stress challenge on day 10. Furthermore, the enzymes that perform these modifications are altered both during stress conditioning and challenge. Finally, these modifications are both necessary and sufficient, since antisense "knockdown" of these enzymes affects histone modifications, and as a consequence stress resilience. DNA methylation was also demonstrated at the promoters of genes involved in heat stress regulation and long-term resilience. It should be noted that the only goal that we did not meet because of technical reasons was No. 7. In conclusion: The outcome of this research may provide information for the improvement of stress responses in high yield poultry breeds using epigenetic adaptation approaches during critical periods in the course of early development in order to improve animal welfare even under suboptimum environmental conditions.
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Yahav, Shlomo, John Brake, and Noam Meiri. Development of Strategic Pre-Natal Cycling Thermal Treatments to Improve Livability and Productivity of Heavy Broilers. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7593395.bard.

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The necessity to improve broiler thermotolerance and live performance led to the following hypothesis: Appropriate comprehensive incubation treatments that include significant temperature management changes will promote angiogenesis and will improve acquisition of thermotolerance and carcass quality of heavy broilers through epigenetic adaptation. It was based on the following questions: 1. Can TM during embryogenesis of broilers induce a longer-lasting thermoregulatory memory (up to marketing age of 10 wk) that will improve acquisition of thermotolerance as well as increased breast meat yield in heavy broilers? 2. The improved sensible heat loss (SHL) suggests an improved peripheral vasodilation process. Does elevated temperature during incubation affect vasculogenesis and angiogenesis processes in the chick embryo? Will such create subsequent advantages for heavy broilers coping with adverse hot conditions? 3. What are the changes that occur in the PO/AH that induce the changes in the threshold response for heat production/heat loss based on the concept of epigenetic temperature adaptation? The original objectives of this study were as follow: a. to assess the improvement of thermotolerance efficiency and carcass quality of heavy broilers (~4 kg); b. toimproveperipheral vascularization and angiogenesis that improve sensible heat loss (SHL); c. to study the changes in the PO/AH thermoregulatory response for heat production/losscaused by modulating incubation temperature. To reach the goals: a. the effect of TM on performance and thermotolerance of broilers reared to 10 wk of age was studied. b. the effect of preincubation heating with an elevated temperature during the 1ˢᵗ 3 to 5 d of incubation in the presence of modified fresh air flow coupled with changes in turning frequency was elucidated; c.the effect of elevated temperature on vasculogenesis and angiogenesis was determined using in ovo and whole embryo chick culture as well as HIF-1α VEGF-α2 VEGF-R, FGF-2, and Gelatinase A (MMP2) gene expression. The effects on peripheral blood system of post-hatch chicks was determined with an infrared thermal imaging technique; c. the expression of BDNF was determined during the development of the thermal control set-point in the preoptic anterior hypothalamus (PO/AH). Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” Recently, Piestunet al. (2008) demonstrated for the first time that TM (an elevated incubation temperature of 39.5°C for 12 h/d from E7 to E16) during the development/maturation of the hypothalamic-hypophyseal-thyroid axis (thermoregulation) and the hypothalamic-hypophyseal-adrenal axis (stress) significantly improved the thermotolerance and performance of broilers at 35 d of age. These phenomena raised two questions that were addressed in this project: 1. was it possible to detect changes leading to the determination of the “set point”; 2. Did TM have a similar long lasting effect (up to 70 d of age)? 3. Did other TM combinations (pre-heating and heating during the 1ˢᵗ 3 to 5 d of incubation) coupled with changes in turning frequency have any performance effect? The improved thermotolerance resulted mainly from an efficient capacity to reduce heat production and the level of stress that coincided with an increase in SHL (Piestunet al., 2008; 2009). The increase in SHL (Piestunet al., 2009) suggested an additional positive effect of TM on vasculogenesis and angiogensis. 4. In order to sustain or even improve broiler performance, TM during the period of the chorioallantoic membrane development was thought to increase vasculogenesis and angiogenesis providing better vasodilatation and by that SHL post-hatch.
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