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Journal articles on the topic 'Epigenetic switch'

Author: Grafiati

Published: 22 February 2025

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1

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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2

Holding, Cathy. "Epigenetic switch for Igf2." Genome Biology 5 (2004): spotlight—20040728–01. http://dx.doi.org/10.1186/gb-spotlight-20040728-01.

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3

Domann, Frederick E., and Bernard W. Futscher. "Flipping the Epigenetic Switch." American Journal of Pathology 164, no. 6 (June 2004): 1883–86. http://dx.doi.org/10.1016/s0002-9440(10)63748-0.

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4

Socolovsky, Merav. "Systems Biology and Epigenetic Mechanisms in Erythropoiesis." Blood 122, no. 21 (November 15, 2013): SCI—11—SCI—11. http://dx.doi.org/10.1182/blood.v122.21.sci-11.sci-11.

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Abstract Irreversible rapid cellular decisions are often controlled by network motifs known as bistable switches. We identified a cell-cycle regulated bistable switch that controls activation of the erythroid transcriptional program during early S phase of the last generation of erythroid colony-forming-unit progenitors (CFUe). This switch drives a rapid, multi-layered commitment event that activates GATA-1 transcription, renders the cells dependent on erythropoietin, and brings about chromatin reconfiguration at erythroid gene loci. In addition, it triggers an unusual process of genome-wide DNA demethylation, the first known example of such a process in somatic cell development. Approximately 25 to 30 percent of all methylation marks are lost from essentially all genomic elements during erythroid terminal differentiation. The bistable switch activating erythroid transcription consists of two linked double-negative feedback interactions of the erythroid transcriptional repressor PU.1, which antagonizes both S phase progression, and the erythroid master transcriptional regulator GATA-1. During operation of the switch, a rapid S phase-dependent decline in PU.1 activates GATA-1 transcription. The dependence of this switch on S phase progression coincides with a dramatic change in the nature of S phase itself, which becomes shorter and 50 percent faster. The accelerated intra-S phase DNA synthesis rate is essential for the loss of genome-wide DNA methylation, which in turn is required for the rapid induction of erythroid genes. Disclosures: No relevant conflicts of interest to declare.

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5

Pedini, Giorgia, and Claudia Bagni. "Epigenetic switch controls social actions." Neuron 110, no. 7 (April 2022): 1085–87. http://dx.doi.org/10.1016/j.neuron.2022.03.028.

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6

Attar, Naomi. "SMRT-seq reveals an epigenetic switch." Nature Reviews Microbiology 14, no. 9 (August 1, 2016): 546. http://dx.doi.org/10.1038/nrmicro.2016.122.

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7

Song, J., A. Angel, M. Howard, and C. Dean. "Vernalization - a cold-induced epigenetic switch." Journal of Cell Science 125, no. 16 (August 15, 2012): 3723–31. http://dx.doi.org/10.1242/jcs.084764.

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8

Fawal, Mohamad-Ali, and Alice Davy. "Impact of Metabolic Pathways and Epigenetics on Neural Stem Cells." Epigenetics Insights 11 (January 2018): 251686571882094. http://dx.doi.org/10.1177/2516865718820946.

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Balancing self-renewal with differentiation is crucial for neural stem cells (NSC) functions to ensure tissue development and homeostasis. Over the last years, multiple studies have highlighted the coupling of either metabolic or epigenetic reprogramming to NSC fate decisions. Metabolites are essential as they provide the energy and building blocks for proper cell function. Moreover, metabolites can also function as substrates and/or cofactors for epigenetic modifiers. It is becoming more evident that metabolic alterations and epigenetics rewiring are highly intertwined; however, their relation regarding determining NSC fate is not well understood. In this review, we summarize the major metabolic pathways and epigenetic modifications that play a role in NSC. We then focus on the notion that nutrients availability can function as a switch to modify the epigenetic machinery and drive NSC sequential differentiation during embryonic neurogenesis.

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9

Li, Xudong, and Ye Zheng. "Treg identity protection by an epigenetic switch." Cell Cycle 13, no. 20 (October 15, 2014): 3159–60. http://dx.doi.org/10.4161/15384101.2014.969996.

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10

Dai, Xiaofeng, Xinyu Lv, Erik W. Thompson, and Kostya (Ken) Ostrikov. "Histone lactylation: epigenetic mark of glycolytic switch." Trends in Genetics 38, no. 2 (February 2022): 124–27. http://dx.doi.org/10.1016/j.tig.2021.09.009.

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11

Ben-Shahar, Yehuda. "Epigenetic switch turns on genetic behavioral variations." Proceedings of the National Academy of Sciences 114, no. 47 (November 7, 2017): 12365–67. http://dx.doi.org/10.1073/pnas.1717376114.

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12

Pires, Nuno D., and Ueli Grossniklaus. "How to Fine-Tune an Epigenetic Switch." Developmental Cell 23, no. 3 (September 2012): 453–54. http://dx.doi.org/10.1016/j.devcel.2012.08.014.

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13

Costa, Silvia, and Caroline Dean. "Storing memories: the distinct phases of Polycomb-mediated silencing of Arabidopsis FLC." Biochemical Society Transactions 47, no. 4 (July 5, 2019): 1187–96. http://dx.doi.org/10.1042/bst20190255.

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Abstract Polycomb-mediated epigenetic silencing is central to correct growth and development in higher eukaryotes. The evolutionarily conserved Polycomb repressive complex 2 (PRC2) transcriptionally silences target genes through a mechanism requiring the histone modification H3K27me3. However, we still do not fully understand what defines Polycomb targets, how their expression state is switched from epigenetically ON to OFF and how silencing is subsequently maintained through many cell divisions. An excellent system in which to dissect the sequence of events underlying an epigenetic switch is the Arabidopsis FLC locus. Exposure to cold temperatures progressively induces a PRC2-dependent switch in an increasing proportion of cells, through a mechanism that is driven by the local chromatin environment. Temporally distinct phases of this silencing mechanism have been identified. First, the locus is transcriptionally silenced in a process involving cold-induced antisense transcripts; second, nucleation at the first exon/intron boundary of a Polycomb complex containing cold-induced accessory proteins induces a metastable epigenetically silenced state; third, a Polycomb complex with a distinct composition spreads across the locus in a process requiring DNA replication to deliver long-term epigenetic silencing. Detailed understanding from this system is likely to provide mechanistic insights important for epigenetic silencing in eukaryotes generally.

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14

Jeevan-Raj, Beena Patricia, Isabelle Robert, Vincent Heyer, Adeline Page, Jing H. Wang, Florence Cammas, Frederick W. Alt, Régine Losson, and Bernardo Reina-San-Martin. "Epigenetic tethering of AID to the donor switch region during immunoglobulin class switch recombination." Journal of Experimental Medicine 208, no. 8 (July 11, 2011): 1649–60. http://dx.doi.org/10.1084/jem.20110118.

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Immunoglobulin class switch recombination (CSR) is initiated by double-stranded DNA breaks (DSBs) in switch regions triggered by activation-induced cytidine deaminase (AID). Although CSR correlates with epigenetic modifications at the IgH locus, the relationship between these modifications and AID remains unknown. In this study, we show that during CSR, AID forms a complex with KAP1 (KRAB domain–associated protein 1) and HP1 (heterochromatin protein 1) that is tethered to the donor switch region (Sμ) bearing H3K9me3 (trimethylated histone H3 at lysine 9) in vivo. Furthermore, in vivo disruption of this complex results in impaired AID recruitment to Sμ, inefficient DSB formation, and a concomitant defect in CSR but not in somatic hypermutation. We propose that KAP1 and HP1 tether AID to H3K9me3 residues at the donor switch region, thus providing a mechanism linking AID to epigenetic modifications during CSR.

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15

Kramer, Beat P., Alessandro Usseglio Viretta, Marie Daoud-El Baba, Dominique Aubel, Wilfried Weber, and Martin Fussenegger. "An engineered epigenetic transgene switch in mammalian cells." Nature Biotechnology 22, no. 7 (June 6, 2004): 867–70. http://dx.doi.org/10.1038/nbt980.

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16

Angel, Andrew, Jie Song, Caroline Dean, and Martin Howard. "A Polycomb-based switch underlying quantitative epigenetic memory." Nature 476, no. 7358 (July 24, 2011): 105–8. http://dx.doi.org/10.1038/nature10241.

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17

Margulies, Carla E., and Andreas G. Ladurner. "PARP-1 Flips the Epigenetic Switch on Obesity." Molecular Cell 79, no. 6 (September 2020): 874–75. http://dx.doi.org/10.1016/j.molcel.2020.08.019.

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18

Hernday, Aaron D., Bruce A. Braaten, Gina Broitman-Maduro, Patrick Engelberts, and David A. Low. "Regulation of the Pap Epigenetic Switch by CpxAR." Molecular Cell 16, no. 4 (November 2004): 537–47. http://dx.doi.org/10.1016/j.molcel.2004.10.020.

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19

Pray, Leslie. "At the Flick of a Switch: Epigenetic Drugs." Chemistry & Biology 15, no. 7 (July 2008): 640–41. http://dx.doi.org/10.1016/j.chembiol.2008.07.003.

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20

Jeevan-Raj, Beena Patricia, Isabelle Robert, Vincent Heyer, Adeline Page, Jing H. Wang, Florence Cammas, Frederick W. Alt, Régine Losson, and Bernardo Reina-San-Martin. "Epigenetic tethering of AID to the donor switch region during immunoglobulin class switch recombination." Journal of Cell Biology 194, no. 2 (July 25, 2011): i5. http://dx.doi.org/10.1083/jcb1942oia5.

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21

Yosefzon, Yahav, Cfir David, Anna Tsukerman, Lilach Pnueli, Sen Qiao, Ulrich Boehm, and Philippa Melamed. "An epigenetic switch repressingTet1in gonadotropes activates the reproductive axis." Proceedings of the National Academy of Sciences 114, no. 38 (August 30, 2017): 10131–36. http://dx.doi.org/10.1073/pnas.1704393114.

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The TET enzymes catalyze conversion of 5-methyl cytosine (5mC) to 5-hydroxymethyl cytosine (5hmC) and play important roles during development. TET1 has been particularly well-studied in pluripotent stem cells, butTet1-KO mice are viable, and the most marked defect is abnormal ovarian follicle development, resulting in impaired fertility. We hypothesized that TET1 might play a role in the central control of reproduction by regulating expression of the gonadotropin hormones, which are responsible for follicle development and maturation and ovarian function. We find that all three TET enzymes are expressed in gonadotrope-precursor cells, butTet1mRNA levels decrease markedly with completion of cell differentiation, corresponding with an increase in expression of the luteinizing hormone gene,Lhb. We demonstrate that poorly differentiated gonadotropes express a TET1 isoform lacking the N-terminal CXXC-domain, which repressesLhbgene expression directly and does not catalyze 5hmC at the gene promoter. We show that this isoform is also expressed in other differentiated tissues, and that it is regulated by an alternative promoter whose activity is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic gonadotropin-releasing hormone through activation of PKA. Its expression is also regulated by DNA methylation, including at an upstream enhancer that is protected by TET2, to allowTet1expression. The down-regulation of TET1 relieves its repression of the methylatedLhbgene promoter, which is then hydroxymethylated and activated by TET2 for full reproductive competence.

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22

Stafford, James M., and K. Matthew Lattal. "Is an epigenetic switch the key to persistent extinction?" Neurobiology of Learning and Memory 96, no. 1 (July 2011): 35–40. http://dx.doi.org/10.1016/j.nlm.2011.04.012.

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23

Amasino, Richard. "Vernalization: Remembering winter with an environmentally induced epigenetic switch." Developmental Biology 295, no. 1 (July 2006): 323. http://dx.doi.org/10.1016/j.ydbio.2006.04.022.

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24

Harvey, Zachary H., Anupam K. Chakravarty, Raymond A. Futia, and Daniel F. Jarosz. "A Prion Epigenetic Switch Establishes an Active Chromatin State." Cell 180, no. 5 (March 2020): 928–40. http://dx.doi.org/10.1016/j.cell.2020.02.014.

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25

Erokhin, Maksim, Pavel Elizar’ev, Aleksander Parshikov, Paul Schedl, Pavel Georgiev, and Darya Chetverina. "Transcriptional read-through is not sufficient to induce an epigenetic switch in the silencing activity of Polycomb response elements." Proceedings of the National Academy of Sciences 112, no. 48 (October 26, 2015): 14930–35. http://dx.doi.org/10.1073/pnas.1515276112.

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In Drosophila, Polycomb (PcG) and Trithorax (TrxG) group proteins are assembled on Polycomb response elements (PREs) to maintain tissue and stage-specific patterns of gene expression. Critical to coordinating gene expression with the process of differentiation, the activity of PREs can be switched “on” and “off.” When on, the PRE imposes a silenced state on the genes in the same domain that is stably inherited through multiple rounds of cell division. When the PRE is switched off, the domain is in a state permissive for gene expression that can be stably inherited. Previous studies have suggested that a burst of transcription through a PRE sequence displaces PcG proteins and provides a universal mechanism for inducing a heritable switch in PRE activity from on to off; however, the evidence favoring this model is indirect. Here, we have directly tested the transcriptional read-through mechanism. Contrary to previous suggestions, we show that transcription through the PRE is not sufficient for inducing an epigenetic switch in PRE activity. In fact, even high levels of continuous transcription through a PRE fails to dislodge the PcG proteins, nor does it remove repressive histone marks. Our results indicate that other mechanisms involving adjacent DNA regulatory elements must be implicated in heritable switch of PRE activity.

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26

Chen, Siyuan, Jing Yang, Yuquan Wei, and Xiawei Wei. "Epigenetic regulation of macrophages: from homeostasis maintenance to host defense." Cellular & Molecular Immunology 17, no. 1 (October 29, 2019): 36–49. http://dx.doi.org/10.1038/s41423-019-0315-0.

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Abstract Macrophages are crucial members of the innate immune response and important regulators. The differentiation and activation of macrophages require the timely regulation of gene expression, which depends on the interaction of a variety of factors, including transcription factors and epigenetic modifications. Epigenetic changes also give macrophages the ability to switch rapidly between cellular programs, indicating the ability of epigenetic mechanisms to affect phenotype plasticity. In this review, we focus on key epigenetic events associated with macrophage fate, highlighting events related to the maintenance of tissue homeostasis, responses to different stimuli and the formation of innate immune memory. Further understanding of the epigenetic regulation of macrophages will be helpful for maintaining tissue integrity, preventing chronic inflammatory diseases and developing therapies to enhance host defense.

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27

Chai, Y., T. Norman, R. Kolter, and R. Losick. "An epigenetic switch governing daughter cell separation in Bacillus subtilis." Genes & Development 24, no. 8 (March 29, 2010): 754–65. http://dx.doi.org/10.1101/gad.1915010.

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28

Iglesias, Nahid, Mark A. Currie, Gloria Jih, Joao A. Paulo, Nertila Siuti, Marian Kalocsay, Steven P. Gygi, and Danesh Moazed. "Automethylation-induced conformational switch in Clr4 (Suv39h) maintains epigenetic stability." Nature 560, no. 7719 (July 23, 2018): 504–8. http://dx.doi.org/10.1038/s41586-018-0398-2.

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29

Lin, Sheng-Chieh, Yu-Ting Chou, Shih Sheng Jiang, Junn-Liang Chang, Chih-Hung Chung, Yu-Rung Kao, I.-Shou Chang, and Cheng-Wen Wu. "Epigenetic Switch between SOX2 and SOX9 Regulates Cancer Cell Plasticity." Cancer Research 76, no. 23 (October 7, 2016): 7036–48. http://dx.doi.org/10.1158/0008-5472.can-15-3178.

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30

Norregaard, K., M. Andersson, K. Sneppen, P. E. Nielsen, S. Brown, and L. B. Oddershede. "DNA supercoiling enhances cooperativity and efficiency of an epigenetic switch." Proceedings of the National Academy of Sciences 110, no. 43 (October 7, 2013): 17386–91. http://dx.doi.org/10.1073/pnas.1215907110.

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31

Nørregaard, Kamilla, Magnus Andersson, Peter E. Nielsen, Stanley Brown, and Lene B. Oddershede. "DNA Supercoiling Enhances Cooperativity and Efficiency of an Epigenetic Switch." Biophysical Journal 108, no. 2 (January 2015): 188a. http://dx.doi.org/10.1016/j.bpj.2014.11.1037.

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32

Knipper, Johanna A., Xiaolei Ding, and Sabine A. Eming. "Diabetes Impedes the Epigenetic Switch of Macrophages into Repair Mode." Immunity 51, no. 2 (August 2019): 199–201. http://dx.doi.org/10.1016/j.immuni.2019.07.009.

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33

Nedjai, Belinda, Caroline Reuter, Amar Ahmad, Rawinder Banwait, Rhian Warman, James Carton, Sabrina Boer, Jack Cuzick, and Attila T. Lorincz. "Molecular progression to cervical precancer, epigenetic switch or sequential model?" International Journal of Cancer 143, no. 7 (July 3, 2018): 1720–30. http://dx.doi.org/10.1002/ijc.31549.

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34

Srivastava, Anusha, Ankit Srivastava, and Rajnish Kumar Singh. "Insight into the Epigenetics of Kaposi’s Sarcoma-Associated Herpesvirus." International Journal of Molecular Sciences 24, no. 19 (October 6, 2023): 14955. http://dx.doi.org/10.3390/ijms241914955.

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Epigenetic reprogramming represents a series of essential events during many cellular processes including oncogenesis. The genome of Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic herpesvirus, is predetermined for a well-orchestrated epigenetic reprogramming once it enters into the host cell. The initial epigenetic reprogramming of the KSHV genome allows restricted expression of encoded genes and helps to hide from host immune recognition. Infection with KSHV is associated with Kaposi’s sarcoma, multicentric Castleman’s disease, KSHV inflammatory cytokine syndrome, and primary effusion lymphoma. The major epigenetic modifications associated with KSHV can be labeled under three broad categories: DNA methylation, histone modifications, and the role of noncoding RNAs. These epigenetic modifications significantly contribute toward the latent–lytic switch of the KSHV lifecycle. This review gives a brief account of the major epigenetic modifications affiliated with the KSHV genome in infected cells and their impact on pathogenesis.

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35

Thon, Geneviève, and Tove Friis. "Epigenetic Inheritance of Transcriptional Silencing and Switching Competence in Fission Yeast." Genetics 145, no. 3 (March 1, 1997): 685–96. http://dx.doi.org/10.1093/genetics/145.3.685.

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Epigenetic events allow the inheritance of phenotypic changes that are not caused by an alteration in DNA sequence. Here we characterize an epigenetic phenomenon occuring in the mating-type region of fission yeast. Cells of fission yeast switch between the P and M mating-type by interconverting their expressed mating-type cassette between two allelic forms, mat1-P and mat1-M. The switch results from gene conversions of mat1 by two silent cassettes, mat2-P and mat3-M, which are linked to each other and to mat1. Grewal and Klar observed that the ability to both switch mat1 and repress transcription near mat2-P and mat3-M was maintained epigenetically in a strain with an 8-kb deletion between mat2 and mat3. Using a strain very similar to theirs, we determined that interconversions between the switching- and silencing-proficient state and the switching and silencing-deficient state occurred less frequently than once per 1000 cell divisions. Although transcriptional silencing was alleviated by the 8-kb deletion, it was not abolished. We performed a mutant search and obtained a class of trans-acting mutations that displayed a strong cumulative effect with the 8-kb deletion. These mutations allow to assess the extent to which silencing is affected by the deletion and provide new insights on the redundancy of the silencing mechanism.

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36

Ntziachristos, Panagiotis, Aristotelis Tsirigos, Grant Welstead, Thomas Trimarchi, Linda Holmfeldt, Takashi Satoh, Elisabeth M. Paietta, et al. "An Oncogene-Regulated Epigenetic Switch in T Cell Acute Lymphoblastic Leukemia." Blood 124, no. 21 (December 6, 2014): 56. http://dx.doi.org/10.1182/blood.v124.21.56.56.

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Abstract Although the cure rate for acute lymphoblastic leukemia (ALL), a frequent pediatric leukemia, has improved dramatically, the overall prognosis remains dismal due to frequent disease relapse and the absence of non-cytotoxic targeted therapy options. Up to 25% of children fail frontline therapy and in these cases prognosis is dismal and the cure rate is approximate 20%. Main current therapies are based on intensive induction chemotherapy that is most frequently coupled to intrathecal chemotherapy alone or with cranial irradiation for central nervous system prophylaxis, which has severe short and long-term side effects. Thus, the ultimate and most critical aim for developing new treatments in different types of leukemia is to block the effects of specific cancer-inducing oncogenes. Others and we have previously shown that T cell ALL (T-ALL) is characterized by activating mutations in the NOTCH signaling pathway. It is currently unclear how key transcription factors in T-ALL such as NOTCH1 recruit the epigenetic machinery and bring together different chromosomal domain, in order to carry out the oncogenic transformation program. We generated evidence that NOTCH1 oncogenic action leads to important epigenetic changes through antagonizing the polycomb repressive complex 2 (PRC2) and leads to loss of the repressive mark histone 3 lysine 27 di/tri-methylation (H3K27me2/3). Moreover, we identified inactivating mutations of the polycomb repressive complex 2 (PRC2), the “writer” of Histone 3 lysine 27 methylation, in primary samples from human patients revealing a tumor suppressor role for the complex in T-ALL. Further extending our work on the H3K27me3 mark, we showed the oncogenic role for the Jumonji d3 (JMJD3) demethylase. Functionally, genomic ablation of the JMJD3 modulator as well as targeting with a specific chemical inhibitor, GSKJ4, generated by GlaxoSmithKline, leads to apoptosis and cell cycle arrest of T-ALL lines and primary cells. Genetic ablation of JMJD3 leads to slower initiation of the disease with significantly improved survival rates of the mice. Surprisingly, UTX acts as a tumor suppressor in the context of the same disease, as part of different transcriptional complexes, and we found that it is genetically inactivated in T-ALL patients. In light of recent developments on novel epigenetic inhibitors against JMJD3, these findings pave the way to specific pharmacological targeting of T cell leukemia. Based on this activity of Notch1 oncogene on epigenetic marks we further hypothesized that the switch from physiological to oncogenic activity might be mediated by changes in enhancer-promoter interaction networks forming chromosomal domains. A substantial percentage of these interactions are likely to be specific for the malignant state, and their disruption with epigenetic pharmacological inhibitors would not potentially affect healthy tissues. Studies in our laboratory show for the first time in leukemia that NOTCH1 chromatin binding sites are associated with enhancer-promoter interactions at oncogenic loci, using up-to-date chromosome conformation capture technology. We hereby show the importance of these interactions for oncogenic gene expression and pharmacological targeting of leukemic cells. These findings lend further rationale to the use of epigenetic drugs for targeted treatment of T cell leukemia. Disclosures Kruidenier: GlaxoSmithKline: Employment. Prinjha:GlaxoSmithKline: Employment.

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37

Sullivan, Adrienne E. "Epigenetic Control of Cell Potency and Fate Determination during Mammalian Gastrulation." Genes 14, no. 6 (May 25, 2023): 1143. http://dx.doi.org/10.3390/genes14061143.

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Pluripotent embryonic stem cells have a unique and characteristic epigenetic profile, which is critical for differentiation to all embryonic germ lineages. When stem cells exit the pluripotent state and commit to lineage-specific identities during the process of gastrulation in early embryogenesis, extensive epigenetic remodelling mediates both the switch in cellular programme and the loss of potential to adopt alternative lineage programmes. However, it remains to be understood how the stem cell epigenetic profile encodes pluripotency, or how dynamic epigenetic regulation helps to direct cell fate specification. Recent advances in stem cell culture techniques, cellular reprogramming, and single-cell technologies that can quantitatively profile epigenetic marks have led to significant insights into these questions, which are important for understanding both embryonic development and cell fate engineering. This review provides an overview of key concepts and highlights exciting new advances in the field.

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38

Chondrou, Vasiliki, Athanasios-Nasir Shaukat, Georgios Psarias, Katerina Athanasopoulou, Evanthia Iliopoulou, Ariadne Damanaki, Constantinos Stathopoulos, and Argyro Sgourou. "LRF Promotes Indirectly Advantageous Chromatin Conformation via BGLT3-lncRNA Expression and Switch from Fetal to Adult Hemoglobin." International Journal of Molecular Sciences 23, no. 13 (June 24, 2022): 7025. http://dx.doi.org/10.3390/ijms23137025.

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The hemoglobin switch from fetal (HbF) to adult (HbA) has been studied intensively as an essential model for gene expression regulation, but also as a beneficial therapeutic approach for β-hemoglobinopathies, towards the objective of reactivating HbF. The transcription factor LRF (Leukemia/lymphoma-related), encoded from the ZBTB7A gene has been implicated in fetal hemoglobin silencing, though has a wide range of functions that have not been fully clarified. We thus established the LRF/ZBTB7A-overexpressing and ZBTB7A-knockdown K562 (human erythroleukemia cell line) clones to assess fetal vs. adult hemoglobin production pre- and post-induction. Transgenic K562 clones were further developed and studied under the influence of epigenetic chromatin regulators, such as DNA methyl transferase 3 (DNMT3) and Histone Deacetylase 1 (HDAC1), to evaluate LRF’s potential disturbance upon the aberrant epigenetic background and provide valuable information of the preferable epigenetic frame, in which LRF unfolds its action on the β-type globin’s expression. The ChIP-seq analysis demonstrated that LRF binds to γ-globin genes (HBG2/1) and apparently associates BCL11A for their silencing, but also during erythropoiesis induction, LRF binds the BGLT3 gene, promoting BGLT3-lncRNA production through the γ-δ intergenic region of β-type globin’s locus, triggering the transcriptional events from γ- to β-globin switch. Our findings are supported by an up-to-date looping model, which highlights chromatin alterations during erythropoiesis at late stages of gestation, to establish an “open” chromatin conformation across the γ-δ intergenic region and accomplish β-globin expression and hemoglobin switch.

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39

Ciesielski, Oskar, Marta Biesiekierska, Baptiste Panthu, Varvara Vialichka, Luciano Pirola, and Aneta Balcerczyk. "The Epigenetic Profile of Tumor Endothelial Cells. Effects of Combined Therapy with Antiangiogenic and Epigenetic Drugs on Cancer Progression." International Journal of Molecular Sciences 21, no. 7 (April 9, 2020): 2606. http://dx.doi.org/10.3390/ijms21072606.

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Tumors require a constant supply of nutrients to grow which are provided through tumor blood vessels. To metastasize, tumors need a route to enter circulation, that route is also provided by tumor blood vessels. Thus, angiogenesis is necessary for both tumor progression and metastasis. Angiogenesis is tightly regulated by a balance of angiogenic and antiangiogenic factors. Angiogenic factors of the vascular endothelial growth factor (VEGF) family lead to the activation of endothelial cells, proliferation, and neovascularization. Significant VEGF-A upregulation is commonly observed in cancer cells, also due to hypoxic conditions, and activates endothelial cells (ECs) by paracrine signaling stimulating cell migration and proliferation, resulting in tumor-dependent angiogenesis. Conversely, antiangiogenic factors inhibit angiogenesis by suppressing ECs activation. One of the best-known anti-angiogenic factors is thrombospondin-1 (TSP-1). In pathological angiogenesis, the balance shifts towards the proangiogenic factors and an angiogenic switch that promotes tumor angiogenesis. Here, we review the current literature supporting the notion of the existence of two different endothelial lineages: normal endothelial cells (NECs), representing the physiological form of vascular endothelium, and tumor endothelial cells (TECs), which are strongly promoted by the tumor microenvironment and are biologically different from NECs. The angiogenic switch would be also important for the explanation of the differences between NECs and TECs, as angiogenic factors, cytokines and growth factors secreted into the tumor microenvironment may cause genetic instability. In this review, we focus on the epigenetic differences between the two endothelial lineages, which provide a possible window for pharmacological targeting of TECs.

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Raffan, Sarah, Navneet Kaur, and Nigel G. Halford. "Epigenetic switch reveals CRISPR /Cas9 response to cytosine methylation in plants." New Phytologist 235, no. 6 (August 18, 2022): 2146–48. http://dx.doi.org/10.1111/nph.18405.

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Serandour, A. A., S. Avner, F. Percevault, F. Demay, M. Bizot, C. Lucchetti-Miganeh, F. Barloy-Hubler, et al. "Epigenetic switch involved in activation of pioneer factor FOXA1-dependent enhancers." Genome Research 21, no. 4 (January 13, 2011): 555–65. http://dx.doi.org/10.1101/gr.111534.110.

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Dean, Caroline. "PL-02 Vernalization – Cold-mediated epigenetic regulation of a developmental switch." Mechanisms of Development 126 (August 2009): S1. http://dx.doi.org/10.1016/j.mod.2009.06.1073.

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Li, Xi-Yin, and Jian-Fang Gui. "An epigenetic regulatory switch controlling temperature-dependent sex determination in vertebrates." Science China Life Sciences 61, no. 8 (June 25, 2018): 996–98. http://dx.doi.org/10.1007/s11427-018-9314-3.

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Wagner, Verena, and Jesús Gil. "An Epigenetic Switch: From Senescent Melanocytes to Malignant Melanoma (and Back)." Cancer Cell 33, no. 2 (February 2018): 162–63. http://dx.doi.org/10.1016/j.ccell.2018.01.013.

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Deblois, Geneviève, Seyed Ali Madani Tonekaboni, Giacomo Grillo, Constanza Martinez, Yunchi Ingrid Kao, Felicia Tai, Ilias Ettayebi, et al. "Epigenetic Switch–Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer." Cancer Discovery 10, no. 9 (June 16, 2020): 1312–29. http://dx.doi.org/10.1158/2159-8290.cd-19-1493.

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Hitchler, Michael J., and Frederick E. Domann. "Metabolic defects provide a spark for the epigenetic switch in cancer." Free Radical Biology and Medicine 47, no. 2 (July 2009): 115–27. http://dx.doi.org/10.1016/j.freeradbiomed.2009.04.010.

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Günthel, Marie, Karel van Duijvenboden, Dennis E. M. de Bakker, Ingeborg B. Hooijkaas, Jeroen Bakkers, Phil Barnett, and Vincent M. Christoffels. "Epigenetic State Changes Underlie Metabolic Switch in Mouse Post-Infarction Border Zone Cardiomyocytes." Journal of Cardiovascular Development and Disease 8, no. 11 (October 22, 2021): 134. http://dx.doi.org/10.3390/jcdd8110134.

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Myocardial infarction causes ventricular muscle loss and formation of scar tissue. The surviving myocardium in the border zone, located adjacent to the infarct, undergoes profound changes in function, structure and composition. How and to what extent these changes of border zone cardiomyocytes are regulated epigenetically is not fully understood. Here, we obtained transcriptomes of PCM-1-sorted mouse cardiomyocyte nuclei of healthy left ventricle and 7 days post myocardial infarction border zone tissue. We validated previously observed downregulation of genes involved in fatty acid metabolism, oxidative phosphorylation and mitochondrial function in border zone-derived cardiomyocytes, and observed a modest induction of genes involved in glycolysis, including Slc2a1 (Glut1) and Pfkp. To gain insight into the underlying epigenetic regulatory mechanisms, we performed H3K27ac profiling of healthy and border zone cardiomyocyte nuclei. We confirmed the switch from Mef2- to AP-1 chromatin association in border zone cardiomyocytes, and observed, in addition, an enrichment of PPAR/RXR binding motifs in the sites with reduced H3K27ac signal. We detected downregulation and accompanying epigenetic state changes at several key PPAR target genes including Ppargc1a (PGC-1α), Cpt2, Ech1, Fabpc3 and Vldrl in border zone cardiomyocytes. These data indicate that changes in epigenetic state and gene regulation underlie the maintained metabolic switch in border zone cardiomyocytes.

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Sharma, Mahima, and Sreedharan Sajikumar. "G9a/GLP Complex Acts as a Bidirectional Switch to Regulate Metabotropic Glutamate Receptor-Dependent Plasticity in Hippocampal CA1 Pyramidal Neurons." Cerebral Cortex 29, no. 7 (July 6, 2018): 2932–46. http://dx.doi.org/10.1093/cercor/bhy161.

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Abstract Metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) is conventionally considered to be solely dependent on local protein synthesis. Given the impact of epigenetics on memory, the intriguing question is whether epigenetic regulation influences mGluR-LTD as well. G9a/GLP histone lysine methyltransferase complex is crucial for brain development and goal-directed learning as well as for drug-addiction. In this study, we analyzed whether the epigenetic regulation by G9a/GLP complex affects mGluR-LTD in CA1 hippocampal pyramidal neurons of 5–7 weeks old male Wistar rats. In hippocampal slices with intact CA1 dendritic regions, inhibition of G9a/GLP activity abolished mGluR-LTD. The inhibition of this complex upregulated the expression of plasticity proteins like PKMζ, which mediated the prevention of mGluR-LTD expression by regulating the NSF-GluA2-mediated trafficking of AMPA receptors towards the postsynaptic site. G9a/GLP inhibition during the induction of mGluR-LTD also downregulated the protein levels of phosphorylated-GluA2 and Arc. Interestingly, G9a/GLP inhibition could not impede the mGluR-LTD when the cell-body was severed. Our study highlights the role of G9a/GLP complex in intact neuronal network as a bidirectional switch; when turned on, it facilitates the expression of mGluR-LTD, and when turned off, it promotes the expression of long-term potentiation.

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Forte, Amalia, Umberto Galderisi, Marilena Cipollaro, Marisa De Feo, and Alessandro Della Corte. "Epigenetic regulation of TGF-β1 signalling in dilative aortopathy of the thoracic ascending aorta." Clinical Science 130, no. 16 (July 7, 2016): 1389–405. http://dx.doi.org/10.1042/cs20160222.

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The term ‘epigenetics’ refers to heritable, reversible DNA or histone modifications that affect gene expression without modifying the DNA sequence. Epigenetic modulation of gene expression also includes the RNA interference mechanism. Epigenetic regulation of gene expression is fundamental during development and throughout life, also playing a central role in disease progression. The transforming growth factor β1 (TGF-β1) and its downstream effectors are key players in tissue repair and fibrosis, extracellular matrix remodelling, inflammation, cell proliferation and migration. TGF-β1 can also induce cell switch in epithelial-to-mesenchymal transition, leading to myofibroblast transdifferentiation. Cellular pathways triggered by TGF-β1 in thoracic ascending aorta dilatation have relevant roles to play in remodelling of the vascular wall by virtue of their association with monogenic syndromes that implicate an aortic aneurysm, including Loeys–Dietz and Marfan's syndromes. Several studies and reviews have focused on the progression of aneurysms in the abdominal aorta, but research efforts are now increasingly being focused on pathogenic mechanisms of thoracic ascending aorta dilatation. The present review summarizes the most recent findings concerning the epigenetic regulation of effectors of TGF-β1 pathways, triggered by sporadic dilative aortopathy of the thoracic ascending aorta in the presence of a tricuspid or bicuspid aortic valve, a congenital malformation occurring in 0.5–2% of the general population. A more in-depth comprehension of the epigenetic alterations associated with TGF-β1 canonical and non-canonical pathways in dilatation of the ascending aorta could be helpful to clarify its pathogenesis, identify early potential biomarkers of disease, and, possibly, develop preventive and therapeutic strategies.

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Gan, Huoqun, Tian Shen, Daniel P. Chupp, Julia R. Taylor, Helia N. Sanchez, Xin Li, Zhenming Xu, Hong Zan, and Paolo Casali. "B cell Sirt1 deacetylates histone and non-histone proteins for epigenetic modulation of AID expression and the antibody response." Science Advances 6, no. 14 (April 2020): eaay2793. http://dx.doi.org/10.1126/sciadv.aay2793.

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Activation-induced cytidine deaminase (AID) mediates immunoglobulin class switch DNA recombination (CSR) and somatic hypermutation (SHM), critical processes for maturation of the antibody response. Epigenetic factors, such as histone deacetylases (HDACs), would underpin B cell differentiation stage–specific AID expression. Here, we showed that NAD+-dependent class III HDAC sirtuin 1 (Sirt1) is highly expressed in resting B cells and down-regulated by stimuli inducing AID. B cell Sirt1 down-regulation, deprivation of NAD+ cofactor, or genetic Sirt1 deletion reduced deacetylation of Aicda promoter histones, Dnmt1, and nuclear factor–κB (NF-κB) p65 and increased AID expression. This promoted class-switched and hypermutated T-dependent and T-independent antibody responses or led to generation of autoantibodies. Genetic Sirt1 overexpression, Sirt1 boost by NAD+, or allosteric Sirt1 enhancement by SRT1720 repressed AID expression and CSR/SHM. By deacetylating histone and nonhistone proteins (Dnmt1 and NF-κB p65), Sirt1 transduces metabolic cues into epigenetic changes to play an important B cell–intrinsic role in modulating antibody and autoantibody responses.

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