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Journal articles on the topic 'Epigenetic regulator'

Author: Grafiati
Published: 11 March 2023

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1

Abdullah, Omeima, and Mahmoud Alhosin. "HAUSP Is a Key Epigenetic Regulator of the Chromatin Effector Proteins." Genes 13, no. 1 (December 24, 2021): 42. http://dx.doi.org/10.3390/genes13010042.

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HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP is a main partner of the “Epigenetic Code Replication Machinery,” ECREM, a large protein complex that includes several epigenetic players, such as the ubiquitin-like containing plant homeodomain (PHD) and an interesting new gene (RING), finger domains 1 (UHRF1), as well as DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), histone methyltransferase G9a, and histone acetyltransferase TIP60. Due to its deubiquitinase activity and its ability to team up through direct interactions with several epigenetic regulators, mainly UHRF1, DNMT1, TIP60, the histone lysine methyltransferase EZH2, and the lysine-specific histone demethylase LSD1, HAUSP positions itself at the top of the regulatory hierarchies involved in epigenetic silencing of tumor suppressor genes in cancer. This review highlights the increasing role of HAUSP as an epigenetic master regulator that governs a set of epigenetic players involved in both the maintenance of DNA methylation and histone post-translational modifications.
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Albogami, Sarah. "Epigenetic Regulator Signatures in Regenerative Capacity." Current Stem Cell Research & Therapy 14, no. 7 (September 23, 2019): 598–606. http://dx.doi.org/10.2174/1574888x14666190618125111.

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Background:: Regeneration is the process by which body parts lost as a result of injury are replaced, as observed in certain animal species. The root of regenerative differences between organisms is still not very well understood; if regeneration merely recycles developmental pathways in the adult form, why can some animals regrow organs whereas others cannot? In the regulation of the regeneration process as well as other biological phenomena, epigenetics plays an essential role. Objective:: This review aims to demonstrate the role of epigenetic regulators in determining regenerative capacity. Results:: In this review, we discuss the basis of regenerative differences between organisms. In addition, we present the current knowledge on the role of epigenetic regulation in regeneration, including DNA methylation, histone modification, lysine methylation, lysine methyltransferases, and the SET1 family. Conclusion:: An improved understanding of the regeneration process and the epigenetic regulation thereof through the study of regeneration in highly regenerative species will help in the field of regenerative medicine in future.
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Barneda-Zahonero, Bruna, Lidia Roman-Gonzalez, Olga Collazo, Tokameh Mahmoudi, and Maribel Parra. "Epigenetic Regulation of B Lymphocyte Differentiation, Transdifferentiation, and Reprogramming." Comparative and Functional Genomics 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/564381.

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B cell development is a multistep process that is tightly regulated at the transcriptional level. In recent years, investigators have shed light on the transcription factor networks involved in all the differentiation steps comprising B lymphopoiesis. The interplay between transcription factors and the epigenetic machinery involved in establishing the correct genomic landscape characteristic of each cellular state is beginning to be dissected. The participation of “epigenetic regulator-transcription factor” complexes is also crucial for directing cells during reprogramming into pluripotency or lineage conversion. In this context, greater knowledge of epigenetic regulation during B cell development, transdifferentiation, and reprogramming will enable us to understand better how epigenetics can control cell lineage commitment and identity. Herein, we review the current knowledge about the epigenetic events that contribute to B cell development and reprogramming.
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McCoy, Rachel M., Russell Julian, Shoban R. V. Kumar, Rajeev Ranjan, Kranthi Varala, and Ying Li. "A Systems Biology Approach to Identify Essential Epigenetic Regulators for Specific Biological Processes in Plants." Plants 10, no. 2 (February 13, 2021): 364. http://dx.doi.org/10.3390/plants10020364.

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Upon sensing developmental or environmental cues, epigenetic regulators transform the chromatin landscape of a network of genes to modulate their expression and dictate adequate cellular and organismal responses. Knowledge of the specific biological processes and genomic loci controlled by each epigenetic regulator will greatly advance our understanding of epigenetic regulation in plants. To facilitate hypothesis generation and testing in this domain, we present EpiNet, an extensive gene regulatory network (GRN) featuring epigenetic regulators. EpiNet was enabled by (i) curated knowledge of epigenetic regulators involved in DNA methylation, histone modification, chromatin remodeling, and siRNA pathways; and (ii) a machine-learning network inference approach powered by a wealth of public transcriptome datasets. We applied GENIE3, a machine-learning network inference approach, to mine public Arabidopsis transcriptomes and construct tissue-specific GRNs with both epigenetic regulators and transcription factors as predictors. The resultant GRNs, named EpiNet, can now be intersected with individual transcriptomic studies on biological processes of interest to identify the most influential epigenetic regulators, as well as predicted gene targets of the epigenetic regulators. We demonstrate the validity of this approach using case studies of shoot and root apical meristem development.
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Skalnik, David G. "The epigenetic regulator Cfp1." BioMolecular Concepts 1, no. 5-6 (December 1, 2010): 325–34. http://dx.doi.org/10.1515/bmc.2010.031.

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AbstractNumerous epigenetic modifications have been identified and correlated with transcriptionally active euchromatin or repressed heterochromatin and many enzymes responsible for the addition and removal of these marks have been characterized. However, less is known regarding how these enzymes are regulated and targeted to appropriate genomic locations. Mammalian CXXC finger protein 1 is an epigenetic regulator that was originally identified as a protein that binds specifically to any DNA sequence containing an unmethylated CpG dinucleotide. Mouse embryos lacking CXXC finger protein 1 die prior to gastrulation, and embryonic stem cells lacking CXXC finger protein 1 are viable but are unable to achieve cellular differentiation and lineage commitment. CXXC finger protein 1 is a regulator of both cytosine and histone methylation. It physically interacts with DNA methyltransferase 1 and facilitates maintenance cytosine methylation. Rescue studies reveal that CXXC finger protein 1 contains redundant functional domains that are sufficient to support cellular differentiation and proper levels of cytosine methylation. CXXC finger protein 1 is also a component of the Setd1 histone H3-Lys4 methyltransferase complexes and functions to target these enzymes to unmethylated CpG islands. Depletion of CXXC finger protein 1 leads to loss of histone H3-Lys4 tri-methylation at CpG islands and inappropriate drifting of this euchromatin mark into areas of hetero-chromatin. Thus, one function of CXXC finger protein 1 is to serve as an effector protein that interprets cytosine methylation patterns and facilitates crosstalk with histone-modifying enzymes.
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Theys, Claudia, Dorien Lauwers, Claudina Perez-Novo, and Wim Vanden Berghe. "PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?" Biomedicines 10, no. 12 (November 25, 2022): 3041. http://dx.doi.org/10.3390/biomedicines10123041.

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Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic and the most common cause of chronic liver disease worldwide. It consists of a spectrum of liver disorders ranging from simple steatosis to NASH which predisposes patients to further fibrosis, cirrhosis and even hepatocarcinoma. Despite much research, an approved treatment is still lacking. Finding new therapeutic targets has therefore been a main priority. Known as a main regulator of the lipid metabolism and highly expressed in the liver, the nuclear receptor peroxisome proliferator-activated receptor-α (PPARα) has been identified as an attractive therapeutic target. Since its expression is silenced by DNA hypermethylation in NAFLD patients, many research strategies have aimed to restore the expression of PPARα and its target genes involved in lipid metabolism. Although previously tested PPARα agonists did not ameliorate the disease, current research has shown that PPARα also interacts and regulates epigenetic DNMT1, JMJD3, TET and SIRT1 enzymes. Moreover, there is a growing body of evidence suggesting the orchestrating role of epigenetics in the development and progression of NAFLD. Therefore, current therapeutic strategies are shifting more towards epigenetic drugs. This review provides a concise overview of the epigenetic regulation of NAFLD with a focus on PPARα regulation and highlights recently identified epigenetic interaction partners of PPARα.
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7

Dey, Anusree, Sheetal Uppal, Jayeeta Giri, and Hari Sharan Misra. "Emerging Roles of Bromodomain Protein 4 in Regulation of Stem Cell Identity." Stem Cells 39, no. 12 (September 25, 2021): 1615–24. http://dx.doi.org/10.1002/stem.3454.

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Abstract Understanding the mechanism of fate decision and lineage commitment is the key step for developing novel stem cell applications in therapeutics. This process is coordinately regulated through systematic epigenetic reprogramming and concomitant changes in the transcriptional landscape of the stem cells. One of the bromo- and extra-terminal domain (BET) family member proteins, bromodomain protein 4 (BRD4), performs the role of epigenetic reader and modulates gene expression by recruiting other transcription factors and directly regulating RNA polymerase II elongation. Controlled gene regulation is the critical step in maintenance of stem cell potency and dysregulation may lead to tumor formation. As a key transcriptional factor and epigenetic regulator, BRD4 contributes to stem cell maintenance in several ways. Being a druggable target, BRD4 is an attractive candidate for exploiting its potential in stem cell therapeutics. Therefore, it is crucial to elucidate how BRD4, through its interplay with pluripotency transcriptional regulators, control lineage commitment in stem cells. Here, we systemically review the role of BRD4 in complex gene regulatory network during three specific states of stem cell transitions: cell differentiation, cell reprogramming and transdifferentiation. A thorough understanding of BRD4 mediated epigenetic regulation in the maintenance of stem cell potency will be helpful to strategically control stem cell fates in regenerative medicine.
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Sarne, Victoria, Sandrina Braunmueller, Lisa Rakob, and Rita Seeboeck. "The Relevance of Gender in Tumor-Influencing Epigenetic Traits." Epigenomes 3, no. 1 (January 28, 2019): 6. http://dx.doi.org/10.3390/epigenomes3010006.

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Tumorigenesis as well as the molecular orchestration of cancer progression are very complex mechanisms that comprise numerous elements of influence and regulation. Today, many of the major concepts are well described and a basic understanding of a tumor’s fine-tuning is given. Throughout the last decade epigenetics has been featured in cancer research and it is now clear that the underlying mechanisms, especially DNA and histone modifications, are important regulators of carcinogenesis and tumor progression. Another key regulator, which is well known but has been neglected in scientific approaches as well as molecular diagnostics and, consequently, treatment conceptualization for a long time, is the subtle influence patient gender has on molecular processes. Naturally, this is greatly based on hormonal differences, but from an epigenetic point of view, the diverse susceptibility to stress and environmental influences is of prime interest. In this review we present the current view on which and how epigenetic modifications, emphasizing DNA methylation, regulate various tumor diseases. It is our aim to elucidate gender and epigenetics and their interconnectedness, which will contribute to understanding of the prospect molecular orchestration of cancer in individual tumors.
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9

Bithell, Angela. "REST: transcriptional and epigenetic regulator." Epigenomics 3, no. 1 (February 2011): 47–58. http://dx.doi.org/10.2217/epi.10.76.

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10

Bahia, Ravinder, Xiaoguang Hao, Rozina Hassam, Orsolya Cseh, Danielle Bozek, H. Artee Luchman, and Samuel Weiss. "STEM-18. EPIGENETIC AND MOLECULAR COORDINATION BETWEEN HDAC2 AND SMAD3-SKI IS REQUIRED FOR GROWTH AND STEM CELL CHARACTERISTICS OF BRAIN TUMOUR STEM CELLS." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii34—vii35. http://dx.doi.org/10.1093/neuonc/noac209.135.

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Abstract Brain tumour stem cell population in glioblastoma (GBM) display key cancer stem cell characteristics of high self-renewal and drug resistance that are maintained by the coordinated functions of epigenetic and molecular regulators. Yet, specific epigenetic mechanisms that, in collaboration with relevant molecular pathways, help maintain a stem-like state in BTSCs remain poorly understood. Here, we identify HDAC2 as a foremost epigenetic regulator in BTSCs that specifically utilizes the transforming growth factor-β (TGF-β) pathway related proteins, SMAD3-SKI, for remodelling BTSC chromatin accessibility and transcriptional programs to facilitate their stemness and tumorigenic potentials. Our initial drug screening revealed that selective inhibition of HDAC1 and 2 with romidepsin was effective in targeting BTSC viability, cell proliferation and self-renewal in vitro. Using CRISPR-cas9 knockout and shRNA knockdown strategies, we further demonstrated that loss of HDAC2 disrupts an epigenetic and molecular coordination between HDAC2 and SMAD-SKI proteins, which negatively impacts BTSC survival, cell proliferation and self-renewal in vitro and improves median survival in orthotopic xenograft mouse models. Loss of HDAC2 showed reduction in the protein abundance of transcriptional regulator, SMAD3 and negative regulator protein, SKI. However, overexpression of SMAD3 in HDAC2 deficient BTSCs could partially rescues their cell functional deficits. These findings suggest that context-specific epigenetic regulations by HDAC2 and its interaction with the critical transcriptional regulators, SMAD3-SKI, maintains the stemness and growth characteristics of BTSCs. Further HDAC2 overexpression increases cell proliferation and self-renewal abilities in normal neural stem cells (NSCs). These findings thus support the role of HDAC2 as a key epigenetic determinant of stemness in normal NSCs and of cancer stem cell characteristics and tumorigenic potential in BTSCs. Collectively, our data raises the potential that disruption of the coordinated mechanisms regulated by HDAC2-SMAD3-SKI axis may be an effective therapeutic approach for targeting GBM BTSCs.
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11

Guo, Mengnan, Ning Li, Jianxia Zheng, Wei Wang, Yan Wu, Xu Han, Jiapei Guo, et al. "Epigenetic Regulation of Hepatocellular Carcinoma Progression through the mTOR Signaling Pathway." Canadian Journal of Gastroenterology and Hepatology 2021 (May 25, 2021): 1–9. http://dx.doi.org/10.1155/2021/5596712.

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Hepatocellular carcinoma (HCC), the most common type of primary liver cancer, is an aggressive tumor with a high mortality rate because of the limited systemic and locoregional treatment modalities. The development and progression of HCC depend on epigenetic changes that result in the activation or inhibition of some signaling pathways. The mTOR signaling pathway is essential for many pathophysiological processes and is considered a major regulator of cancer. Increasing evidence has shown that epigenetics plays a key role in HCC biology by regulating the mTOR signaling pathway. Therefore, epigenetic regulation through the mTOR signaling pathway to diagnose and treat HCC will become a very promising strategy.
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12

Lal, Girdhari, and Jonathan S. Bromberg. "Epigenetic mechanisms of regulation of Foxp3 expression." Blood 114, no. 18 (October 29, 2009): 3727–35. http://dx.doi.org/10.1182/blood-2009-05-219584.

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Abstract Regulatory T cells play important roles in the control of autoimmunity and maintenance of transplantation tolerance. Foxp3, a member of the forkhead/winged-helix family of transcription factors, acts as the master regulator for regulatory T-cell (Treg) development and function. Mutation of the Foxp3 gene causes the scurfy phenotype in mouse and IPEX syndrome (immune dysfunction, polyendocrinopathy, enteropathy, X-linked syndrome) in humans. Epigenetics is defined by regulation of gene expression without altering nucleotide sequence in the genome. Several epigenetic markers, such as histone acetylation and methylation, and cytosine residue methylation in CpG dinucleotides, have been reported at the Foxp3 locus. In particular, CpG dinucleotides at the Foxp3 locus are methylated in naive CD4+CD25− T cells, activated CD4+ T cells, and TGF-β–induced adaptive Tregs, whereas they are completely demethylated in natural Tregs. The DNA methyltransferases DNMT1 and DNMT3b are associated with the Foxp3 locus in CD4+ T cells. Methylation of CpG residues represses Foxp3 expression, whereas complete demethylation is required for stable Foxp3 expression. In this review, we discuss how different cis-regulatory elements at the Foxp3 locus are subjected to epigenetic modification in different subsets of CD4+ T cells and regulate Foxp3 expression, and how these mechanisms can be exploited to generate efficiently large numbers of suppressive Tregs for therapeutic purposes.
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Schick, Sandra, Kolja Becker, Sudhir Thakurela, David Fournier, Mareike Hildegard Hampel, Stefan Legewie, and Vijay K. Tiwari. "Identifying Novel Transcriptional Regulators with Circadian Expression." Molecular and Cellular Biology 36, no. 4 (December 7, 2015): 545–58. http://dx.doi.org/10.1128/mcb.00701-15.

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Organisms adapt their physiology and behavior to the 24-h day-night cycle to which they are exposed. On a cellular level, this is regulated by intrinsic transcriptional-translational feedback loops that are important for maintaining the circadian rhythm. These loops are organized by members of the core clock network, which further regulate transcription of downstream genes, resulting in their circadian expression. Despite progress in understanding circadian gene expression, only a few players involved in circadian transcriptional regulation, including transcription factors, epigenetic regulators, and long noncoding RNAs, are known. Aiming to discover such genes, we performed a high-coverage transcriptome analysis of a circadian time course in murine fibroblast cells. In combination with a newly developed algorithm, we identified many transcription factors, epigenetic regulators, and long intergenic noncoding RNAs that are cyclically expressed. In addition, a number of these genes also showed circadian expression in mouse tissues. Furthermore, the knockdown of one such factor, Zfp28, influenced the core clock network. Mathematical modeling was able to predict putative regulator-effector interactions between the identified circadian genes and may help for investigations into the gene regulatory networks underlying circadian rhythms.
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Nothof, Sophie A., Frédérique Magdinier, and Julien Van-Gils. "Chromatin Structure and Dynamics: Focus on Neuronal Differentiation and Pathological Implication." Genes 13, no. 4 (April 2, 2022): 639. http://dx.doi.org/10.3390/genes13040639.

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Chromatin structure is an essential regulator of gene expression. Its state of compaction contributes to the regulation of genetic programs, in particular during differentiation. Epigenetic processes, which include post-translational modifications of histones, DNA methylation and implication of non-coding RNA, are powerful regulators of gene expression. Neurogenesis and neuronal differentiation are spatio-temporally regulated events that allow the formation of the central nervous system components. Here, we review the chromatin structure and post-translational histone modifications associated with neuronal differentiation. Studying the impact of histone modifications on neuronal differentiation improves our understanding of the pathophysiological mechanisms of chromatinopathies and opens up new therapeutic avenues. In addition, we will discuss techniques for the analysis of histone modifications on a genome-wide scale and the pathologies associated with the dysregulation of the epigenetic machinery.
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15

Grosswendt, Stefanie, Helene Kretzmer, Zachary D. Smith, Abhishek Sampath Kumar, Sara Hetzel, Lars Wittler, Sven Klages, Bernd Timmermann, Shankar Mukherji, and Alexander Meissner. "Epigenetic regulator function through mouse gastrulation." Nature 584, no. 7819 (July 29, 2020): 102–8. http://dx.doi.org/10.1038/s41586-020-2552-x.

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Cantariño, Neus, Julien Douet, and Marcus Buschbeck. "MacroH2A – An epigenetic regulator of cancer." Cancer Letters 336, no. 2 (August 2013): 247–52. http://dx.doi.org/10.1016/j.canlet.2013.03.022.

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Caprio, Cinzia, Antonio Sacco, Viviana Giustini, and Aldo M. Roccaro. "Epigenetic Aberrations in Multiple Myeloma." Cancers 12, no. 10 (October 15, 2020): 2996. http://dx.doi.org/10.3390/cancers12102996.

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Multiple myeloma (MM) is a plasma cell dyscrasia characterized by proliferation of clonal plasma cells within the bone marrow. Several advances in defining key processes responsible for MM pathogenesis and disease progression have been made; and dysregulation of epigenetics, including DNA methylation and histone modification, has emerged as a crucial regulator of MM pathogenesis. In the present review article, we will focus on the role of epigenetic modifications within the specific context of MM.
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18

Martinez-Moreno, Julio M., Miguel Fontecha-Barriuso, Diego Martin-Sanchez, Juan Guerrero-Mauvecin, Elena Goma-Garces, Beatriz Fernandez-Fernandez, Sol Carriazo, et al. "Epigenetic Modifiers as Potential Therapeutic Targets in Diabetic Kidney Disease." International Journal of Molecular Sciences 21, no. 11 (June 9, 2020): 4113. http://dx.doi.org/10.3390/ijms21114113.

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Diabetic kidney disease is one of the fastest growing causes of death worldwide. Epigenetic regulators control gene expression and are potential therapeutic targets. There is functional interventional evidence for a role of DNA methylation and the histone post-translational modifications—histone methylation, acetylation and crotonylation—in the pathogenesis of kidney disease, including diabetic kidney disease. Readers of epigenetic marks, such as bromodomain and extra terminal (BET) proteins, are also therapeutic targets. Thus, the BD2 selective BET inhibitor apabetalone was the first epigenetic regulator to undergo phase-3 clinical trials in diabetic kidney disease with an endpoint of kidney function. The direct therapeutic modulation of epigenetic features is possible through pharmacological modulators of the specific enzymes involved and through the therapeutic use of the required substrates. Of further interest is the characterization of potential indirect effects of nephroprotective drugs on epigenetic regulation. Thus, SGLT2 inhibitors increase the circulating and tissue levels of β-hydroxybutyrate, a molecule that generates a specific histone modification, β-hydroxybutyrylation, which has been associated with the beneficial health effects of fasting. To what extent this impact on epigenetic regulation may underlie or contribute to the so-far unclear molecular mechanisms of cardio- and nephroprotection offered by SGLT2 inhibitors merits further in-depth studies.
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Yi, Mei, Yixin Tan, Li Wang, Jing Cai, Xiaoling Li, Zhaoyang Zeng, Wei Xiong, et al. "TP63 links chromatin remodeling and enhancer reprogramming to epidermal differentiation and squamous cell carcinoma development." Cellular and Molecular Life Sciences 77, no. 21 (May 23, 2020): 4325–46. http://dx.doi.org/10.1007/s00018-020-03539-2.

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Abstract Squamous cell carcinoma (SCC) is an aggressive malignancy that can originate from various organs. TP63 is a master regulator that plays an essential role in epidermal differentiation. It is also a lineage-dependent oncogene in SCC. ΔNp63α is the prominent isoform of TP63 expressed in epidermal cells and SCC, and overexpression promotes SCC development through a variety of mechanisms. Recently, ΔNp63α was highlighted to act as an epidermal-specific pioneer factor that binds closed chromatin and enhances chromatin accessibility at epidermal enhancers. ΔNp63α coordinates chromatin-remodeling enzymes to orchestrate the tissue-specific enhancer landscape and three-dimensional high-order architecture of chromatin. Moreover, ΔNp63α establishes squamous-like enhancer landscapes to drive oncogenic target expression during SCC development. Importantly, ΔNp63α acts as an upstream regulator of super enhancers to activate a number of oncogenic transcripts linked to poor prognosis in SCC. Mechanistically, ΔNp63α activates genes transcription through physically interacting with a number of epigenetic modulators to establish enhancers and enhance chromatin accessibility. In contrast, ΔNp63α also represses gene transcription via interacting with repressive epigenetic regulators. ΔNp63α expression is regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational levels. In this review, we summarize recent advances of p63 in epigenomic and transcriptional control, as well as the mechanistic regulation of p63.
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Picard, Nathalie, and Michela Fagiolini. "MeCP2: an epigenetic regulator of critical periods." Current Opinion in Neurobiology 59 (December 2019): 95–101. http://dx.doi.org/10.1016/j.conb.2019.04.004.

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21

Liu, Ruijie, Kelan Chen, Natasha Jansz, Marnie E. Blewitt, and Matthew E. Ritchie. "Transcriptional profiling of the epigenetic regulator Smchd1." Genomics Data 7 (March 2016): 144–47. http://dx.doi.org/10.1016/j.gdata.2015.12.027.

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Teiten, Marie-Hélène, Mario Dicato, and Marc Diederich. "Curcumin as a regulator of epigenetic events." Molecular Nutrition & Food Research 57, no. 9 (June 11, 2013): 1619–29. http://dx.doi.org/10.1002/mnfr.201300201.

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23

Angelini, Francesco, Francesca Pagano, Antonella Bordin, Marika Milan, Isotta Chimenti, Mariangela Peruzzi, Valentina Valenti, et al. "The Impact of Environmental Factors in Influencing Epigenetics Related to Oxidative States in the Cardiovascular System." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–18. http://dx.doi.org/10.1155/2017/2712751.

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Oxidative states exert a significant influence on a wide range of biological and molecular processes and functions. When their balance is shifted towards enhanced amounts of free radicals, pathological phenomena can occur, as the generation of reactive oxygen species (ROS) in tissue microenvironment or in the systemic circulation can be detrimental. Epidemic chronic diseases of western societies, such as cardiovascular disease, obesity, and diabetes correlate with the imbalance of redox homeostasis. Current advances in our understanding of epigenetics have revealed a parallel scenario showing the influence of oxidative stress as a major regulator of epigenetic gene regulation via modification of DNA methylation, histones, and microRNAs. This has provided both the biological link and a potential molecular explanation between oxidative stress and cardiovascular/metabolic phenomena. Accordingly, in this review, we will provide current insights on the physiological and pathological impact of changes in oxidative states on cardiovascular disorders, by specifically focusing on the influence of epigenetic regulation. A special emphasis will highlight the effect on epigenetic regulation of human’s current life habits, external and environmental factors, including food intake, tobacco, air pollution, and antioxidant-based approaches. Additionally, the strategy to quantify oxidative states in humans in order to determine which biological marker could best match a subject’s profile will be discussed.
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Yang, Haiqing, Yuting Li, Linying Huang, Miaochun Fang, and Shun Xu. "The Epigenetic Regulation of RNA N6-Methyladenosine Methylation in Glycolipid Metabolism." Biomolecules 13, no. 2 (February 1, 2023): 273. http://dx.doi.org/10.3390/biom13020273.

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The highly conserved and dynamically reversible N6-methyladenine (m6A) modification has emerged as a critical gene expression regulator by affecting RNA splicing, translation efficiency, and stability at the post-transcriptional level, which has been established to be involved in various physiological and pathological processes, including glycolipid metabolism and the development of glycolipid metabolic disease (GLMD). Hence, accumulating studies have focused on the effects and regulatory mechanisms of m6A modification on glucose metabolism, lipid metabolism, and GLMD. This review summarizes the underlying mechanism of how m6A modification regulates glucose and lipid metabolism-related enzymes, transcription factors, and signaling pathways and the advances of m6A regulatory mechanisms in GLMD in order to deepen the understanding of the association of m6A modification with glycolipid metabolism and GLMD.
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Oh, Sungryong, Kyungjin Boo, Jaebeom Kim, Seon Ah Baek, Yoon Jeon, Junghyun You, Ho Lee, et al. "The chromatin-binding protein PHF6 functions as an E3 ubiquitin ligase of H2BK120 via H2BK12Ac recognition for activation of trophectodermal genes." Nucleic Acids Research 48, no. 16 (July 31, 2020): 9037–52. http://dx.doi.org/10.1093/nar/gkaa626.

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Abstract Epigenetic regulation is important for establishing lineage-specific gene expression during early development. Although signaling pathways have been well-studied for regulation of trophectoderm reprogramming, epigenetic regulation of trophectodermal genes with histone modification dynamics have been poorly understood. Here, we identify that plant homeodomain finger protein 6 (PHF6) is a key epigenetic regulator for activation of trophectodermal genes using RNA-sequencing and ChIP assays. PHF6 acts as an E3 ubiquitin ligase for ubiquitination of H2BK120 (H2BK120ub) via its extended plant homeodomain 1 (PHD1), while the extended PHD2 of PHF6 recognizes acetylation of H2BK12 (H2BK12Ac). Intriguingly, the recognition of H2BK12Ac by PHF6 is important for exerting its E3 ubiquitin ligase activity for H2BK120ub. Together, our data provide evidence that PHF6 is crucial for epigenetic regulation of trophectodermal gene expression by linking H2BK12Ac to H2BK120ub modification.
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Hernández-Muñoz, Inmaculada. "Chromatin regulators: weaving epigenetic nets." BioMolecular Concepts 1, no. 3-4 (October 1, 2010): 225–38. http://dx.doi.org/10.1515/bmc.2010.023.

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AbstractIn multicellular organisms differentiated cells must maintain their cellular memory, which will be faithfully inherited and maintained by their progeny. In addition, these specialized cells are exposed to specific environmental and cell-intrinsic signals and will have to appropriately respond to them. Some of these stimuli lead to changes in a subset of genes or to a genome-wide reprogramming of the cells that will remain after stimuli removal and, in some instances, will be inherited by the daughter cells. The molecular substrate that integrates cellular memory and plasticity is the chromatin, a complex of DNA and histones unique to eukaryotes. The nucleosome is the fundamental unit of the chromatin and nucleosomal organization defines different chromatin conformations. Chromatin regulators affect chromatin conformation and accessibility by covalently modifying the DNA or the histones, substituting histone variants, remodeling the nucleosome position or modulating chromatin looping and folding. These regulators frequently act in multiprotein complexes and highly specific interplays among chromatin marks and different chromatin regulators allow a remarkable array of possibilities. Therefore, chromatin regulator nets act to propagate the conformation of different chromatin regions through DNA replication and mitosis, and to remodel the chromatin fiber to regulate the accessibility of the DNA to transcription factors and to the transcription and repair machineries. Here, the state-of-the-art of the best-known chromatin regulators is reviewed.
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Al-Radhawi, M. Ali, Shubham Tripath, Yun Zhang, Eduardo Sontag, and Herbert Levine. "Abstract A026: Epigenetic factor competition reshapes the EMT landscape." Cancer Research 82, no. 23_Supplement_2 (December 1, 2022): A026. http://dx.doi.org/10.1158/1538-7445.cancepi22-a026.

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Abstract The emergence of and transitions between distinct phenotypes in isogenic cells can be attributed to the intricate interplay of epigenetic marks, external signals, and gene regulatory elements. These elements include chromatin remodelers, histone modifiers, transcription factors, and regulatory RNAs. Mathematical models known as Gene Regulatory Networks (GRNs) are an increasingly important tool to unravel the workings of such complex networks. In such models, epigenetic factors are usually proposed to act on the chromatin regions directly involved in the expression of relevant genes. However, it has been well-established that these factors operate globally and compete with each other for targets genome-wide. Therefore, a perturbation of the activity of a regulator can redistribute epigenetic marks across the genome and modulate the levels of competing regulators. These interactions have been brought to the fore by recent experiments (Zhang, Donaher et al, 2022) reporting that the knockouts of different histone methyltransferases can induce two distinct trajectories of EMT, characterized by distinct and unexpected changes in gene expression profiles. In this work, we propose a new modeling framework that combines local transcriptional regulation with global epigenetic control, and show that complex interplay between transcriptional and epigenetic control can lead to rich gene expression dynamics. We use our modeling framework to understand the effects of various epigenetic perturbations on the epithelial-mesenchymal transition, a crucial cellular process involved in both health and disease. We note that the interplay between epigenetic competition, the EMT transcriptional network, and the baseline transcriptional context can result in counter-intuitive experimental observations, and generate unique paths for cells to transition between epithelial and mesenchymal states. We apply our modeling framework to explain the aforementioned recent experimental findings (Zhang, Donaher et al, 2022), and we use it to offer verifiable predictions. One crucial takeaway from our modeling is that experiments involving epigenetic perturbations must be analyzed with care due to the possibility of widespread cross-talk between the genomic targets of different epigenetic factors. This means that the biological consequence of perturbation to an epigenetic modifier could be an outcome of changes in the expression levels of its direct genomic targets or simply a side-effect from the dilution and distribution of an entirely different epigenetic modifier. Citation Format: M. Ali Al-Radhawi, Shubham Tripath, Yun Zhang, Eduardo Sontag, Herbert Levine. Epigenetic factor competition reshapes the EMT landscape. [abstract]. In: Proceedings of the AACR Special Conference: Cancer Epigenomics; 2022 Oct 6-8; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_2):Abstract nr A026.
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Pedrotti, Simona, Roberta Caccia, Maria Victoria Neguembor, Jose Manuel Garcia-Manteiga, Giulia Ferri, Clara de Palma, Tamara Canu, et al. "The Suv420h histone methyltransferases regulate PPAR-γ and energy expenditure in response to environmental stimuli." Science Advances 5, no. 4 (April 2019): eaav1472. http://dx.doi.org/10.1126/sciadv.aav1472.

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Obesity and its associated metabolic abnormalities have become a global emergency with considerable morbidity and mortality. Epidemiologic and animal model data suggest an epigenetic contribution to obesity. Nevertheless, the cellular and molecular mechanisms through which epigenetics contributes to the development of obesity remain to be elucidated. Suv420h1 and Suv420h2 are histone methyltransferases responsible for chromatin compaction and gene repression. Through in vivo, ex vivo, and in vitro studies, we found that Suv420h1 and Suv420h2 respond to environmental stimuli and regulate metabolism by down-regulating peroxisome proliferator–activated receptor gamma (PPAR-γ), a master transcriptional regulator of lipid storage and glucose metabolism. Accordingly, mice lacking Suv420h proteins activate PPAR-γ target genes in brown adipose tissue to increase mitochondria respiration, improve glucose tolerance, and reduce adipose tissue to fight obesity. We conclude that Suv420h proteins are key epigenetic regulators of PPAR-γ and the pathways controlling metabolism and weight balance in response to environmental stimuli.
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Schauder, David M., Jian Shen, Yao Chen, Moujtaba Y. Kasmani, Matthew R. Kudek, Robert Burns, and Weiguo Cui. "E2A-regulated epigenetic landscape promotes memory CD8 T cell differentiation." Proceedings of the National Academy of Sciences 118, no. 16 (April 15, 2021): e2013452118. http://dx.doi.org/10.1073/pnas.2013452118.

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During an acute viral infection, CD8 T cells encounter a myriad of antigenic and inflammatory signals of variable strength, which sets off individual T cells on their own differentiation trajectories. However, the developmental path for each of these cells will ultimately lead to one of only two potential outcomes after clearance of the infection—death or survival and development into memory CD8 T cells. How this cell fate decision is made remains incompletely understood. In this study, we explore the transcriptional changes during effector and memory CD8 T cell differentiation at the single-cell level. Using single-cell, transcriptome-derived gene regulatory network analysis, we identified two main groups of regulons that govern this differentiation process. These regulons function in concert with changes in the enhancer landscape to confer the establishment of the regulatory modules underlying the cell fate decision of CD8 T cells. Furthermore, we found that memory precursor effector cells maintain chromatin accessibility at enhancers for key memory-related genes and that these enhancers are highly enriched for E2A binding sites. Finally, we show that E2A directly regulates accessibility of enhancers of many memory-related genes and that its overexpression increases the frequency of memory precursor effector cells and accelerates memory cell formation while decreasing the frequency of short-lived effector cells. Overall, our results suggest that effector and memory CD8 T cell differentiation is largely regulated by two transcriptional circuits, with E2A serving as an important epigenetic regulator of the memory circuit.
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Melnik, Bodo C., and Gerd Schmitz. "DNA methyltransferase 1-targeting miRNA-148a of dairy milk: a potential bioactive modifier of the human epigenome." Functional Foods in Health and Disease 7, no. 9 (September 30, 2017): 671. http://dx.doi.org/10.31989/ffhd.v7i9.379.

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Background: The perception of milk has changed from a “simple food” to a more sophisticated bioactive functional signaling system that promotes mTORC1-driven postnatal anabolism, growth, and development of the newborn infant. Accumulating evidence supports the view that milk´s miRNAs significantly contribute to these processes. The most abundant miRNA of milk found in milk fat and milk exosomes is miRNA-148a, which targets DNA methyltransferase 1 (DNMT1), a pivotal epigenetic regulator that suppresses transcription. Furthermore, milk-derived miRNA-125b, miRNA-30d, and miRNA-25 target TP53, the guardian of the genome that interacts with DNMT1 and regulates metabolism, cell kinetics, and apoptosis. Thus, the question arose whether cow´s milk-derived miRNAs may modify epigenetic regulation of the human milk consumer. Methods: To understand the potential impact of dairy milk consumption on human epigenetics, we have analyzed all relevant research-based bioinformatics data related to milk, milk miRNAs, epigenetic regulation, and lactation performance with special attention to bovine miRNAs that modify gene expression of DNA methyltransferase 1 (DNMT1) and p53 (TP53), the two guardians of the mammalian genome. By means of translational research and comparative functional genomics, we investigated the potential impact of cow´s milk miRNAs on epigenetic regulation of human DNMT1, TP53, FOXP3, and FTO, which are critically involved in immunologic and metabolic programming respectively. miRNA sequences have been obtained from mirbase.org. miRNA-target site prediction has been performed using TargetScan release 7.0.Results: The most abundant miRNA of cow´s milk is miRNA-148a, which represents more than 10% of all miRNAs of cow´s milk, survives pasteurization and refrigerated storage. The seed sequence of human and bovine miRNA-148a-3p is identical. Furthermore, human and bovine DNMT1 mRNA share 88% identity. The miRNA-148a 7mer seed is conserved in human and bovine DNMT1 mRNA respectively, which may allow for the strong binding of bovine miRNA-148a to human DNMT1 mRNA. Consequently, we hypothesize that bovine milk miRNA-148a - protected by highly resistant milk exosome membranes - may reach the systemic circulation of the milk consumer targeting and suppressing human DNMT1 mRNA. Attenuated DNMT1 expression associated with reduced CpG promoter methylation upregulates gene expression of developmental genes such as FOXP3 and FTO. Milk-derived miRNA-125b, miRNA-30d, and miRNA-25 via targeting TP53 may downregulate p53, which physically interacts with and stabilizes DNMT1. Enhancement of dairy lactation performance is associated with increased expression of bovine milk miRNA-148a, a modification that may further increase the miRNA-148a load of dairy milk.Conclusions: Translational evidence and comparative functional genomics support our hypothesis that bovine milk miRNA signaling may suppress human DNMT1-mediated epigenetic regulation and p53 signaling, which closely interacts with the epigenetic and transcriptional regulation of growth, metabolism, cell cycle progression, and apoptosis. Human and bovine milk miRNAs are able to target DNMT1 and TP53 mRNAs, share identical seed sequences, and resist pasteurization. Pasteurization and refrigeration of dairy milk conserves the gene regulatory software of milk and allows its unrestricted entry into the human food chain. The continued exposure of modern humans to milk´s epigenetic machinery since the widespread distribution of refrigerators is a novel change of human nutrition which may promote diseases of Western civilization.Keywords: adipogenesis, dairy, DNA methyltransferase 1, epigenetics, exosome, miRNA-148a, miRNA-125b, milk, obesity, p53, Parkinson disease, prostate cancer
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Raihan, Tajbir, Robert L. Geneve, Sharyn E. Perry, and Carlos M. Rodriguez Lopez. "The Regulation of Plant Vegetative Phase Transition and Rejuvenation: miRNAs, a Key Regulator." Epigenomes 5, no. 4 (October 18, 2021): 24. http://dx.doi.org/10.3390/epigenomes5040024.

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In contrast to animals, adult organs in plants are not formed during embryogenesis but generated from meristematic cells as plants advance through development. Plant development involves a succession of different phenotypic stages and the transition between these stages is termed phase transition. Phase transitions need to be tightly regulated and coordinated to ensure they occur under optimal seasonal, environmental conditions. Polycarpic perennials transition through vegetative stages and the mature, reproductive stage many times during their lifecycles and, in both perennial and annual species, environmental factors and culturing methods can reverse the otherwise unidirectional vector of plant development. Epigenetic factors regulating gene expression in response to internal cues and external (environmental) stimuli influencing the plant’s phenotype and development have been shown to control phase transitions. How developmental and environmental cues interact to epigenetically alter gene expression and influence these transitions is not well understood, and understanding this interaction is important considering the current climate change scenarios, since epigenetic maladaptation could have catastrophic consequences for perennial plants in natural and agricultural ecosystems. Here, we review studies focusing on the epigenetic regulators of the vegetative phase change and highlight how these mechanisms might act in exogenously induced plant rejuvenation and regrowth following stress.
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Natsume, Atsushi, Motokazu Ito, Keisuke Katsushima, Fumiharu Ohka, Akira Hatanaka, Keiko Shinjo, Shinya Sato, et al. "Chromatin Regulator PRC2 Is a Key Regulator of Epigenetic Plasticity in Glioblastoma." Cancer Research 73, no. 14 (May 29, 2013): 4559–70. http://dx.doi.org/10.1158/0008-5472.can-13-0109.

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Liu, Mengying, Nirmalya Saha, Ambikai Gajan, Nadia Saadat, Smiti V. Gupta, and Lori A. Pile. "A complex interplay between SAM synthetase and the epigenetic regulator SIN3 controls metabolism and transcription." Journal of Biological Chemistry 295, no. 2 (November 27, 2019): 375–89. http://dx.doi.org/10.1074/jbc.ra119.010032.

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The SIN3 histone-modifying complex regulates the expression of multiple methionine catabolic genes, including SAM synthetase (Sam-S), as well as SAM levels. To further dissect the relationship between methionine catabolism and epigenetic regulation by SIN3, we sought to identify genes and metabolic pathways controlled by SIN3 and SAM synthetase (SAM-S) in Drosophila melanogaster. Using several approaches, including RNAi-mediated gene silencing, RNA-Seq– and quantitative RT-PCR–based transcriptomics, and ultra-high-performance LC-MS/MS– and GC/MS–based metabolomics, we found that, as a global transcriptional regulator, SIN3 impacted a wide range of genes and pathways. In contrast, SAM-S affected only a narrow range of genes and pathways. The expression and levels of additional genes and metabolites, however, were altered in Sin3A+Sam-S dual knockdown cells. This analysis revealed that SIN3 and SAM-S regulate overlapping pathways, many of which involve one-carbon and central carbon metabolisms. In some cases, the factors acted independently; in some others, redundantly; and for a third set, in opposition. Together, these results, obtained from experiments with the chromatin regulator SIN3 and the metabolic enzyme SAM-S, uncover a complex relationship between metabolism and epigenetic regulation.
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Narayanan, Sathiya Pandi, Smriti Singh, and Sanjeev Shukla. "A saga of cancer epigenetics: linking epigenetics to alternative splicing." Biochemical Journal 474, no. 6 (March 7, 2017): 885–96. http://dx.doi.org/10.1042/bcj20161047.

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The discovery of an increasing number of alternative splicing events in the human genome highlighted that ∼94% of genes generate alternatively spliced transcripts that may produce different protein isoforms with diverse functions. It is now well known that several diseases are a direct and indirect consequence of aberrant splicing events in humans. In addition to the conventional mode of alternative splicing regulation by ‘cis’ RNA-binding sites and ‘trans’ RNA-binding proteins, recent literature provides enormous evidence for epigenetic regulation of alternative splicing. The epigenetic modifications may regulate alternative splicing by either influencing the transcription elongation rate of RNA polymerase II or by recruiting a specific splicing regulator via different chromatin adaptors. The epigenetic alterations and aberrant alternative splicing are known to be associated with various diseases individually, but this review discusses/highlights the latest literature on the role of epigenetic alterations in the regulation of alternative splicing and thereby cancer progression. This review also points out the need for further studies to understand the interplay between epigenetic modifications and aberrant alternative splicing in cancer progression.
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Barde, Isabelle, Elisa Laurenti, Sonia Verp, Anna Claire Groner, Christopher Towne, Viviane Padrun, Patrick Aebischer, Andreas Trumpp, and Didier Trono. "Regulation of Episomal Gene Expression by KRAB/KAP1-Mediated Histone Modifications." Journal of Virology 83, no. 11 (March 11, 2009): 5574–80. http://dx.doi.org/10.1128/jvi.00001-09.

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ABSTRACT KAP1 is an essential cofactor of KRAB zinc finger proteins, a family of vertebrate-specific epigenetic repressors of largely unknown functions encoded in the hundreds by the mouse and human genomes. So far, KRAB/KAP1-mediated gene regulation has been studied within the environment of chromosomal DNA. Here we demonstrate that KRAB/KAP1 regulation is fully functional within the context of episomal DNA, such as adeno-associated viral and nonintegrated lentiviral vectors, and is correlated with histone modifications typically associated with this epigenetic regulator.
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Ma, Shixin, Xiaoling Wan, Zihou Deng, Lei Shi, Congfang Hao, Zhenyuan Zhou, Chun Zhou, et al. "Epigenetic regulator CXXC5 recruits DNA demethylase Tet2 to regulate TLR7/9-elicited IFN response in pDCs." Journal of Experimental Medicine 214, no. 5 (April 17, 2017): 1471–91. http://dx.doi.org/10.1084/jem.20161149.

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TLR7/9 signals are capable of mounting massive interferon (IFN) response in plasmacytoid dendritic cells (pDCs) immediately after viral infection, yet the involvement of epigenetic regulation in this process has not been documented. Here, we report that zinc finger CXXC family epigenetic regulator CXXC5 is highly expressed in pDCs, where it plays a crucial role in TLR7/9- and virus-induced IFN response. Notably, genetic ablation of CXXC5 resulted in aberrant methylation of the CpG-containing island (CGI) within the Irf7 gene and impaired IRF7 expression in steady-state pDCs. Mechanistically, CXXC5 is responsible for the recruitment of DNA demethylase Tet2 to maintain the hypomethylation of a subset of CGIs, a process coincident with active histone modifications and constitutive transcription of these CGI-containing genes. Consequently, CXXC5-deficient mice had compromised early IFN response and became highly vulnerable to infection by herpes simplex virus and vesicular stomatitis virus. Together, our results identify CXXC5 as a novel epigenetic regulator for pDC-mediated antiviral response.
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Woods, David, Karrune Woan, Dapeng Wang, Yu Yu, John Powers, Eva Sahakian, Fengdong Cheng, et al. "Histone deacetylase 11 is an epigenetic regulator of cytotoxic T-lymphocyte effector function and memory formation (P1404)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 117.2. http://dx.doi.org/10.4049/jimmunol.190.supp.117.2.

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Abstract The roles of individual histone deacetylases in the regulation of T-cell development and function remain largely unknown. Here we provide evidence for HDAC11 as an epigenetic regulator of T-cell inflammatory response as well as CTL central memory formation. To investigate the role of HDAC11 in T-cells, an HDAC11 knockout (HDAC11KO) mouse model was utilized. HDAC11KO mice display no gross phenotypic abnormalities and no alterations in T-cell development or CD4+/CD8+ population distributions. However, HDAC11KO CTLs are hyper-proliferative and secrete significantly higher levels of IL-2, TNF, and IFN-γ upon activation, and HDAC11KO mice accumulate higher percentages of central memory CTLs. In an allogeneic bone marrow transfer model, HDAC11KO T-cells mediate more potent and robust graft vs host disease associated with increased inflammatory cytokines. Mechanistically, we provide evidence that in CTLs HDAC11 interacts with the Eomes gene promoter, a known regulator of IFN-γ production and memory formation. HDAC11KO CTLs, at both basal state and post stimulation, display higher levels of acetylation at the Eomes promoter, indicative of a permissive transcriptional state. Correspondingly, eomes mRNA levels in HDAC11KO cells are elevated. Finally, chromatin immunoprecipitation of HDAC11 reveals interaction between HDAC11 and the Eomes promoter in CTLs. These results support HDAC11 as an epigenetic regulator of CTL function and memory formation through epigenetic regulation of Eomes.
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Batlle-López, Ana, María G. Cortiguera, and M. Dolores Delgado. "The epigenetic regulator CTCF modulates BCL6 in lymphoma." Oncoscience 2, no. 10 (September 14, 2015): 783–84. http://dx.doi.org/10.18632/oncoscience.239.

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Leong, Huei San, Kelan Chen, Yifang Hu, Stanley Lee, Jason Corbin, Miha Pakusch, James M. Murphy, et al. "Epigenetic Regulator Smchd1 Functions as a Tumor Suppressor." Cancer Research 73, no. 5 (December 26, 2012): 1591–99. http://dx.doi.org/10.1158/0008-5472.can-12-3019.

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Wan, Le-Ben, Hua Pan, Yong Cheng, Jun Ma, Andrew Fedoriw, Victor Lobanenkov, Keith E. Latham, Richard M. Schultz, and Marisa S. Bartolomei. "Maternal effects of CTCF, a multifunctional epigenetic regulator." Developmental Biology 319, no. 2 (July 2008): 571. http://dx.doi.org/10.1016/j.ydbio.2008.05.369.

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Fabini, Edoardo, Vladimir O. Talibov, Filip Mihalic, Marina Naldi, Manuela Bartolini, Carlo Bertucci, Alberto Del Rio, and U. Helena Danielson. "Unveiling the Biochemistry of the Epigenetic Regulator SMYD3." Biochemistry 58, no. 35 (August 7, 2019): 3634–45. http://dx.doi.org/10.1021/acs.biochem.9b00420.

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42

Glastad, Karl M., Riley J. Graham, Linyang Ju, Julian Roessler, Cristina M. Brady, and Shelley L. Berger. "Epigenetic Regulator CoREST Controls Social Behavior in Ants." Molecular Cell 77, no. 2 (January 2020): 338–51. http://dx.doi.org/10.1016/j.molcel.2019.10.012.

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Zhang, Jian, Hamed I. Ali, Yudhishtar Singh Bedi, and Mahua Choudhury. "The plasticizer BBP selectively inhibits epigenetic regulator sirtuins." Toxicology 338 (December 2015): 130–41. http://dx.doi.org/10.1016/j.tox.2015.10.004.

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Jansz, Natasha, Kelan Chen, James M. Murphy, and Marnie E. Blewitt. "The Epigenetic Regulator SMCHD1 in Development and Disease." Trends in Genetics 33, no. 4 (April 2017): 233–43. http://dx.doi.org/10.1016/j.tig.2017.01.007.

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45

Luo, Dan, Antoine de Morree, Stephane Boutet, Navaline Quach, Vanita Natu, Arjun Rustagi, and Thomas A. Rando. "Deltex2 represses MyoD expression and inhibits myogenic differentiation by acting as a negative regulator of Jmjd1c." Proceedings of the National Academy of Sciences 114, no. 15 (March 28, 2017): E3071—E3080. http://dx.doi.org/10.1073/pnas.1613592114.

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The myogenic regulatory factor MyoD has been implicated as a key regulator of myogenesis, and yet there is little information regarding its upstream regulators. We found that Deltex2 inhibits myogenic differentiation in vitro, and that skeletal muscle stem cells from Deltex2 knockout mice exhibit precocious myogenic differentiation and accelerated regeneration in response to injury. Intriguingly, Deltex2 inhibits myogenesis by suppressing MyoD transcription, and the Deltex2 knockout phenotype can be rescued by a loss-of-function allele for MyoD. In addition, we obtained evidence that Deltex2 regulates MyoD expression by promoting the enrichment of histone 3 modified by dimethylation at lysine 9 at a key regulatory region of the MyoD locus. The enrichment is attributed to a Deltex2 interacting protein, Jmjd1c, whose activity is directly inhibited by Deltex2 and whose expression is required for MyoD expression in vivo and in vitro. Finally, we find that Deltex2 causes Jmjd1c monoubiquitination and inhibits its demethylase activity. Mutation of the monoubiquitination site in Jmjd1c abolishes the inhibitory effect of Deltex2 on Jmjd1c demethylase activity. These results reveal a mechanism by which a member of the Deltex family of proteins can inhibit cellular differentiation, and demonstrate a role of Deltex in the epigenetic regulation of myogenesis.
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Seong, Rho H., Sungkyu Lee, Jieun Kim, and Hyungyu Min. "RORγt-driven TH17 cell differentiation requires epigenetic control by the Swi/Snf chromatin remodeling complex." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 230.14. http://dx.doi.org/10.4049/jimmunol.204.supp.230.14.

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Abstract Epigenetic regulation, including chromatin accessibility and posttranslational modifications of histones, is of importance for T cell lineage decision. TH17 cells play a critical role in protective mucosal immunity and pathogenic multiple autoimmune diseases. The differentiation of TH17 cells is dictated by a master transcription factor, RORγt. However, the epigenetic mechanism that controls TH17 cell differentiation remains poorly understood. Here we show that the Swi/Snf complex is required for TH17-mediated cytokine production both in vitro and in vivo. We demonstrate that RORγt recruits and forms a complex with the Swi/Snf complex to cooperate for the RORγt mediated epigenetic modifications of target genes, including both permissive and repressive ones for TH17 cell differentiation. Our findings thus highlight the Swi/Snf complex as an essential epigenetic regulator of TH17 cell differentiation and provide a basis for the understanding of how a master transcription factor RORγt collaborates with the Swi/Snf complex to govern epigenetic regulation.
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Yan, Fangxue, Jinyang Li, Jelena Milosevic, Ricardo Petroni, Suying Liu, Zhennan Shi, Salina Yuan, et al. "KAT6A and ENL Form an Epigenetic Transcriptional Control Module to Drive Critical Leukemogenic Gene-Expression Programs." Cancer Discovery 12, no. 3 (March 1, 2022): 792–811. http://dx.doi.org/10.1158/2159-8290.cd-20-1459.

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Abstract Epigenetic programs are dysregulated in acute myeloid leukemia (AML) and help enforce an oncogenic state of differentiation arrest. To identify key epigenetic regulators of AML cell fate, we performed a differentiation-focused CRISPR screen in AML cells. This screen identified the histone acetyltransferase KAT6A as a novel regulator of myeloid differentiation that drives critical leukemogenic gene-expression programs. We show that KAT6A is the initiator of a newly described transcriptional control module in which KAT6A-catalyzed promoter H3K9ac is bound by the acetyl-lysine reader ENL, which in turn cooperates with a network of chromatin factors to induce transcriptional elongation. Inhibition of KAT6A has strong anti-AML phenotypes in vitro and in vivo, suggesting that KAT6A small-molecule inhibitors could be of high therapeutic interest for mono-therapy or combinatorial differentiation-based treatment of AML. Significance: AML is a poor-prognosis disease characterized by differentiation blockade. Through a cell-fate CRISPR screen, we identified KAT6A as a novel regulator of AML cell differentiation. Mechanistically, KAT6A cooperates with ENL in a “writer–reader” epigenetic transcriptional control module. These results uncover a new epigenetic dependency and therapeutic opportunity in AML. This article is highlighted in the In This Issue feature, p. 587
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Fujikura, Kohei, Makoto Yoshida, and Kazuma Uesaka. "Transcriptome complexity in intravascular NK/T-cell lymphoma." Journal of Clinical Pathology 73, no. 10 (March 18, 2020): 671–75. http://dx.doi.org/10.1136/jclinpath-2020-206461.

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AimsIntravascular NK/T-cell lymphoma (IVNKTCL) is a rare disease, which is characterised by exclusive growth of large cells within the lumen of small vessels, Epstein–Barr virus infection and somatic mutations in epigenetic regulator genes. Here, we elucidate the transcriptomic complexity of IVNKTCL.MethodsIVNKTCL cases were retrieved from a single-centre cohort of 25 intravascular lymphomas. RNA-seq and whole exome sequencing (WES) were performed to analyse transcriptomic abnormalities and mutations in splicing factors.ResultsApproximately 88% of the total reads from the RNA-seq were considered exonic, while the remaining reads (12%) were mapped to intronic or intergenic regions. We detected 28,941 alternative splicing events, some of which would produce abnormal proteins rarely found in normal cells. The detected events also included tumour-specific splicing alterations in oncogenes and tumour suppressors (e.g., HRAS, MDM2 and VEGFA). WES identified premature termination mutations or copy number losses in a total of 15 splicing regulator genes, including SF3B5, SRSF12 and TNPO3.ConclusionsThis study raises the possibility that IVNKTCL may be driven by multiple complex regulatory loops, including non-exonic expression and aberrant splicing, in addition to defects in epigenetic regulation.
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Balint, Balint L., Attila Szanto, Andras Madi, Uta-Maria Bauer, Petra Gabor, Szilvia Benko, Laszlo G. Puskás, Peter J. A. Davies, and Laszlo Nagy. "Arginine Methylation Provides Epigenetic Transcription Memory for Retinoid-Induced Differentiation in Myeloid Cells." Molecular and Cellular Biology 25, no. 13 (July 1, 2005): 5648–63. http://dx.doi.org/10.1128/mcb.25.13.5648-5663.2005.

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ABSTRACT Cellular differentiation is governed by changes in gene expression, but at the same time, a cell's identity needs to be maintained through multiple cell divisions during maturation. In myeloid cell lines, retinoids induce gene expression and a well-characterized two-step lineage-specific differentiation. To identify mechanisms that contribute to cellular transcriptional memory, we analyzed the epigenetic changes taking place on regulatory regions of tissue transglutaminase, a gene whose expression is tightly linked to retinoid-induced differentiation. Here we report that the induction of an intermediary or “primed” state of myeloid differentiation is associated with increased H4 arginine 3 and decreased H3 lysine 4 methylation. These modifications occur before transcription and appear to prime the chromatin for subsequent hormone-regulated transcription. Moreover, inhibition of methyltransferase activity, preacetylation, or activation of the enzyme PAD4 attenuated retinoid-regulated gene expression, while overexpression of PRMT1, a methyltransferase, enhanced retinoid responsiveness. Taken together, our results suggest that H4 arginine 3 methylation is a bona fide positive epigenetic marker and regulator of transcriptional responsiveness as well as a signal integration mechanism during cell differentiation and, as such, may provide epigenetic memory.
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Gupta, P. D. "The Mighty Microbiota: Regulator of the Human Body." Clinical Research and Clinical Trials 3, no. 5 (June 25, 2021): 01–08. http://dx.doi.org/10.31579/2693-4779/048.

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Microbiota is a life line for human being, however if the balance in interspecies of microbiota is disturb, it can cause not only serious diseases but can kill also. Collectively the microbiotal species act as epigenetic factor for humans. First exposure to microbiota is in utero. The whole health programming of the individuals stars even before birth. C-section or fed formula fed babies are immunologically weaker than that of normal delivered and beast fed babies. For the lifelong good health of babies, Mothers should opt for vaginal delivery and breastfeeding for healthy newborn
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