G2 Histone Methylation Is Required for the Proper Segregation of Chromosomes
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The C-Terminal Region of Histone H4 Recognized by Antinucleosome Th Cells in Identification of a Minimal T Cell Epitope
Identification of a Minimal T Cell Epitope Recognized by Antinucleosome Th Cells in the C-Terminal Region of Histone H4 This information is current as Patrice Decker, Anne Le Moal, Jean-Paul Briand and of October 2, 2021. Sylviane Muller J Immunol 2000; 165:654-662; ; doi: 10.4049/jimmunol.165.2.654 http://www.jimmunol.org/content/165/2/654 Downloaded from References This article cites 34 articles, 13 of which you can access for free at: http://www.jimmunol.org/content/165/2/654.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 2, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Identification of a Minimal T Cell Epitope Recognized by Antinucleosome Th Cells in the C-Terminal Region of Histone H41 Patrice Decker, Anne Le Moal, Jean-Paul Briand, and Sylviane Muller2 Autoreactive T cells responding to systemic autoantigens have been characterized in patients and mice with autoimmune diseases and in healthy individuals. -
The Molecular Hallmarks of Epigenetic Control
PERSPECTIVES EPIGENETICS mainly highlight important mechanistic TIMELINE and conceptual advances. Seminal primary papers are cited, but for in-depth discussions The molecular hallmarks of epigenetic and additional references the reader is at times referred to the textbook Epigenetics3 control or other timely reviews. Foundation of epigenetics C. David Allis and Thomas Jenuwein Pioneering work carried out between Abstract | Over the past 20 years, breakthrough discoveries of chromatin-modifying 1869 and 1928 by Miescher, Flemming, Kossel and Heitz defined nucleic acids, enzymes and associated mechanisms that alter chromatin in response to chromatin and histone proteins, which physiological or pathological signals have transformed our knowledge of led to the cytological distinction between epigenetics from a collection of curious biological phenomena to a functionally euchromatin and heterochromatin4 (FIG. 1a). dissected research field. Here, we provide a personal perspective on the This was followed by ground-breaking 5 development of epigenetics, from its historical origins to what we define as studies by Muller (in Drosophila melanogaster) and McClintock6 (in maize) ‘the modern era of epigenetic research’. We primarily highlight key molecular on position-effect variegation (PEV) and mechanisms of and conceptual advances in epigenetic control that have changed transposable elements, providing early our understanding of normal and perturbed development. hints of non-Mendelian inheritance. Descriptions of the phenomena of X-chromosome inactivation7 -
Role of STAT1 in the Resistance of HBV to IFN‑Α
EXPERIMENTAL AND THERAPEUTIC MEDICINE 21: 550, 2021 Role of STAT1 in the resistance of HBV to IFN‑α BINGFA XU1, BO TANG2 and JIAJIA WEI3 1Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061; 2Department of Pharmacy, Huainan First People's Hospital, Huainan, Anhui 232007; 3Department of Pharmacy, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China Received February 26, 2020; Accepted February 17, 2021 DOI: 10.3892/etm.2021.9982 Abstract. The objective of the present study was to explore of the receptor. This subsequently changes the intracellular the mechanism of hepatitis B virus (HBV) resistance to inter‑ conformation of the receptor and activates janus kinase (JAK). feron (IFN), and the role of signal transducer and activator JAK phosphorylates signal transducer and activator of tran‑ of transcription 1 (STAT1). HepG2.2.15 cells were stimulated scription (STAT) in the cytoplasm, which then forms STAT1/2 with a long‑term (6‑24 weeks) low‑dose interferon (IFN)α‑2b heterodimers and is transported to the nucleus to interact with (10‑70 IU/ml), so as to construct and screen a HepG2.2.15 IFN‑stimulated response elements (ISRE). This initiates the cell model resistant to IFNα‑2b. The changes of STAT1 and transcription of IFN‑stimulated genes (ISGs), resulting in other proteins in the JAK‑STAT signaling pathway, before and proteins which exert direct or indirect antiviral effects (8), after drug resistance, were compared. The phosphorylation of such as double‑stranded RNA‑dependent protease (Protein STAT1 in HepG2.2.15 cells resistant to IFNα‑2b was signifi‑ Kinase r; RKR) and 2',5'‑oligoadenylate synthetase 1 (OAS1), cantly decreased, and the expression level of 2',5'‑oligoadenylate anti‑myxovirus protein (myxovirus resistance protein A; synthetase 1 was downregulated. -
PRMT5-CATALYZED ARGININE METHYLATION of NF-Κb P65 IN
PRMT5-CATALYZED ARGININE METHYLATION OF NF-κB p65 IN THE ENDOTHELIAL CELL INDUCTION OF PRO-INFLAMMATORY CHEMOKINES by DANIEL PELLERIN HARRIS Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Dissertation Advisor: Paul E. DiCorleto, Ph.D. Department of Physiology and Biophysics CASE WESTERN RESERVE UNIVERSITY January, 2016 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of Daniel P. Harris candidate for the Doctor of Philosophy degree *. Thomas N. Nosek, Ph.D., Committee Chair Paul E. DiCorleto, Ph.D. Cathleen R. Carlin, Ph.D. George R. Dubyak, Ph.D. Paul L. Fox, Ph.D. Mukesh K. Jain, M.D. July 27th, 2015 *We also certify that written approval has been obtained for any proprietary material contained therein. iii DEDICATION This dissertation is dedicated to my great-grandparents, Mark and Madeline Pellerin, and my parents Steve and Madeline Harris, for showing me how to live with grace and kindness. i TABLE OF CONTENTS List of Tables ....................................................................................................... 4 List of Figures ...................................................................................................... 5 Acknowledgements ............................................................................................ 6 List of Abbreviations ......................................................................................... 11 Abstract ............................................................................................................. -
The Role of Histone H2av Variant Replacement and Histone H4 Acetylation in the Establishment of Drosophila Heterochromatin
The role of histone H2Av variant replacement and histone H4 acetylation in the establishment of Drosophila heterochromatin Jyothishmathi Swaminathan, Ellen M. Baxter, and Victor G. Corces1 Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA Activation and repression of transcription in eukaryotes involve changes in the chromatin fiber that can be accomplished by covalent modification of the histone tails or the replacement of the canonical histones with other variants. Here we show that the histone H2A variant of Drosophila melanogaster, H2Av, localizes to the centromeric heterochromatin, and it is recruited to an ectopic heterochromatin site formed by a transgene array. His2Av behaves genetically as a PcG gene and mutations in His2Av suppress position effect variegation (PEV), suggesting that this histone variant is required for euchromatic silencing and heterochromatin formation. His2Av mutants show reduced acetylation of histone H4 at Lys 12, decreased methylation of histone H3 at Lys 9, and a reduction in HP1 recruitment to the centromeric region. H2Av accumulation or histone H4 Lys 12 acetylation is not affected by mutations in Su(var)3-9 or Su(var)2-5. The results suggest an ordered cascade of events leading to the establishment of heterochromatin and requiring the recruitment of the histone H2Av variant followed by H4 Lys 12 acetylation as necessary steps before H3 Lys 9 methylation and HP1 recruitment can take place. [Keywords: Chromatin; silencing; transcription; histone; nucleus] Received September 8, 2004; revised version accepted November 4, 2004. The basic unit of chromatin is the nucleosome, which is guchi et al. 2004). The role of histone variants, and spe- made up of 146 bp of DNA wrapped around a histone cially those of H3 and H2A, in various nuclear processes octamer composed of two molecules each of the histones has been long appreciated (Wolffe and Pruss 1996; Ah- H2A, H2B, H3, and H4. -
From 1957 to Nowadays: a Brief History of Epigenetics
International Journal of Molecular Sciences Review From 1957 to Nowadays: A Brief History of Epigenetics Paul Peixoto 1,2, Pierre-François Cartron 3,4,5,6,7,8, Aurélien A. Serandour 3,4,6,7,8 and Eric Hervouet 1,2,9,* 1 Univ. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, F-25000 Besançon, France; [email protected] 2 EPIGENEXP Platform, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France 3 CRCINA, INSERM, Université de Nantes, 44000 Nantes, France; [email protected] (P.-F.C.); [email protected] (A.A.S.) 4 Equipe Apoptose et Progression Tumorale, LaBCT, Institut de Cancérologie de l’Ouest, 44805 Saint Herblain, France 5 Cancéropole Grand-Ouest, Réseau Niches et Epigénétique des Tumeurs (NET), 44000 Nantes, France 6 EpiSAVMEN Network (Région Pays de la Loire), 44000 Nantes, France 7 LabEX IGO, Université de Nantes, 44000 Nantes, France 8 Ecole Centrale Nantes, 44300 Nantes, France 9 DImaCell Platform, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France * Correspondence: [email protected] Received: 9 September 2020; Accepted: 13 October 2020; Published: 14 October 2020 Abstract: Due to the spectacular number of studies focusing on epigenetics in the last few decades, and particularly for the last few years, the availability of a chronology of epigenetics appears essential. Indeed, our review places epigenetic events and the identification of the main epigenetic writers, readers and erasers on a historic scale. This review helps to understand the increasing knowledge in molecular and cellular biology, the development of new biochemical techniques and advances in epigenetics and, more importantly, the roles played by epigenetics in many physiological and pathological situations. -
Sleeping Beauty Transposon Mutagenesis Identifies Genes That
Sleeping Beauty transposon mutagenesis identifies PNAS PLUS genes that cooperate with mutant Smad4 in gastric cancer development Haruna Takedaa,b, Alistair G. Rustc,d, Jerrold M. Warda, Christopher Chin Kuan Yewa, Nancy A. Jenkinsa,e, and Neal G. Copelanda,e,1 aDivision of Genomics and Genetics, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore 138673; bDepartment of Pathology, School of Medicine, Kanazawa Medical University, Ishikawa 920-0293, Japan; cExperimental Cancer Genetics, Wellcome Trust Sanger Institute, Cambridge CB10 1HH, United Kingdom; dTumour Profiling Unit, The Institute of Cancer Research, Chester Beatty Laboratories, London SW3 6JB, United Kingdom; and eCancer Research Program, Houston Methodist Research Institute, Houston, TX 77030 Contributed by Neal G. Copeland, February 27, 2016 (sent for review October 15, 2015; reviewed by Yoshiaki Ito and David A. Largaespada) Mutations in SMAD4 predispose to the development of gastroin- animal models that mimic human GC, researchers have infected testinal cancer, which is the third leading cause of cancer-related mice with H. pylori and then, treated them with carcinogens. They deaths. To identify genes driving gastric cancer (GC) development, have also used genetic engineering to develop a variety of trans- we performed a Sleeping Beauty (SB) transposon mutagenesis genic and KO mouse models of GC (10). Smad4 KO mice are one + − screen in the stomach of Smad4 / mutant mice. This screen iden- GC model that has been of particular interest to us (11, 12). tified 59 candidate GC trunk drivers and a much larger number of Heterozygous Smad4 KO mice develop polyps in the pyloric re- candidate GC progression genes. -
Histone H4 Lysine 20 Mono-Methylation Directly Facilitates Chromatin Openness and Promotes Transcription of Housekeeping Genes
ARTICLE https://doi.org/10.1038/s41467-021-25051-2 OPEN Histone H4 lysine 20 mono-methylation directly facilitates chromatin openness and promotes transcription of housekeeping genes Muhammad Shoaib 1,8,9, Qinming Chen2,9, Xiangyan Shi 3, Nidhi Nair1, Chinmayi Prasanna 2, Renliang Yang2,4, David Walter1, Klaus S. Frederiksen 5, Hjorleifur Einarsson1, J. Peter Svensson 6, ✉ ✉ ✉ Chuan Fa Liu 2, Karl Ekwall6, Mads Lerdrup 7 , Lars Nordenskiöld 2 & Claus S. Sørensen 1 1234567890():,; Histone lysine methylations have primarily been linked to selective recruitment of reader or effector proteins that subsequently modify chromatin regions and mediate genome functions. Here, we describe a divergent role for histone H4 lysine 20 mono-methylation (H4K20me1) and demonstrate that it directly facilitates chromatin openness and accessibility by disrupting chromatin folding. Thus, accumulation of H4K20me1 demarcates highly accessible chromatin at genes, and this is maintained throughout the cell cycle. In vitro, H4K20me1-containing nucleosomal arrays with nucleosome repeat lengths (NRL) of 187 and 197 are less compact than unmethylated (H4K20me0) or trimethylated (H4K20me3) arrays. Concordantly, and in contrast to trimethylated and unmethylated tails, solid-state NMR data shows that H4K20 mono-methylation changes the H4 conformational state and leads to more dynamic histone H4-tails. Notably, the increased chromatin accessibility mediated by H4K20me1 facilitates gene expression, particularly of housekeeping genes. Altogether, we show how the methy- lation state of a single histone H4 residue operates as a focal point in chromatin structure control. While H4K20me1 directly promotes chromatin openness at highly transcribed genes, it also serves as a stepping-stone for H4K20me3-dependent chromatin compaction. -
Human Brain Organoids Reveal Accelerated Development of Cortical Neuron Classes As a Shared Feature of Autism Risk Genes
bioRxiv preprint doi: https://doi.org/10.1101/2020.11.10.376509; this version posted November 12, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Human brain organoids reveal accelerated development of cortical neuron classes as a shared feature of autism risk genes Bruna Paulsen1,2,†, Silvia Velasco1,2,†,#, Amanda J. Kedaigle1,2,3,†, Martina Pigoni1,2,†, Giorgia Quadrato4,5 Anthony Deo2,6,7,8, Xian Adiconis2,3, Ana Uzquiano1,2, Kwanho Kim1,2,3, Sean K. Simmons2,3, Kalliopi Tsafou2, Alex Albanese9, Rafaela Sartore1,2, Catherine Abbate1,2, Ashley Tucewicz1,2, Samantha Smith1,2, Kwanghun Chung9,10,11,12, Kasper Lage2,13, Aviv Regev3,14, Joshua Z. Levin2,3, Paola Arlotta1,2,# † These authors contributed equally to the work # Correspondence should be addressed to [email protected] and [email protected] 1 Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA 2 Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA 3 Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA 4 Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; 5 Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at the University of Southern California, Los Angeles, CA 90033, USA. 6 Department of Psychiatry, -
SETD3 Is an Actin Histidine Methyltransferase That Prevents Primary Dystocia
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nature. Manuscript Author Author manuscript; Manuscript Author available in PMC 2019 June 10. Published in final edited form as: Nature. 2019 January ; 565(7739): 372–376. doi:10.1038/s41586-018-0821-8. SETD3 is an Actin Histidine Methyltransferase that Prevents Primary Dystocia Alex W. Wilkinson1,*, Jonathan Diep2,*, Shaobo Dai3,*, Shuo Liu1, Yaw shin Ooi2, Dan Song4, Tie-Mei Li1, John R. Horton3, Xing Zhang3, Chao Liu4, Darshan V. Trivedi4, Katherine M. Ruppel4, José G. Vilches-Moure5, Kerriann M. Casey5, Justin Mak6, Tina Cowan7, Joshua E. Elias8, Claude M. Nagamine5, James A. Spudich4, Xiaodong Cheng3,#, Jan E. Carette2,#, and Or Gozani1,# 1Department of Biology, Stanford University, Stanford, CA 94305, USA 2Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA 3Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA 4Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA 5Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA 6Stanford Healthcare, Palo Alto, CA 94305 USA 7Departent of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA 8Deparment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford CA 94305, USA Abstract For over fifty years, the methylation of mammalian actin at histidine 73 (actin-H73me) has been known to exist1. Beyond mammals, we find that actin-H73me is conserved in several additional model animal and plant organisms. Despite the pervasiveness of H73me, its function is enigmatic, and the enzyme generating this modification is unknown. -
Histones H3 and H4 Are Components of Upstream Activation Factor Required for the High-Level Transcription of Yeast Rdna by RNA Polymerase I
Proc. Natl. Acad. Sci. USA Vol. 94, pp. 13458–13462, December 1997 Biochemistry Histones H3 and H4 are components of upstream activation factor required for the high-level transcription of yeast rDNA by RNA polymerase I JOHN KEENER*, JONATHAN A. DODD*, DOMINIQUE LALO, AND MASAYASU NOMURA† Department of Biological Chemistry, University of California, Irvine, CA 92697-1700 Contributed by Masayasu Nomura, October 16, 1997 ABSTRACT RNA polymerase I (Pol I) transcription in consisting of Rrn6p, Rrn7p, and Rrn11p; refs. 3, 9, and 10), the yeast Saccharomyces cerevisiae is greatly stimulated in vivo Rrn3p (5), and Pol I are required. In addition to these factors, and in vitro by the multiprotein complex, upstream activation upstream activation factor (UAF) and TATA box-binding factor (UAF). UAF binds tightly to the upstream element of the protein, as well as the upstream element, are required for a rDNA promoter, such that once bound (in vitro), UAF does not high level of transcription from the yeast rDNA promoter (4, readily exchange onto a competing template. Of the polypep- 11). Purified UAF previously was shown to contain three tides previously identified in purified UAF, three are encoded genetically defined subunits, Rrn5p, Rrn9p, and Rrn10p, and by genes required for Pol I transcription in vivo: RRN5, RRN9, two uncharacterized subunits, p30 and p18 (4). and RRN10. Two others, p30 and p18, have remained unchar- DNA in the eukaryotic nucleus is organized as chromatin, acterized. We report here that the N-terminal amino acid consisting mostly of regularly repeating nucleosomes in which sequence, its mobility in gel electrophoresis, and the immu- DNA is wrapped around an octameric structure of core noreactivity of p18 shows that it is histone H3. -
Comparative Transcriptomics Reveals Similarities and Differences
Seifert et al. BMC Cancer (2015) 15:952 DOI 10.1186/s12885-015-1939-9 RESEARCH ARTICLE Open Access Comparative transcriptomics reveals similarities and differences between astrocytoma grades Michael Seifert1,2,5*, Martin Garbe1, Betty Friedrich1,3, Michel Mittelbronn4 and Barbara Klink5,6,7 Abstract Background: Astrocytomas are the most common primary brain tumors distinguished into four histological grades. Molecular analyses of individual astrocytoma grades have revealed detailed insights into genetic, transcriptomic and epigenetic alterations. This provides an excellent basis to identify similarities and differences between astrocytoma grades. Methods: We utilized public omics data of all four astrocytoma grades focusing on pilocytic astrocytomas (PA I), diffuse astrocytomas (AS II), anaplastic astrocytomas (AS III) and glioblastomas (GBM IV) to identify similarities and differences using well-established bioinformatics and systems biology approaches. We further validated the expression and localization of Ang2 involved in angiogenesis using immunohistochemistry. Results: Our analyses show similarities and differences between astrocytoma grades at the level of individual genes, signaling pathways and regulatory networks. We identified many differentially expressed genes that were either exclusively observed in a specific astrocytoma grade or commonly affected in specific subsets of astrocytoma grades in comparison to normal brain. Further, the number of differentially expressed genes generally increased with the astrocytoma grade with one major exception. The cytokine receptor pathway showed nearly the same number of differentially expressed genes in PA I and GBM IV and was further characterized by a significant overlap of commonly altered genes and an exclusive enrichment of overexpressed cancer genes in GBM IV. Additional analyses revealed a strong exclusive overexpression of CX3CL1 (fractalkine) and its receptor CX3CR1 in PA I possibly contributing to the absence of invasive growth.