Natural Antisense Transcript PEBP1P3 Regulates the RNA Expression, DNA Methylation and Histone Modification of CD45 Gene
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PCAF-Dependent Epigenetic Changes Promote Axonal Regeneration in the Central Nervous System
ARTICLE Received 13 Dec 2013 | Accepted 27 Feb 2014 | Published 1 Apr 2014 DOI: 10.1038/ncomms4527 PCAF-dependent epigenetic changes promote axonal regeneration in the central nervous system Radhika Puttagunta1,*, Andrea Tedeschi2,*, Marilia Grando So´ria1,3, Arnau Hervera1,4, Ricco Lindner1,3, Khizr I. Rathore1, Perrine Gaub1,3, Yashashree Joshi1,3,5, Tuan Nguyen1, Antonio Schmandke1, Claudia J. Laskowski2, Anne-Laurence Boutillier6, Frank Bradke2 & Simone Di Giovanni1,4 Axonal regenerative failure is a major cause of neurological impairment following central nervous system (CNS) but not peripheral nervous system (PNS) injury. Notably, PNS injury triggers a coordinated regenerative gene expression programme. However, the molecular link between retrograde signalling and the regulation of this gene expression programme that leads to the differential regenerative capacity remains elusive. Here we show through systematic epigenetic studies that the histone acetyltransferase p300/CBP-associated factor (PCAF) promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury. Furthermore, we find that extracellular signal-regulated kinase (ERK)-mediated retrograde signalling is required for PCAF-dependent regenerative gene reprogramming. Finally, PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury. Thus, we find a specific epigenetic mechanism that regulates axonal regeneration of CNS axons, suggesting novel targets for clinical application. 1 Laboratory for NeuroRegeneration and Repair, Center for Neurology, Hertie Institute for Clinical Brain Research, University of Tu¨bingen, 72076 Tu¨bingen, Germany. 2 Department of Axonal Growth and Regeneration, German Center for Neurodegenerative Disease, 53175 Bonn, Germany. -
Histone Modifications of H3k4me3, H3k9me3 and Lineage Gene Expressions in Chimeric Mouse Embryo
Original Article Histone Modifications of H3K4me3, H3K9me3 and Lineage Gene Expressions in Chimeric Mouse Embryo Maryam Salimi, Ph.D.1, Abolfazl Shirazi, Ph.D.2, 3*, Mohsen Norouzian, Ph.D.1*, Mohammad Mehdi Mehrazar, M.Sc.2, Mohammad Mehdi Naderi, Ph.D.2, Mohammad Ali Shokrgozar, Ph.D.4, Mirdavood Omrani, Ph.D.5, Seyed Mahmoud Hashemi, Ph.D.6 1. Department of Biology and Anatomical Sciences, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran 2. Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran 3. Department of Gametes and Cloning, Research Institute of Animal Embryo Technology, Shahrekord University, Shahrekord, Iran 4. National Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran 5. Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran 6. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran *Corresponding Addresses: P.O.Box: 19615/1177, Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran P.O.Box: 1985717-443, Department of Biology and Anatomical Sciences, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Emails: [email protected], [email protected] Received: 4/October/2018, Accepted: 18/February/2019 Abstract Objective: Chimeric animal exhibits less viability and more fetal and placental abnormalities than normal animal. This study was aimed to determine the impact of mouse embryonic stem cells (mESCs) injection into the mouse embryos on H3K9me3 and H3K4me3 and cell lineage gene expressions in chimeric blastocysts. Materials and Methods: In our experiment, at the first step, incorporation of the GFP positive mESCs (GFP-mESCs) 129/Sv into the inner cell mass (ICM) of pre-compacted and compacted morula stage embryos was compared. -
Simultaneous Epigenetic Perturbation and Genome Imaging Reveal Distinct Roles of H3k9me3 in Chromatin Architecture and Transcription
University of Massachusetts Medical School eScholarship@UMMS Open Access Publications by UMMS Authors 2020-12-08 Simultaneous epigenetic perturbation and genome imaging reveal distinct roles of H3K9me3 in chromatin architecture and transcription Ying Feng East China University of Science and Technology Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/oapubs Part of the Amino Acids, Peptides, and Proteins Commons, Genetics and Genomics Commons, and the Structural Biology Commons Repository Citation Feng Y, Wang Y, Wang X, He X, Yang C, Naseri A, Pederson T, Zheng J, Zhang S, Xiao X, Xie W, Ma H. (2020). Simultaneous epigenetic perturbation and genome imaging reveal distinct roles of H3K9me3 in chromatin architecture and transcription. Open Access Publications by UMMS Authors. https://doi.org/ 10.1186/s13059-020-02201-1. Retrieved from https://escholarship.umassmed.edu/oapubs/4502 Creative Commons License This work is licensed under a Creative Commons Attribution 4.0 License. This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Open Access Publications by UMMS Authors by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. Feng et al. Genome Biology (2020) 21:296 https://doi.org/10.1186/s13059-020-02201-1 RESEARCH Open Access Simultaneous epigenetic perturbation and genome imaging reveal distinct roles of H3K9me3 in chromatin architecture and transcription Ying Feng1†, Yao Wang2,3†, Xiangnan Wang4, Xiaohui He4, Chen Yang5, Ardalan Naseri6, Thoru Pederson7, Jing Zheng5, Shaojie Zhang6, Xiao Xiao8, Wei Xie2,3* and Hanhui Ma4* * Correspondence: xiewei121@ tsinghua.edu.cn; mahh@ Abstract shanghaitech.edu.cn †Ying Feng and Yao Wang Introduction: Despite the long-observed correlation between H3K9me3, chromatin contributed equally to this work. -
Intronic Mir-26B Controls Neuronal Differentiation by Repressing Its Host Transcript, Ctdsp2
Downloaded from genesdev.cshlp.org on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press RESEARCH COMMUNICATION CTDSPL. As part of the REST complex, these enzymes Intronic miR-26b controls dephosphorylate the C-terminal domain (CTD) of RNA neuronal differentiation polymerase II (PolII) and thereby inhibit the expression of genes that have an RE1 signature sequence (Yeo et al. by repressing its host 2005; Visvanathan et al. 2007). During neural fate com- ctdsp2 mitment and terminal differentiation, the REST/CTDSP transcript, pathway is gradually inactivated to allow the expression Holger Dill,1 Bastian Linder,1 Alexander Fehr,2 of RE1-containing genes (Ballas et al. 2005; Yeo et al. 3 2005; Visvanathan et al. 2007). Neuronal gene activation and Utz Fischer in mice and humans is known to depend on the action of Department of Biochemistry, Theodor Boveri-Institute, miR-124, which prevents expression of CTDSPs (Lim University of Wu¨ rzburg, D-97074 Wu¨ rzburg, Germany et al. 2005; Conaco et al. 2006; Visvanathan et al. 2007). However, as shown in mice, the neuron-specific miR-124 Differentiation of neural stem cells (NSCs) to neurons is itself repressed by the REST/CTDSP pathway, since all of its loci contain an RE1 (Conaco et al. 2006). As mRNAs requires the activation of genes controlled by the re- often are under the control of a collection of microRNAs pressor element 1 (RE1) silencing transcription factor (miRNAs) (Krek et al. 2005), we therefore hypothesized (REST)/neuron-restrictive silencer factor (NRSF) protein that additional miRNAs might be involved in the regu- complex. Important components of REST/NRSF are phos- lation of CTDSP activity. -
Deciphering the Histone Code to Build the Genome Structure
bioRxiv preprint doi: https://doi.org/10.1101/217190; this version posted November 20, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. Deciphering the histone code to build the genome structure Kirti Prakasha,b,c,* and David Fournierd,* aPhysico-Chimie Curie, Institut Curie, CNRS UMR 168, 75005 Paris, France; bOxford Nanoimaging Ltd, OX1 1JD, Oxford, UK; cMicron Advanced Bioimaging Unit, Department of Biochemistry, University of Oxford, Oxford, UK; dFaculty of Biology and Center for Computational Sciences, Johannes Gutenberg University Mainz, 55128 Mainz, Germany; *Correspondence: [email protected], [email protected] Histones are punctuated with small chemical modifications that alter their interaction with DNA. One attractive hypothesis stipulates that certain combinations of these histone modifications may function, alone or together, as a part of a predictive histone code to provide ground rules for chromatin folding. We consider four features that relate histone modifications to chromatin folding: charge neutrali- sation, molecular specificity, robustness and evolvability. Next, we present evidence for the association among different histone modi- fications at various levels of chromatin organisation and show how these relationships relate to function such as transcription, replica- tion and cell division. Finally, we propose a model where the histone code can set critical checkpoints for chromatin to fold reversibly be- tween different orders of the organisation in response to a biological stimulus. DNA | nucleosomes | histone modifications | chromatin domains | chro- mosomes | histone code | chromatin folding | genome structure Introduction The genetic information within chromosomes of eukaryotes is packaged into chromatin, a long and folded polymer of double-stranded DNA, histones and other structural and non- structural proteins. -
Dynamics of Transcription-Dependent H3k36me3 Marking by the SETD2:IWS1:SPT6 Ternary Complex
bioRxiv preprint doi: https://doi.org/10.1101/636084; this version posted May 14, 2019. 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. Dynamics of transcription-dependent H3K36me3 marking by the SETD2:IWS1:SPT6 ternary complex Katerina Cermakova1, Eric A. Smith1, Vaclav Veverka2, H. Courtney Hodges1,3,4,* 1 Department of Molecular & Cellular Biology, Center for Precision Environmental Health, and Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, 77030, USA 2 Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic 3 Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA 4 Department of Bioengineering, Rice University, Houston, TX, 77005, USA * Lead contact; Correspondence to: [email protected] Abstract The genome-wide distribution of H3K36me3 is maintained SETD2 contributes to gene expression by marking gene through various mechanisms. In human cells, H3K36 is bodies with H3K36me3, which is thought to assist in the mono- and di-methylated by eight distinct histone concentration of transcription machinery at the small portion methyltransferases; however, the predominant writer of the of the coding genome. Despite extensive genome-wide data trimethyl mark on H3K36 is SETD21,11,12. Interestingly, revealing the precise localization of H3K36me3 over gene SETD2 is a major tumor suppressor in clear cell renal cell bodies, the physical basis for the accumulation, carcinoma13, breast cancer14, bladder cancer15, and acute maintenance, and sharp borders of H3K36me3 over these lymphoblastic leukemias16–18. In these settings, mutations sites remains rudimentary. -
Assessing the Epigenetic Status of Human Telomeres
cells Perspective Assessing the Epigenetic Status of Human Telomeres María I. Vaquero-Sedas and Miguel A. Vega-Palas * Instituto de Bioquímica Vegetal y Fotosíntesis, CSIC-Universidad de Sevilla, 41092 Seville, Spain * Correspondence: [email protected] Received: 19 July 2019; Accepted: 5 September 2019; Published: 7 September 2019 Abstract: The epigenetic modifications of human telomeres play a relevant role in telomere functions and cell proliferation. Therefore, their study is becoming an issue of major interest. These epigenetic modifications are usually analyzed by microscopy or by chromatin immunoprecipitation (ChIP). However, these analyses could be challenged by subtelomeres and/or interstitial telomeric sequences (ITSs). Whereas telomeres and subtelomeres cannot be differentiated by microscopy techniques, telomeres and ITSs might not be differentiated in ChIP analyses. In addition, ChIP analyses of telomeres should be properly controlled. Hence, studies focusing on the epigenetic features of human telomeres have to be carefully designed and interpreted. Here, we present a comprehensive discussion on how subtelomeres and ITSs might influence studies of human telomere epigenetics. We specially focus on the influence of ITSs and some experimental aspects of the ChIP technique on ChIP analyses. In addition, we propose a specific pipeline to accurately perform these studies. This pipeline is very simple and can be applied to a wide variety of cells, including cancer cells. Since the epigenetic status of telomeres could influence cancer cells proliferation, this pipeline might help design precise epigenetic treatments for specific cancer types. Keywords: telomeres; epigenetics; chromatin immunoprecipitation; microscopy; human; cancer 1. The Epigenetic Nature of Human Telomeres Has Remained Controversial The length of telomeres and the chromatin organization of telomeric regions influence telomeres function [1]. -
Synthesis of Orthogonal Transcription- Translation Networks
Synthesis of orthogonal transcription- translation networks Wenlin An and Jason W. Chin1 Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, United Kingdom Edited by Susan Gottesman, National Institutes of Health, Bethesda, MD, and approved April 2, 2009 (received for review January 11, 2009) Orthogonal, parallel and independent, systems are one key foun- O-ribosomes for the translation of an O-mRNA arises from the dation for synthetic biology. The synthesis of orthogonal systems altered 16S rRNA in the O-ribosome that recognizes an altered that are uncoupled from evolutionary constraints, and selectively Shine-Dalgarno sequence in the leader sequence of the O-mRNA abstracted from cellular regulation, is an emerging approach to in the initiation phase of translation (12). In previous work O- making biology more amenable to engineering. Here, we combine ribosomes have been evolved that decode genetic information in orthogonal transcription by T7 RNA polymerase and translation by orthogonal mRNAs in new ways. In combination with orthogonal orthogonal ribosomes (O-ribosomes), creating an orthogonal gene aminoacyl-tRNA synthetases and tRNAs that recognize unnatural expression pathway in Escherichia coli. We design and implement amino acids the evolved O-ribosomes have allowed us to begin to compact, orthogonal gene expression networks. In particular we undo the ‘‘frozen accident’’ of the natural genetic code and direct focus on creating transcription–translation feed-forward loops the efficient incorporation of unnatural amino acids into proteins (FFLs). The transcription–translation FFLs reported cannot be cre- encoded on O-mRNAs (13, 14). O-ribosomes have also been used ated by using the cells’ gene expression machinery and introduce to create new translational Boolean logic functions that would not information-processing delays on the order of hours into gene be possible to create by using the essential cellular ribosome (15) expression. -
A Small Nucleolar RNA Is Processed from an Intron of the Human Gene Encoding Ribosomal Protein $3
Downloaded from genesdev.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press A small nucleolar RNA is processed from an intron of the human gene encoding ribosomal protein $3 Kazimierz Tyc Tycowski, Mei-Di Shu, and Joan A. Steitz Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06536-0812 USA A human small nucleolar RNA, identified previously in HeLa cells by anti-fibrillarin autoantibody precipitation and termed RNA X, has been characterized. It comprises two uridine-rich variants (148 and 146 nucleotides}, which we refer to as snRNA U15A and U15B. Secondary structure models predict for both variants a U15-specific stem-loop structure, as well as a new structural motif that contains conserved sequences and can also be recognized in the other fibrillarin-associated nucleolar snRNAs, U3, U14, and RNA Y. The single-copy gene for human U15A has been found unexpectedly to reside in intron 1 of the ribosomal protein $3 gene; the U15A sequence appears on the same strand as the $3 mRNA and does not exhibit canonical transcription signals for nuclear RNA polymerases. U15A RNA is processed in vitro from $3 intron 1 transcripts to yield the correct 5' end with a 5'-monophosphate; the in vitro system requires ATP for 3' cleavage, which occurs a few nucleotides downstream of the mature end. The production of a single primary transcript specifying the mRNA for a ribosomal or nucleolar protein and a nucleolar snRNA may constitute a general mechanism for balancing the levels of nucleolar components in vertebrate cells. -
Screening HDAC Inhibitors
APPLICATION NOTE Cellular Imaging and Analysis Key Features • Identify candidate compounds using high throughput biochemical AlphaLISA® assays • Validate candidates in a high content imaging approach HDAC inhibitor Screening HDAC Inhibitors – A Workflow Introduction Comprising High An epigenetic trait is a stably inherited phenotype resulting from changes in a Throughput and High chromosome without alterations in the Content Screening DNA sequence [Berger et al., 2009]. Key mechanisms of epigenetic gene regulation are pathways which affect the packaging of DNA into chromatin, thereby determining the accessibility of DNA to transcription. These pathways include DNA methylation, chromatin remodeling and histone modifications. Aberrations in epigenetic mechanisms are well known to be associated with the biology of cancer, which suggests that epigenetic enzymes may be promising cancer drug targets [Ducasse and Brown, 2006]. In comparison to normal cells, cancer cell genomes are characterized by, among other things, a decrease in histone modifications such as acetylation [Ropero and Esteller, 2007]. Histone acetylation by histone acetyltransferases leads to loosening of DNA-histone interactions, allowing gene expression. In contrast, histone deacetylation by histone deacetylases (HDACs) increases the interaction between DNA and histones and leads to a decrease in gene expression (Figure 1). To perform the AlphaLISA assay, all steps were performed as previously described [Rodriguez-Suarez et al., 2011]. Briefly, HDAC-1 was pre-incubated with different concentrations of the HDAC inhibitor TSA, or Assay Buffer alone, for 5 min at room temperature, before addition of the H3K9ac peptide (AnaSpec, 64361). After 1h of enzymatic reaction time, AlphaLISA Acceptor Beads (PerkinElmer, AL138C) were added and the reaction mix was incubated for 1h, followed by addition of Streptavidin Figure 1: DNA accessibility is regulated by acetylation of core histones. -
Nucleosome Eviction Along with H3k9ac Deposition Enhances Sox2 Binding During Human Neuroectodermal Commitment
Cell Death and Differentiation (2017) 24, 1121–1131 OPEN Official journal of the Cell Death Differentiation Association www.nature.com/cdd Nucleosome eviction along with H3K9ac deposition enhances Sox2 binding during human neuroectodermal commitment Yanhua Du1,2, Zhenping Liu2, Xinkai Cao2, Xiaolong Chen2, Zhenyu Chen3, Xiaobai Zhang2, Xiaoqing Zhang*,1,3 and Cizhong Jiang*,1,2 Neuroectoderm is an important neural precursor. However, chromatin remodeling and its epigenetic regulatory roles during the differentiation of human neuroectodermal cells (hNECs) from human embryonic stem cells (hESCs) remain largely unexplored. Here, we obtained hNECs through directed differentiation from hESCs, and determined chromatin states in the two cell types. Upon differentiation, H2A.Z-mediated nucleosome depletion leads to an open chromatin structure in promoters and upregulates expression of neuroectodermal genes. Increase in H3K9ac signals and decrease in H3K27me3 signals in promoters result in an active chromatin state and activate neuroectodermal genes. Conversely, decrease in H3K9ac signals and increase in H3K27me3 signals in promoters repress pluripotency genes. Moreover, H3K9ac signals facilitate the pluripotency factor Sox2 binding to target sites unique to hNECs. Knockdown of the acetyltransferase Kat2b erases H3K9ac signals, disrupts Sox2 binding, and fails the differentiation. Our results demonstrate a hierarchy of epigenetic regulation of gene expression during the differentiation of hNECs from hESCs through chromatin remodeling. Cell Death and Differentiation (2017) 24, 1121–1131; doi:10.1038/cdd.2017.62; published online 5 May 2017 Chromatin remodeling offers the epigenetic basis for tran- that H3K4me3 and H3K27me3 effectively distinguish genes scriptional regulation and has a pivotal role in many biological with different expression levels and reflect lineage potential.11 A processes such as cell differentiation, embryonic develop- recent HPLC-MS-based quantitative proteomics identified ment, and so on. -
Untranslated Region of Mrnas As a Site for Ribozyme Cleavage-Dependent Processing and Control in Bacteria
Erschienen in: RNA Biology ; 14 (2017), 11. - S. 1522-1533 https://dx.doi.org/10.1080/15476286.2016.1240141 RESEARCH PAPER The 30-untranslated region of mRNAs as a site for ribozyme cleavage-dependent processing and control in bacteria Michele Fellettia,b, Anna Biebera, and Jorg€ S. Hartiga,b aDepartment of Chemistry, University of Konstanz, Konstanz, Germany; bKonstanz Research School Chemical Biology (Kors-CB), University of Konstanz, Konstanz, Germany ABSTRACT Besides its primary informational role, the sequence of the mRNA (mRNA) including its 50-and30- untranslated regions (UTRs), contains important features that are relevant for post-transcriptional and translational regulation of gene expression. In this work a number of bacterial twister motifs are characterized both in vitro and in vivo. The analysis of their genetic contexts shows that these motifs have the potential of being transcribed as part of KEYWORDS polycistronic mRNAs, thus we suggest the involvement of bacterial twister motifs in the processing of mRNA. 0 Aptazyme; bacteria; Our data show that the ribozyme-mediated cleavage of the bacterial 3 -UTR has major effects on gene hammerhead ribozyme; expression. While the observed effects correlate weakly with the kinetic parameters of the ribozymes, they polyadenylation; riboswitch; show dependence on motif-specific structural features and on mRNA stabilization properties of the secondary RNase; RNA decay; secondary structures that remain on the 30-UTR after ribozyme cleavage. Using these principles, novel artificial twister- structure; twister ribozyme based riboswitches are developed that exert their activity via ligand-dependent cleavage of the 30-UTR and the removal of the protective intrinsic terminator. Our results provide insights into possible biological functions of these recently discovered and widespread catalytic RNA motifs and offer new tools for applications in biotechnology, synthetic biology and metabolic engineering.