Chromatin, Epigenetics & Transcription

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ORGANIZERS Genevieve Almouzni, Curie Institute Hiroyuki Sasaki, Kyushu University Yang Shi, Harvard Medical School Bing Zhu, Institute of Biophysics, CAS KEYNOTE SPEAKERS Shelley Berger, University of Pennsylvania Barbara Meyer, HHMI / U. C. Berkeley Azim Surani, University of Cambridge INVITED SPEAKERS Chromatin, Epigenetics Genevieve Almouzni, Institut Curie Timothy Bestor, Columbia University & Transcription Neil Brockdorff, University of Oxford Xiaofeng Cao, Institute of Genetics & Developmental Biology, CAS Suzhou, China Giacomo Cavalli, Institute of Human Genetics, CNRS September 13-17, 2021 Ling-Ling Chen, Shanghai Institute of Biochemistry and Cell Biology, CAS Abstract deadline: July 2, 2021 Xiaodong Cheng, The University of Texas MD Anderson Cancer Center Wouter De Laat, Hubrecht Institute-KNAW and University Medical Center Utrecht Ines Drinnenberg, Institute Curie Shaorong Gao, Tongji University MAJOR TOPICS: Or Gozani, Stanford School of Medicine Chromatin assembly & structure Anja Groth, University of Copenhagen Dosage compensation & non-coding RNAs Nada Jabado, McGill University Chromatin modifications Cigall Kadoch, Harvard Medical School Chromatin architecture Hitoshi Kurumizaka, The University of Tokyo Epigenetics, development & disease Gaëlle Legube, Université de Toulouse, UT3 Guohong Li, Institute of Biophysics, CAS Bing Ren, University of California San Diego Noriko Saitoh, Kumamoto University FELLOWSHIPS Hiroyuki Sasaki, Kyushu University We are eager to have as many young people as possible attend Yang Shi, Harvard Medical School since they are likely to beneﬁt most from this meeting. A number of Yoichi Shinkai, RIKEN presentations by graduate students and postdocs in this conference Jane Skok, New York University School of Medicine will be selected for majorfellowship awards. Fuchou Tang, Peking University Chao-ting Wu, Harvard University Yi Zhang, HHMI, Harvard Medical School / Boston Children's Hospital Cold Spring Harbor Asia (CSHA) is the Asia-Pacific subsidiary of New York based Cold Spring Harbor Laboratory (CSHL). Inaugurated in 2010, CSHA is dedicated to promoting international scientific Bing Zhu, Institute of Biophysics, CAS exchange in the Asia-Pacific region by offering cutting-edge scientific conferences and advanced training courses. Tel: +86-512-62729029 Email: [email protected] Address: No. 299, Qiyue Road, Suzhou, China www.csh-asia.org.

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Genetic and Epigenetic Mechanisms of the Regulation of Mouse Embryonic Stem Cells Self-Renewal by the Pluripotency Transcription Factor Nanog
Genetic and epigenetic mechanisms of the regulation of mouse embryonic stem cells self-renewal by the pluripotency transcription factor Nanog Victor HEURTIER Thèse de doctorat de Biologie Dirigée par Pablo NAVARRO GIL Laboratoire Epigénétique des cellules souches – Institut Pasteur Sorbonne Université Ecole doctorale Complexité du Vivant (ED 515) Présentée et soutenue publiquement le 18/09/2018 Devant un jury composé de : Président : Pr MOUCHEL-VIELH Emmanuèle, Professeur Rapporteur : Dr SAVATIER Pierre, Directeur de Recherche Rapporteur : Dr RADA-IGLESIAS Alvaro, Chef d’équipe Examinateur : Dr AZUARA Veronique, Maître de conférences Examinateur : Dr PINSKAYA Marina, Maître de conférences Directeur de thèse : Dr NAVARRO GIL Pablo, Chef d’équipe Abstract Mouse embryonic stem (ES) cells are derived from the pre-implantation blastocyst and are able to maintain their pluripotent state through virtually limitless cell divisions in vitro. The study of the mechanisms regulating the specific features of ES cells led to the discovery of the transcription factors (TFs) governing their unique transcriptome. Among those TFs, Nanog plays a central role in the gene regulatory network that supports ES cells self-renewal. However, the molecular mechanisms by which Nanog exerts its functions are not fully elucidated. We adapted an inducible CRISPR activation (CRISPRa) system in mouse ES cells and demonstrated its functionality to stimulate transcription at endogenous loci. We then accurately determined the list of Nanog responsive genes using gain (CRISPRa cell line) and loss of function experiments and total RNA sequencing. Moreover, the DNA binding profiles of distinct pluripotency TFs were assessed genome-wide by chromatin immunoprecipitation (ChIP) and sequencing upon Nanog depletion and revealed the importance of the latter in the regulation of the pluripotency network activity at thousands of loci.
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