Micropattern Differentiation of Mouse Pluripotent Stem Cells Recapitulates
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Prospective Isolation of NKX2-1–Expressing Human Lung Progenitors Derived from Pluripotent Stem Cells
The Journal of Clinical Investigation RESEARCH ARTICLE Prospective isolation of NKX2-1–expressing human lung progenitors derived from pluripotent stem cells Finn Hawkins,1,2 Philipp Kramer,3 Anjali Jacob,1,2 Ian Driver,4 Dylan C. Thomas,1 Katherine B. McCauley,1,2 Nicholas Skvir,1 Ana M. Crane,3 Anita A. Kurmann,1,5 Anthony N. Hollenberg,5 Sinead Nguyen,1 Brandon G. Wong,6 Ahmad S. Khalil,6,7 Sarah X.L. Huang,3,8 Susan Guttentag,9 Jason R. Rock,4 John M. Shannon,10 Brian R. Davis,3 and Darrell N. Kotton1,2 2 1Center for Regenerative Medicine, and The Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA. 3Center for Stem Cell and Regenerative Medicine, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA. 4Department of Anatomy, UCSF, San Francisco, California, USA. 5Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA. 6Department of Biomedical Engineering and Biological Design Center, Boston University, Boston, Massachusetts, USA. 7Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, Massachusetts, USA. 8Columbia Center for Translational Immunology & Columbia Center for Human Development, Columbia University Medical Center, New York, New York, USA. 9Department of Pediatrics, Monroe Carell Jr. Children’s Hospital, Vanderbilt University, Nashville, Tennessee, USA. 10Division of Pulmonary Biology, Cincinnati Children’s Hospital, Cincinnati, Ohio, USA. It has been postulated that during human fetal development, all cells of the lung epithelium derive from embryonic, endodermal, NK2 homeobox 1–expressing (NKX2-1+) precursor cells. -
Neuromesodermal Progenitors Are a Conserved Source of Spinal
© 2019. Published by The Company of Biologists Ltd | Development (2019) 146, dev175620. doi:10.1242/dev.175620 CORRECTION Correction: Neuromesodermal progenitors are a conserved source of spinal cord with divergent growth dynamics (doi: 10.1242/dev.166728) Andrea Attardi, Timothy Fulton, Maria Florescu, Gopi Shah, Leila Muresan, Martin O. Lenz, Courtney Lancaster, Jan Huisken, Alexander van Oudenaarden and Benjamin Steventon Light-sheet imaging data associated with Development (2018) 145, dev166728 (doi: 10.1242/dev.166728) are now available in the Image Data Repository with an explanatory Data Note hosted by Wellcome Open Research. The corrected Data availability section is shown below and both the online full-text and PDF versions have been updated. Data availability (corrected) Sequencing data associated with the ScarTrace lineage tracing study have been deposited in GEO under accession number GSE121114. The Matlab script allowing for user-defined selection of tracking data can be found here: doi.org/10.5281/zenodo.1475146. Light-sheet imaging data associated with Fig. 7 have been deposited in the Image Data Repository (https://idr.openmicroscopy.org/webclient/?show=project-552) with an associated Data Note hosted by Wellcome Open Research (https:// wellcomeopenresearch.org/articles/3-163/v1). Data availability (original) Sequencing data associated with the ScarTrace lineage tracing study have been deposited in GEO under accession number GSE121114. The Matlab script allowing for user-defined selection of tracking data can be found here: doi.org/10.5281/zenodo.1475146. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. -
UNIVERSITY of CALIFORNIA, IRVINE Combinatorial Regulation By
UNIVERSITY OF CALIFORNIA, IRVINE Combinatorial regulation by maternal transcription factors during activation of the endoderm gene regulatory network DISSERTATION submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Biological Sciences by Kitt D. Paraiso Dissertation Committee: Professor Ken W.Y. Cho, Chair Associate Professor Olivier Cinquin Professor Thomas Schilling 2018 Chapter 4 © 2017 Elsevier Ltd. © 2018 Kitt D. Paraiso DEDICATION To the incredibly intelligent and talented people, who in one way or another, helped complete this thesis. ii TABLE OF CONTENTS Page LIST OF FIGURES vii LIST OF TABLES ix LIST OF ABBREVIATIONS X ACKNOWLEDGEMENTS xi CURRICULUM VITAE xii ABSTRACT OF THE DISSERTATION xiv CHAPTER 1: Maternal transcription factors during early endoderm formation in 1 Xenopus Transcription factors co-regulate in a cell type-specific manner 2 Otx1 is expressed in a variety of cell lineages 4 Maternal otx1 in the endodermal conteXt 5 Establishment of enhancers by maternal transcription factors 9 Uncovering the endodermal gene regulatory network 12 Zygotic genome activation and temporal control of gene eXpression 14 The role of maternal transcription factors in early development 18 References 19 CHAPTER 2: Assembly of maternal transcription factors initiates the emergence 26 of tissue-specific zygotic cis-regulatory regions Introduction 28 Identification of maternal vegetally-localized transcription factors 31 Vegt and OtX1 combinatorially regulate the endodermal 33 transcriptome iii -
SUPPLEMENTARY MATERIAL Bone Morphogenetic Protein 4 Promotes
www.intjdevbiol.com doi: 10.1387/ijdb.160040mk SUPPLEMENTARY MATERIAL corresponding to: Bone morphogenetic protein 4 promotes craniofacial neural crest induction from human pluripotent stem cells SUMIYO MIMURA, MIKA SUGA, KAORI OKADA, MASAKI KINEHARA, HIROKI NIKAWA and MIHO K. FURUE* *Address correspondence to: Miho Kusuda Furue. Laboratory of Stem Cell Cultures, National Institutes of Biomedical Innovation, Health and Nutrition, 7-6-8, Saito-Asagi, Ibaraki, Osaka 567-0085, Japan. Tel: 81-72-641-9819. Fax: 81-72-641-9812. E-mail: [email protected] Full text for this paper is available at: http://dx.doi.org/10.1387/ijdb.160040mk TABLE S1 PRIMER LIST FOR QRT-PCR Gene forward reverse AP2α AATTTCTCAACCGACAACATT ATCTGTTTTGTAGCCAGGAGC CDX2 CTGGAGCTGGAGAAGGAGTTTC ATTTTAACCTGCCTCTCAGAGAGC DLX1 AGTTTGCAGTTGCAGGCTTT CCCTGCTTCATCAGCTTCTT FOXD3 CAGCGGTTCGGCGGGAGG TGAGTGAGAGGTTGTGGCGGATG GAPDH CAAAGTTGTCATGGATGACC CCATGGAGAAGGCTGGGG MSX1 GGATCAGACTTCGGAGAGTGAACT GCCTTCCCTTTAACCCTCACA NANOG TGAACCTCAGCTACAAACAG TGGTGGTAGGAAGAGTAAAG OCT4 GACAGGGGGAGGGGAGGAGCTAGG CTTCCCTCCAACCAGTTGCCCCAAA PAX3 TTGCAATGGCCTCTCAC AGGGGAGAGCGCGTAATC PAX6 GTCCATCTTTGCTTGGGAAA TAGCCAGGTTGCGAAGAACT p75 TCATCCCTGTCTATTGCTCCA TGTTCTGCTTGCAGCTGTTC SOX9 AATGGAGCAGCGAAATCAAC CAGAGAGATTTAGCACACTGATC SOX10 GACCAGTACCCGCACCTG CGCTTGTCACTTTCGTTCAG Suppl. Fig. S1. Comparison of the gene expression profiles of the ES cells and the cells induced by NC and NC-B condition. Scatter plots compares the normalized expression of every gene on the array (refer to Table S3). The central line -
Construction of a Cerna Network Combining Transcription Factors in Eutopic Endometrial Tissue of Tubal Factor Infertility and Endometriosis-Related Infertility
Construction of a ceRNA network combining transcription factors in eutopic endometrial tissue of tubal factor infertility and endometriosis-related infertility Junzui Li ( [email protected] ) Xiamen University https://orcid.org/0000-0002-6640-8215 Lulu Ren Xiamen University Medical College Cui Yang Xiamen University Medical College Rongfeng Wu Xiamen University Medical College Zhixiong Huang Xiamen University School of Life Sciences Qionghua Chen Xiamen University Medical College Research article Keywords: TFI, endometriosis-related infertility, DEGs, ceRNA network, TFs Posted Date: December 19th, 2019 DOI: https://doi.org/10.21203/rs.2.19312/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/27 Abstract Purpose Although tubal factor infertility (TFI) and endometriosis-related infertility all can result in female infertility, the pathogenesis of TFI and endometriosis-related infertility were different. The pathophysiologic mechanisms of TFI and endometriosis-related infertility have not been investigated thoroughly. Thus, the aim of the study is to identify the potential crucial genes, pathways, transcription factors (TFs) and long non-coding RNAs (lncRNAs) associated with TFI and endometriosis-related infertility, and further analyze the molecular mechanism implicated in genes. Methods 3 patients with TFI and 3 patients with endometriosis-related infertility were recruited, and microarray hybridization of the eutopic endometrial tissue during the window of implantation (WOI) was performed to examine the expression of mRNAs and lncRNAs. First, differentially expressed genes (DEGs) and differentially expressed lncRNAs (DELs) were screened out based on P < 0.05 and fold change (FC) ≧ 2. Second, gene ontology, pathway and TFs enrichment analyses and PPI network construction of DEGs were performed. -
A Sox2 Distal Enhancer Cluster Regulates Embryonic Stem Cell Differentiation Potential
Downloaded from genesdev.cshlp.org on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press A Sox2 distal enhancer cluster regulates embryonic stem cell differentiation potential Harry Y. Zhou,1,3 Yulia Katsman,1,3 Navroop K. Dhaliwal,1 Scott Davidson,1 Neil N. Macpherson,1 Moorthy Sakthidevi,1 Felicia Collura,1 and Jennifer A. Mitchell1,2 1Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada; 2Center for the Analysis of Genome Evolution and Function, University of Toronto, Toronto, Ontario M5S 3G5, Canada The Sox2 transcription factor must be robustly transcribed in embryonic stem (ES) cells to maintain pluripotency. Two gene-proximal enhancers, Sox2 regulatory region 1 (SRR1) and SRR2, display activity in reporter assays, but deleting SRR1 has no effect on pluripotency. We identified and functionally validated the sequences required for Sox2 transcription based on a computational model that predicted transcriptional enhancer elements within 130 kb of Sox2. Our reporter assays revealed three novel enhancers—SRR18, SRR107, and SRR111—that, through the formation of chromatin loops, form a chromatin complex with the Sox2 promoter in ES cells. Using the CRISPR/ Cas9 system and F1 ES cells (Mus musculus129 3 Mus castaneus), we generated heterozygous deletions of each enhancer region, revealing that only the distal cluster containing SRR107 and SRR111, located >100 kb downstream from Sox2, is required for cis-regulation of Sox2 in ES cells. Furthermore, homozygous deletion of this distal Sox2 control region (SCR) caused significant reduction in Sox2 mRNA and protein levels, loss of ES cell colony morphology, genome-wide changes in gene expression, and impaired neuroectodermal formation upon spontaneous differentiation to embryoid bodies. -
Pancreas-Specific Deletion of Mouse Gata4 and Gata6 Causes Pancreatic Agenesis
Pancreas-specific deletion of mouse Gata4 and Gata6 causes pancreatic agenesis Shouhong Xuan, … , Raymond J. Macdonald, Lori Sussel J Clin Invest. 2012;122(10):3516-3528. https://doi.org/10.1172/JCI63352. Research Article Pancreatic agenesis is a human disorder caused by defects in pancreas development. To date, only a few genes have been linked to pancreatic agenesis in humans, with mutations in pancreatic and duodenal homeobox 1 (PDX1) and pancreas-specific transcription factor 1a (PTF1A) reported in only 5 families with described cases. Recently, mutations in GATA6 have been identified in a large percentage of human cases, and aG ATA4 mutant allele has been implicated in a single case. In the mouse, Gata4 and Gata6 are expressed in several endoderm-derived tissues, including the pancreas. To analyze the functions of GATA4 and/or GATA6 during mouse pancreatic development, we generated pancreas- specific deletions of Gata4 and Gata6. Surprisingly, loss of either Gata4 or Gata6 in the pancreas resulted in only mild pancreatic defects, which resolved postnatally. However, simultaneous deletion of both Gata4 and Gata6 in the pancreas caused severe pancreatic agenesis due to disruption of pancreatic progenitor cell proliferation, defects in branching morphogenesis, and a subsequent failure to induce the differentiation of progenitor cells expressing carboxypeptidase A1 (CPA1) and neurogenin 3 (NEUROG3). These studies address the conserved and nonconserved mechanisms underlying GATA4 and GATA6 function during pancreas development and provide a new mouse model to characterize the underlying developmental defects associated with pancreatic agenesis. Find the latest version: https://jci.me/63352/pdf Research article Related Commentary, page 3469 Pancreas-specific deletion of mouse Gata4 and Gata6 causes pancreatic agenesis Shouhong Xuan,1 Matthew J. -
KRAS Drives Immune Evasion in a Genetic Model of Pancreatic Cancer
ARTICLE https://doi.org/10.1038/s41467-021-21736-w OPEN KRAS drives immune evasion in a genetic model of pancreatic cancer Irene Ischenko1, Stephen D’Amico1, Manisha Rao2, Jinyu Li2, Michael J. Hayman1, Scott Powers 2, ✉ ✉ Oleksi Petrenko 1,3 & Nancy C. Reich 1,3 Immune evasion is a hallmark of KRAS-driven cancers, but the underlying causes remain unresolved. Here, we use a mouse model of pancreatic ductal adenocarcinoma to inactivate 1234567890():,; KRAS by CRISPR-mediated genome editing. We demonstrate that at an advanced tumor stage, dependence on KRAS for tumor growth is reduced and is manifested in the sup- pression of antitumor immunity. KRAS-deficient cells retain the ability to form tumors in immunodeficient mice. However, they fail to evade the host immune system in syngeneic wild-type mice, triggering strong antitumor response. We uncover changes both in tumor cells and host immune cells attributable to oncogenic KRAS expression. We identify BRAF and MYC as key mediators of KRAS-driven tumor immune suppression and show that loss of BRAF effectively blocks tumor growth in mice. Applying our results to human PDAC we show that lowering KRAS activity is likewise associated with a more vigorous immune environment. 1 Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY, USA. 2 Department of Pathology, Stony Brook University, ✉ Stony Brook, NY, USA. 3These authors jointly supervised this work: Oleksi Petrenko, Nancy C. Reich. email: [email protected]; [email protected] NATURE COMMUNICATIONS | (2021) 12:1482 | https://doi.org/10.1038/s41467-021-21736-w | www.nature.com/naturecommunications 1 ARTICLE NATURE COMMUNICATIONS | https://doi.org/10.1038/s41467-021-21736-w RAS is frequently associated with some of the deadliest and characterization of KRASG12D p53KO mouse cell lines forms of cancer. -
Original Article a Database and Functional Annotation of NF-Κb Target Genes
Int J Clin Exp Med 2016;9(5):7986-7995 www.ijcem.com /ISSN:1940-5901/IJCEM0019172 Original Article A database and functional annotation of NF-κB target genes Yang Yang, Jian Wu, Jinke Wang The State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, People’s Republic of China Received November 4, 2015; Accepted February 10, 2016; Epub May 15, 2016; Published May 30, 2016 Abstract: Backgrounds: The previous studies show that the transcription factor NF-κB always be induced by many inducers, and can regulate the expressions of many genes. The aim of the present study is to explore the database and functional annotation of NF-κB target genes. Methods: In this study, we manually collected the most complete listing of all NF-κB target genes identified to date, including the NF-κB microRNA target genes and built the database of NF-κB target genes with the detailed information of each target gene and annotated it by DAVID tools. Results: The NF-κB target genes database was established (http://tfdb.seu.edu.cn/nfkb/). The collected data confirmed that NF-κB maintains multitudinous biological functions and possesses the considerable complexity and diversity in regulation the expression of corresponding target genes set. The data showed that the NF-κB was a central regula- tor of the stress response, immune response and cellular metabolic processes. NF-κB involved in bone disease, immunological disease and cardiovascular disease, various cancers and nervous disease. NF-κB can modulate the expression activity of other transcriptional factors. Inhibition of IKK and IκBα phosphorylation, the decrease of nuclear translocation of p65 and the reduction of intracellular glutathione level determined the up-regulation or down-regulation of expression of NF-κB target genes. -
Polycomb Repressor Complex 1 Promotes Gene Silencing Through H2AK119 Mono-Ubiquitination in Acinar-To-Ductal Metaplasia and Pancreatic Cancer Cells
www.impactjournals.com/oncotarget/ Oncotarget, Vol. 7, No. 10 Polycomb repressor complex 1 promotes gene silencing through H2AK119 mono-ubiquitination in acinar-to-ductal metaplasia and pancreatic cancer cells Simone Benitz1,*, Ivonne Regel1,3,*, Tobias Reinhard1, Anna Popp1, Isabell Schäffer1, Susanne Raulefs1, Bo Kong1, Irene Esposito3, Christoph W. Michalski2,*, Jörg Kleeff1,4,5,* 1Department of Surgery, Technische Universität München, Munich, Germany 2Department of Surgery, University of Heidelberg, Heidelberg, Germany 3Institute of Pathology, Heinrich-Heine University, Duesseldorf, Germany 4The Royal Liverpool and Broadgreen University Hospitals, Liverpool, United Kingdom 5Department of Surgery, Heinrich-Heine University, Duesseldorf, Germany *These authors contribute equally to the manuscript. Correspondence to: Ivonne Regel, e-mail: [email protected] Keywords: polycomb repressor complex, histone mono-ubiquitination, pancreatic cancer, differentiation gene silencing Abbreviations: ADM (acinar-to-ductal metaplasia), PDAC (pancreatic ductal adenocarcinoma), PRC (polycomb repressor complex), PTF (pancreas specific transcription factor) Received: July 29, 2015 Accepted: November 16, 2015 Published: December 22, 2015 ABSTRACT Acinar-to-ductal metaplasia (ADM) occurring in cerulein-mediated pancreatitis or in oncogenic Kras-driven pancreatic cancer development is accompanied by extensive changes in the transcriptional program. In this process, acinar cells shut down the expression of acinar specific differentiation genes -
GATA Transcription Factors and Their Co-Regulators Guide the Development Of
GATA transcription factors and their co-regulators guide the development of GABAergic and serotonergic neurons in the anterior brainstem Laura Tikker Molecular and Integrative Biosciences Research Programme Faculty of Biological and Environmental Sciences Doctoral Programme Integrative Life Science University of Helsinki ACADEMIC DISSERTATION Doctoral thesis, to be presented for public examination, with the permission of the Faculty of Biological and Environmental Sciences of the University of Helsinki, in Raisio Hall (LS B2) in Forest Sciences building, Latokartanonkaari 7, Helsinki, on the 3rd of April, 2020 at 12 noon. Supervisor Professor Juha Partanen University of Helsinki (Finland) Thesis Committee members Docent Mikko Airavaara University of Helsinki (Finland) Professor Timo Otonkoski University of Helsinki (Finland) Pre-examinators Docent Satu Kuure University of Helsinki (Finland) Research Scientist Siew-Lan Ang, PhD The Francis Crick Institute (United Kingdom) Opponent Research Scientist Johan Holmberg, PhD Karolinska Institutet (Sweden) Custos Professor Juha Partanen University of Helsinki (Finland) The Faculty of Biological and Environmental Sciences, University of Helsinki, uses the Urkund system for plagiarism recognition to examine all doctoral dissertations. ISBN: 978-951-51-5930-4 (paperback) ISBN: 978-951-51-5931-1 (PDF) ISSN: 2342-3161 (paperback) ISSN: 2342-317X (PDF) Printing house: Painosalama Oy Printing location: Turku, Finland Printed on: 03.2020 Cover artwork: Serotonergic neurons in adult dorsal raphe (mouse). -
Resegmentation Is an Ancestral Feature of the Gnathostome Vertebral Skeleton Katharine E Criswell1,2*, J Andrew Gillis1,2
RESEARCH ARTICLE Resegmentation is an ancestral feature of the gnathostome vertebral skeleton Katharine E Criswell1,2*, J Andrew Gillis1,2 1Department of Zoology, University of Cambridge, Cambridge, United Kingdom; 2Marine Biological Laboratory, Woods Hole, United States Abstract The vertebral skeleton is a defining feature of vertebrate animals. However, the mode of vertebral segmentation varies considerably between major lineages. In tetrapods, adjacent somite halves recombine to form a single vertebra through the process of ‘resegmentation’. In teleost fishes, there is considerable mixing between cells of the anterior and posterior somite halves, without clear resegmentation. To determine whether resegmentation is a tetrapod novelty, or an ancestral feature of jawed vertebrates, we tested the relationship between somites and vertebrae in a cartilaginous fish, the skate (Leucoraja erinacea). Using cell lineage tracing, we show that skate trunk vertebrae arise through tetrapod-like resegmentation, with anterior and posterior halves of each vertebra deriving from adjacent somites. We further show that tail vertebrae also arise through resegmentation, though with a duplication of the number of vertebrae per body segment. These findings resolve axial resegmentation as an ancestral feature of the jawed vertebrate body plan. Introduction Axial segmentation is key to the body plan organization of many metazoan groups and has arisen repeatedly throughout animal evolution (Davis and Patel, 1999). Within vertebrates, the axial skele- ton is segmented into repeating vertebral units that provide structural support and protection for *For correspondence: soft tissues. Vertebral segmentation is preceded in the embryo by the segmentation of paraxial [email protected] mesoderm into epithelial blocks called somites (Figure 1a).