Identification of an Rnase That Preferentially Cleaves A/G Nucleotides
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Transcription Factor Zinc Finger and BTB Domain 1 Is Essential for Lymphocyte Development This information is current as Divya Punwani, Karen Simon, Youngnim Choi, Amalia of September 28, 2021. Dutra, Diana Gonzalez-Espinosa, Evgenia Pak, Martin Naradikian, Chang-Hwa Song, Jenny Zhang, David M. Bodine and Jennifer M. Puck J Immunol published online 29 June 2012 http://www.jimmunol.org/content/early/2012/06/29/jimmun Downloaded from ol.1200623 Supplementary http://www.jimmunol.org/content/suppl/2012/06/29/jimmunol.120062 Material 3.DC1 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 by guest on September 28, 2021 • Fast Publication! 4 weeks from acceptance to publication *average 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 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published June 29, 2012, doi:10.4049/jimmunol.1200623 The Journal of Immunology Transcription Factor Zinc Finger and BTB Domain 1 Is Essential for Lymphocyte Development Divya Punwani,*,1 Karen Simon,†,1 Youngnim Choi,‡ Amalia Dutra,† Diana Gonzalez-Espinosa,* Evgenia Pak,† Martin Naradikian,*,x Chang-Hwa Song,*,{ Jenny Zhang,* David M. -
Coupling of Spliceosome Complexity to Intron Diversity
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.19.436190; this version posted March 20, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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-ND 4.0 International license. Coupling of spliceosome complexity to intron diversity Jade Sales-Lee1, Daniela S. Perry1, Bradley A. Bowser2, Jolene K. Diedrich3, Beiduo Rao1, Irene Beusch1, John R. Yates III3, Scott W. Roy4,6, and Hiten D. Madhani1,6,7 1Dept. of Biochemistry and Biophysics University of California – San Francisco San Francisco, CA 94158 2Dept. of Molecular and Cellular Biology University of California - Merced Merced, CA 95343 3Department of Molecular Medicine The Scripps Research Institute, La Jolla, CA 92037 4Dept. of Biology San Francisco State University San Francisco, CA 94132 5Chan-Zuckerberg Biohub San Francisco, CA 94158 6Corresponding authors: [email protected], [email protected] 7Lead Contact 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.19.436190; this version posted March 20, 2021. 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-ND 4.0 International license. SUMMARY We determined that over 40 spliceosomal proteins are conserved between many fungal species and humans but were lost during the evolution of S. cerevisiae, an intron-poor yeast with unusually rigid splicing signals. We analyzed null mutations in a subset of these factors, most of which had not been investigated previously, in the intron-rich yeast Cryptococcus neoformans. -
A Flexible Microfluidic System for Single-Cell Transcriptome Profiling
www.nature.com/scientificreports OPEN A fexible microfuidic system for single‑cell transcriptome profling elucidates phased transcriptional regulators of cell cycle Karen Davey1,7, Daniel Wong2,7, Filip Konopacki2, Eugene Kwa1, Tony Ly3, Heike Fiegler2 & Christopher R. Sibley 1,4,5,6* Single cell transcriptome profling has emerged as a breakthrough technology for the high‑resolution understanding of complex cellular systems. Here we report a fexible, cost‑efective and user‑ friendly droplet‑based microfuidics system, called the Nadia Instrument, that can allow 3′ mRNA capture of ~ 50,000 single cells or individual nuclei in a single run. The precise pressure‑based system demonstrates highly reproducible droplet size, low doublet rates and high mRNA capture efciencies that compare favorably in the feld. Moreover, when combined with the Nadia Innovate, the system can be transformed into an adaptable setup that enables use of diferent bufers and barcoded bead confgurations to facilitate diverse applications. Finally, by 3′ mRNA profling asynchronous human and mouse cells at diferent phases of the cell cycle, we demonstrate the system’s ability to readily distinguish distinct cell populations and infer underlying transcriptional regulatory networks. Notably this provided supportive evidence for multiple transcription factors that had little or no known link to the cell cycle (e.g. DRAP1, ZKSCAN1 and CEBPZ). In summary, the Nadia platform represents a promising and fexible technology for future transcriptomic studies, and other related applications, at cell resolution. Single cell transcriptome profling has recently emerged as a breakthrough technology for understanding how cellular heterogeneity contributes to complex biological systems. Indeed, cultured cells, microorganisms, biopsies, blood and other tissues can be rapidly profled for quantifcation of gene expression at cell resolution. -
CD29 Identifies IFN-Γ–Producing Human CD8+ T Cells With
+ CD29 identifies IFN-γ–producing human CD8 T cells with an increased cytotoxic potential Benoît P. Nicoleta,b, Aurélie Guislaina,b, Floris P. J. van Alphenc, Raquel Gomez-Eerlandd, Ton N. M. Schumacherd, Maartje van den Biggelaarc,e, and Monika C. Wolkersa,b,1 aDepartment of Hematopoiesis, Sanquin Research, 1066 CX Amsterdam, The Netherlands; bLandsteiner Laboratory, Oncode Institute, Amsterdam University Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; cDepartment of Research Facilities, Sanquin Research, 1066 CX Amsterdam, The Netherlands; dDivision of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; and eDepartment of Molecular and Cellular Haemostasis, Sanquin Research, 1066 CX Amsterdam, The Netherlands Edited by Anjana Rao, La Jolla Institute for Allergy and Immunology, La Jolla, CA, and approved February 12, 2020 (received for review August 12, 2019) Cytotoxic CD8+ T cells can effectively kill target cells by producing therefore developed a protocol that allowed for efficient iso- cytokines, chemokines, and granzymes. Expression of these effector lation of RNA and protein from fluorescence-activated cell molecules is however highly divergent, and tools that identify and sorting (FACS)-sorted fixed T cells after intracellular cytokine + preselect CD8 T cells with a cytotoxic expression profile are lacking. staining. With this top-down approach, we performed an un- + Human CD8 T cells can be divided into IFN-γ– and IL-2–producing biased RNA-sequencing (RNA-seq) and mass spectrometry cells. Unbiased transcriptomics and proteomics analysis on cytokine- γ– – + + (MS) analyses on IFN- and IL-2 producing primary human producing fixed CD8 T cells revealed that IL-2 cells produce helper + + + CD8 Tcells. -
Quantitative SUMO Proteomics Reveals the Modulation of Several
www.nature.com/scientificreports OPEN Quantitative SUMO proteomics reveals the modulation of several PML nuclear body associated Received: 10 October 2017 Accepted: 28 March 2018 proteins and an anti-senescence Published: xx xx xxxx function of UBC9 Francis P. McManus1, Véronique Bourdeau2, Mariana Acevedo2, Stéphane Lopes-Paciencia2, Lian Mignacca2, Frédéric Lamoliatte1,3, John W. Rojas Pino2, Gerardo Ferbeyre2 & Pierre Thibault1,3 Several regulators of SUMOylation have been previously linked to senescence but most targets of this modifcation in senescent cells remain unidentifed. Using a two-step purifcation of a modifed SUMO3, we profled the SUMO proteome of senescent cells in a site-specifc manner. We identifed 25 SUMO sites on 23 proteins that were signifcantly regulated during senescence. Of note, most of these proteins were PML nuclear body (PML-NB) associated, which correlates with the increased number and size of PML-NBs observed in senescent cells. Interestingly, the sole SUMO E2 enzyme, UBC9, was more SUMOylated during senescence on its Lys-49. Functional studies of a UBC9 mutant at Lys-49 showed a decreased association to PML-NBs and the loss of UBC9’s ability to delay senescence. We thus propose both pro- and anti-senescence functions of protein SUMOylation. Many cellular mechanisms of defense have evolved to reduce the onset of tumors and potential cancer develop- ment. One such mechanism is cellular senescence where cells undergo cell cycle arrest in response to various stressors1,2. Multiple triggers for the onset of senescence have been documented. While replicative senescence is primarily caused in response to telomere shortening3,4, senescence can also be triggered early by a number of exogenous factors including DNA damage, elevated levels of reactive oxygen species (ROS), high cytokine signa- ling, and constitutively-active oncogenes (such as H-RAS-G12V)5,6. -
Open Data for Differential Network Analysis in Glioma
International Journal of Molecular Sciences Article Open Data for Differential Network Analysis in Glioma , Claire Jean-Quartier * y , Fleur Jeanquartier y and Andreas Holzinger Holzinger Group HCI-KDD, Institute for Medical Informatics, Statistics and Documentation, Medical University Graz, Auenbruggerplatz 2/V, 8036 Graz, Austria; [email protected] (F.J.); [email protected] (A.H.) * Correspondence: [email protected] These authors contributed equally to this work. y Received: 27 October 2019; Accepted: 3 January 2020; Published: 15 January 2020 Abstract: The complexity of cancer diseases demands bioinformatic techniques and translational research based on big data and personalized medicine. Open data enables researchers to accelerate cancer studies, save resources and foster collaboration. Several tools and programming approaches are available for analyzing data, including annotation, clustering, comparison and extrapolation, merging, enrichment, functional association and statistics. We exploit openly available data via cancer gene expression analysis, we apply refinement as well as enrichment analysis via gene ontology and conclude with graph-based visualization of involved protein interaction networks as a basis for signaling. The different databases allowed for the construction of huge networks or specified ones consisting of high-confidence interactions only. Several genes associated to glioma were isolated via a network analysis from top hub nodes as well as from an outlier analysis. The latter approach highlights a mitogen-activated protein kinase next to a member of histondeacetylases and a protein phosphatase as genes uncommonly associated with glioma. Cluster analysis from top hub nodes lists several identified glioma-associated gene products to function within protein complexes, including epidermal growth factors as well as cell cycle proteins or RAS proto-oncogenes. -
Elucidating Biological Roles of Novel Murine Genes in Hearing Impairment in Africa
Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 19 September 2019 doi:10.20944/preprints201909.0222.v1 Review Elucidating Biological Roles of Novel Murine Genes in Hearing Impairment in Africa Oluwafemi Gabriel Oluwole,1* Abdoulaye Yal 1,2, Edmond Wonkam1, Noluthando Manyisa1, Jack Morrice1, Gaston K. Mazanda1 and Ambroise Wonkam1* 1Division of Human Genetics, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Observatory, Cape Town, South Africa. 2Department of Neurology, Point G Teaching Hospital, University of Sciences, Techniques and Technology, Bamako, Mali. *Correspondence to: [email protected]; [email protected] Abstract: The prevalence of congenital hearing impairment (HI) is highest in Africa. Estimates evaluated genetic causes to account for 31% of HI cases in Africa, but the identification of associated causative genes mutations have been challenging. In this study, we reviewed the potential roles, in humans, of 38 novel genes identified in a murine study. We gathered information from various genomic annotation databases and performed functional enrichment analysis using online resources i.e. genemania and g.proflier. Results revealed that 27/38 genes are express mostly in the brain, suggesting additional cognitive roles. Indeed, HERC1- R3250X had been associated with intellectual disability in a Moroccan family. A homozygous 216-bp deletion in KLC2 was found in two siblings of Egyptian descent with spastic paraplegia. Up to 27/38 murine genes have link to at least a disease, and the commonest mode of inheritance is autosomal recessive (n=8). Network analysis indicates that 20 other genes have intermediate and biological links to the novel genes, suggesting their possible roles in HI. -
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in -
Splicing Factors Sf3a2 and Prp31 Have Direct Roles in Mitotic Chromosome Segregation
RESEARCH ARTICLE Splicing factors Sf3A2 and Prp31 have direct roles in mitotic chromosome segregation Claudia Pellacani1†, Elisabetta Bucciarelli1†, Fioranna Renda2‡, Daniel Hayward3, Antonella Palena1, Jack Chen3, Silvia Bonaccorsi2, James G Wakefield3, Maurizio Gatti1,2*, Maria Patrizia Somma1* 1Istituto di Biologia e Patologia Molecolari del CNR, Sapienza Universita` di Roma, Roma, Italy; 2Dipartimento di Biologia e Biotecnologie “C. Darwin”, Sapienza Universita` di Roma, Roma, Italy; 3Biosciences/Living Systems Institute, College of Life and Environmental Sciences, University of Exeter, Exeter, United Kingdom Abstract Several studies have shown that RNAi-mediated depletion of splicing factors (SFs) results in mitotic abnormalities. However, it is currently unclear whether these abnormalities reflect defective splicing of specific pre-mRNAs or a direct role of the SFs in mitosis. Here, we show that two highly conserved SFs, Sf3A2 and Prp31, are required for chromosome segregation in both Drosophila and human cells. Injections of anti-Sf3A2 and anti-Prp31 antibodies into Drosophila *For correspondence: embryos disrupt mitotic division within 1 min, arguing strongly against a splicing-related mitotic [email protected] (MG); function of these factors. We demonstrate that both SFs bind spindle microtubules (MTs) and the [email protected] Ndc80 complex, which in Sf3A2- and Prp31-depleted cells is not tightly associated with the (MPS) kinetochores; in HeLa cells the Ndc80/HEC1-SF interaction is restricted to the M phase. -
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bioRxiv preprint doi: https://doi.org/10.1101/2020.09.02.279679; this version posted September 2, 2020. 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-ND 4.0 International license. A high-throughput CRISPR interference screen for dissecting functional regulators of GPCR/cAMP signaling Khairunnisa Mentari Semesta1, Ruilin Tian2,3,4, Martin Kampmann2,3, Mark von Zastrow5,6 and Nikoleta G. Tsvetanova1* 1 Department of Pharmacology and Cancer Biology, Duke University, Durham, NC 27710, USA 2 Insitute for Neurodegenerative Diseases, Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA 3 Chen-Zuckerberg Biohub, San Francisco, CA 94158, USA 4 Biophysics Graduate Program, University of California, San Francisco, CA 94158, USA 5 Department of Psychiatry, University of California, San Francisco, CA 94158, USA 6 Department of Cellular & Molecular Pharmacology, University of California, San Francisco, CA 94158, USA * Correspondence: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.02.279679; this version posted September 2, 2020. 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-ND 4.0 International license. 1 Abstract 2 G protein-coupled receptors (GPCRs) allow cells to respond to chemical and sensory 3 stimuli through generation of second messengers, such as cyclic AMP (cAMP), which in 4 turn mediate a myriad of processes, including cell survival, proliferation, and 5 differentiation. -
On the Role of Chromosomal Rearrangements in Evolution
On the role of chromosomal rearrangements in evolution: Reconstruction of genome reshuffling in rodents and analysis of Robertsonian fusions in a house mouse chromosomal polymorphism zone by Laia Capilla Pérez A thesis submitted for the degree of Doctor of Philosophy in Animal Biology Supervisors: Dra. Aurora Ruiz-Herrera Moreno and Dr. Jacint Ventura Queija Institut de Biotecnologia i Biomedicina (IBB) Departament de Biologia Cel·lular, Fisiologia i Immunologia Departament de Biologia Animal, Biologia Vegetal i Ecologia Universitat Autònoma de Barcelona Supervisor Supervisor PhD candidate Aurora Ruiz-Herrera Moreno Jacint Ventura Queija Laia Capilla Pérez Bellaterra, 2015 A la mare Al pare Al mano “Visto a la luz de la evolución, la biología es, quizás, la ciencia más satisfactoria e inspiradora. Sin esa luz, se convierte en un montón de hechos varios, algunos de ellos interesantes o curiosos, pero sin formar ninguna visión conjunta.” Theodosius Dobzhansky “La evolución es tan creativa. Por eso tenemos jirafas.” Kurt Vonnegut This thesis was supported by grants from: • Ministerio de Economía y Competitividad (CGL2010-15243 and CGL2010- 20170). • Generalitat de Catalunya, GRQ 1057. • Ministerio de Economía y Competitividad. Beca de Formación de Personal Investigador (FPI) (BES-2011-047722). • Ministerio de Economía y Competitividad. Beca para la realización de estancias breves (EEBB-2011-07350). Covers designed by cintamontserrat.blogspot.com INDEX Abstract 15-17 Acronyms 19-20 1. GENERAL INTRODUCTION 21-60 1.1 Chromosomal rearrangements -
Molecular and Cytogenetic Analysis of the Spreading of X Inactivation in a Girl with Microcephaly, Mild Dysmorphic Features and T(X;5)(Q22.1;Q31.1)
European Journal of Human Genetics (2008) 16, 897–905 & 2008 Nature Publishing Group All rights reserved 1018-4813/08 $30.00 www.nature.com/ejhg ARTICLE Molecular and cytogenetic analysis of the spreading of X inactivation in a girl with microcephaly, mild dysmorphic features and t(X;5)(q22.1;q31.1) Roberto Giorda*,1,7, M Clara Bonaglia2,7, Greta Milani1, Anna Baroncini3, Francesca Spada3, Silvana Beri1, Giorgia Menozzi4, Marianna Rusconi1 and Orsetta Zuffardi5,6 1Molecular Biology Laboratory, ‘E. Medea’ Scientific Institute, Bosisio Parini, Lecco, Italy; 2Cytogenetics Laboratory, ‘E. Medea’ Scientific Institute, Bosisio Parini, Lecco, Italy; 3UO Genetica Medica, AUSL Imola, Imola, Italy; 4Bioinformatic Laboratory, ‘E. Medea’ Scientific Institute, Bosisio Parini, Lecco, Italy; 5Biologia Generale e Genetica Medica, Universita` di Pavia, Pavia, Italy; 6IRCCS Policlinico San Matteo, Pavia, Italy X chromosome inactivation involves initiation, propagation, and maintenance of gene inactivation. Studies of replication pattern and timing in X;autosome translocations have suggested that X inactivation may spread to autosomal DNA. To examine this phenomenon at the molecular level, we have tested the transcriptional activity of a number of chromosome 5 loci in a female subject with microcephaly, mild dysmorphic features and 46,X,der(X)t(X;5)(q22.1;q31.1) karyotype. RT-PCR analysis of 20 transcribed sequences spanning 5q31.1-qter revealed that nine of them were not expressed in somatic cell hybrid clones carrying the translocated chromosome. However, eight genes were expressed and therefore escaped inactivation. This direct expression test demonstrates that spreading of inactivation from the X chromosome to the adjoining autosomal DNA was incomplete and ‘patchy’.