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Nebulette Is a Powerful Cytolinker Organizing Desmin and Actin in Mouse Hearts
M BoC | ARTICLE Nebulette is a powerful cytolinker organizing desmin and actin in mouse hearts Daniel A. Hernandeza,†, Christina M. Bennetta,†, Lyubov Dunina-Barkovskayaa, Tatjana Wedigb, Yassemi Capetanakic, Harald Herrmannb,d, and Gloria M. Conovera,* aDepartment of Biochemistry & Biophysics, Texas A&M University, College Station, TX 77843-3474; bDivision of Molecular Genetics, German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany; cCenter of Basic Research, Biomedi- cal Research Foundation Academy of Athens, Athens 11527, Greece; dInstitute of Neuropathology, University Hospital Erlangen, D-91054 Erlangen, Germany ABSTRACT In the hearts of patients bearing nebulette mutations, a severe general disorgani- Monitoring Editor zation in cardiomyocytes of the extrasarcomeric desmin intermediate filament system is fre- Robert D. Goldman quently observed. However, the molecular and functional relationship between the desmin Northwestern University cytoskeleton and nebulette-containing sarcomeres is still unclear. Here we report a high-affinity Received: Apr 18, 2016 in vitro interaction between nebulette and desmin filaments. A major interaction site has been Revised: Aug 31, 2016 mapped to the desmin α-helical rod domain, indicating that the filament core is directly in- Accepted: Oct 5, 2016 volved in the binding of nebulette. The disease-mutant desmin variants E245D and T453I ex- hibited increased binding affinity for nebulette, delayed filament assembly kinetics, and caused significant weakening of networks. In isolated chick cardiomyocytes and sections from canine heart, we revealed by ground-state depletion and confocal microscopies that module 5 of nebulette extends outward from Z-disk–associated desmin filaments toward the center of the sarcomere. Accordingly, in the myocardium of Des−/− mice, elevated levels of cardiac actin cor- related with alterations in the distribution of nebulette. -
The Role of Z-Disc Proteins in Myopathy and Cardiomyopathy
International Journal of Molecular Sciences Review The Role of Z-disc Proteins in Myopathy and Cardiomyopathy Kirsty Wadmore 1,†, Amar J. Azad 1,† and Katja Gehmlich 1,2,* 1 Institute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK; [email protected] (K.W.); [email protected] (A.J.A.) 2 Division of Cardiovascular Medicine, Radcliffe Department of Medicine and British Heart Foundation Centre of Research Excellence Oxford, University of Oxford, Oxford OX3 9DU, UK * Correspondence: [email protected]; Tel.: +44-121-414-8259 † These authors contributed equally. Abstract: The Z-disc acts as a protein-rich structure to tether thin filament in the contractile units, the sarcomeres, of striated muscle cells. Proteins found in the Z-disc are integral for maintaining the architecture of the sarcomere. They also enable it to function as a (bio-mechanical) signalling hub. Numerous proteins interact in the Z-disc to facilitate force transduction and intracellular signalling in both cardiac and skeletal muscle. This review will focus on six key Z-disc proteins: α-actinin 2, filamin C, myopalladin, myotilin, telethonin and Z-disc alternatively spliced PDZ-motif (ZASP), which have all been linked to myopathies and cardiomyopathies. We will summarise pathogenic variants identified in the six genes coding for these proteins and look at their involvement in myopathy and cardiomyopathy. Listing the Minor Allele Frequency (MAF) of these variants in the Genome Aggregation Database (GnomAD) version 3.1 will help to critically re-evaluate pathogenicity based on variant frequency in normal population cohorts. -
BSCB Newsletter 2017D
2017 BSCB Newsletter BRITISH SOCIETY FOR CELL BIOLOGY Meet the new BSCB President Royal Opening of the Crick Meeting reports 2017 CONTENTS BSCB Newsletter News 2 Book reviews 7 Features 8 Meeting Reports 24 Summer students 30 Society Business 33 Editorial Welcome to the 2017 BSCB newsletter. After several meeting hosted several well received events for our Front cover: years of excellent service, Kate Nobes has stepped PhD and Postdoc members, which we discuss on The head of a Drosophila pupa. The developing down and handed the reins over to me. I’ve enjoyed page 5. Our PhD and Postdoc reps are working hard compound eye (green) is putting together this years’ newsletter. It’s been great to make the event bigger and better for next year! The composed of several hundred simple units called ommatidia to hear what our members have been up to, and I social events were well attended including the now arranged in an extremely hope you will enjoy reading it. infamous annual “Pub Quiz” and disco after the regular array. The giant conference dinner. Members will be relieved to know polyploidy cells of the fat body (red), the fly equivalent of the The 2016 BSCB/DB spring meeting, organised by our we aren’t including any photos from that here. mammalian liver and adipose committee members Buzz Baum (UCL), Silke tissue, occupy a big area of the Robatzek and Steve Royle, had a particular focus on In this issue, we highlight the great work the BSCB head. Cells and Tissue Architecture, Growth & Cell Division, has been doing to engage young scientists. -
List of Genes Associated with Sudden Cardiac Death (Scdgseta) Gene
List of genes associated with sudden cardiac death (SCDgseta) mRNA expression in normal human heart Entrez_I Gene symbol Gene name Uniprot ID Uniprot name fromb D GTEx BioGPS SAGE c d e ATP-binding cassette subfamily B ABCB1 P08183 MDR1_HUMAN 5243 √ √ member 1 ATP-binding cassette subfamily C ABCC9 O60706 ABCC9_HUMAN 10060 √ √ member 9 ACE Angiotensin I–converting enzyme P12821 ACE_HUMAN 1636 √ √ ACE2 Angiotensin I–converting enzyme 2 Q9BYF1 ACE2_HUMAN 59272 √ √ Acetylcholinesterase (Cartwright ACHE P22303 ACES_HUMAN 43 √ √ blood group) ACTC1 Actin, alpha, cardiac muscle 1 P68032 ACTC_HUMAN 70 √ √ ACTN2 Actinin alpha 2 P35609 ACTN2_HUMAN 88 √ √ √ ACTN4 Actinin alpha 4 O43707 ACTN4_HUMAN 81 √ √ √ ADRA2B Adrenoceptor alpha 2B P18089 ADA2B_HUMAN 151 √ √ AGT Angiotensinogen P01019 ANGT_HUMAN 183 √ √ √ AGTR1 Angiotensin II receptor type 1 P30556 AGTR1_HUMAN 185 √ √ AGTR2 Angiotensin II receptor type 2 P50052 AGTR2_HUMAN 186 √ √ AKAP9 A-kinase anchoring protein 9 Q99996 AKAP9_HUMAN 10142 √ √ √ ANK2/ANKB/ANKYRI Ankyrin 2 Q01484 ANK2_HUMAN 287 √ √ √ N B ANKRD1 Ankyrin repeat domain 1 Q15327 ANKR1_HUMAN 27063 √ √ √ ANKRD9 Ankyrin repeat domain 9 Q96BM1 ANKR9_HUMAN 122416 √ √ ARHGAP24 Rho GTPase–activating protein 24 Q8N264 RHG24_HUMAN 83478 √ √ ATPase Na+/K+–transporting ATP1B1 P05026 AT1B1_HUMAN 481 √ √ √ subunit beta 1 ATPase sarcoplasmic/endoplasmic ATP2A2 P16615 AT2A2_HUMAN 488 √ √ √ reticulum Ca2+ transporting 2 AZIN1 Antizyme inhibitor 1 O14977 AZIN1_HUMAN 51582 √ √ √ UDP-GlcNAc: betaGal B3GNT7 beta-1,3-N-acetylglucosaminyltransfe Q8NFL0 -
Sumoylation Regulates Protein Dynamics During Meiotic Chromosome Segregation in C
© 2019. Published by The Company of Biologists Ltd | Journal of Cell Science (2019) 132, jcs232330. doi:10.1242/jcs.232330 RESEARCH ARTICLE Sumoylation regulates protein dynamics during meiotic chromosome segregation in C. elegans oocytes Federico Pelisch*, Laura Bel Borja, Ellis G. Jaffray and Ronald T. Hay ABSTRACT studies of MT-dependent chromosome movement focused on Oocyte meiotic spindles in most species lack centrosomes and pulling forces generated by kinetochore MTs (kMTs) making the mechanisms that underlie faithful chromosome segregation end-on contacts with chromosomes (Cheeseman, 2014), there is in acentrosomal meiotic spindles are not well understood. In also evidence for pushing forces that are exerted on the segregating C. elegans oocytes, spindle microtubules exert a poleward force on chromosomes (Khodjakov et al., 2004; Nahaboo et al., 2015; š ́ chromosomes that is dependent on the microtubule-stabilising Laband et al., 2017; Vuku ic et al., 2017; Yu et al., 2019 preprint). protein CLS-2, the orthologue of the mammalian CLASP proteins. The nematode Caenorhabditis elegans contains holocentric The checkpoint kinase BUB-1 and CLS-2 localise in the central chromosomes (Maddox et al., 2004) and has served as an spindle and display a dynamic localisation pattern throughout extremely useful system to uncover mechanisms of meiosis and anaphase, but the signals regulating their anaphase-specific mitosis for almost 20 years (Oegema et al., 2001; Desai et al., 2003; localisation remains unknown. We have shown previously that Cheeseman et al., 2004, 2005; Monen et al., 2005). Meiosis is a SUMO regulates BUB-1 localisation during metaphase I. Here, we specialised cell division with two successive rounds of chromosome found that SUMO modification of BUB-1 is regulated by the SUMO E3 segregation that reduce the ploidy and generates haploid gametes ligase GEI-17 and the SUMO protease ULP-1. -
Feedback Interactions Between Cell–Cell Adherens Junctions and Cytoskeletal Dynamics in Newt Lung Epithelial Cells□V Clare M
Molecular Biology of the Cell Vol. 11, 2471–2483, July 2000 Feedback Interactions between Cell–Cell Adherens Junctions and Cytoskeletal Dynamics in Newt Lung Epithelial Cells□V Clare M. Waterman-Storer,*†‡ Wendy C. Salmon,†‡ and E.D. Salmon‡ *Department of Cell Biology and Institute for Childhood and Neglected Diseases, The Scripps Research Institute, La Jolla, California 92037; and ‡Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599 Submitted February 3, 2000; Revised April 20, 2000; Accepted May 11, 2000 Monitoring Editor: Jennifer Lippincott-Schwartz To test how cell–cell contacts regulate microtubule (MT) and actin cytoskeletal dynamics, we examined dynamics in cells that were contacted on all sides with neighboring cells in an epithelial cell sheet that was undergoing migration as a wound-healing response. Dynamics were recorded using time-lapse digital fluorescence microscopy of microinjected, labeled tubulin and actin. In fully contacted cells, most MT plus ends were quiescent; exhibiting only brief excursions of growth and shortening and spending 87.4% of their time in pause. This contrasts MTs in the lamella of migrating cells at the noncontacted leading edge of the sheet in which MTs exhibit dynamic instability. In the contacted rear and side edges of these migrating cells, a majority of MTs were also quiescent, indicating that cell–cell contacts may locally regulate MT dynamics. Using photoactivation of fluorescence techniques to mark MTs, we found that MTs in fully contacted cells did not undergo retrograde flow toward the cell center, such as occurs at the leading edge of motile cells. Time-lapse fluorescent speckle microscopy of fluorescently labeled actin in fully contacted cells revealed that actin did not flow rearward as occurs in the leading edge lamella of migrating cells. -
Lipid Rafts and Caveolae
46 Scaffolding SCAFFOLDING 1 NANOCELLBIOLOGY: CELL SURFACE PORTALS – CLATHRIN-COATED PITS, LIPID RAFTS, CAVEOLAE, AND POROSOMES A new field in biology, nanocellbiology (nano cell biol- About 280 years later, the transmission electron micro- ogy), has emerged from the successful use of atomic force scope was invented. Hence, on July 6, 1944 in Rockefeller microscopy, in combination with electron microscopy and Institute for Medical Research, New York, NY, Albert Claude other methods, in understanding the structure and dynamics made the first 13 micrographs taken from (cultured) cells. of cells and biomolecules at nanoscale resolution (1-3) (Fig- Thirty years later, in 1974, Albert Claude, Christian de Duve ure 1). and George Palade shared the Nobel Prize for Physiology or Human “love to knowledge” (from Bulgarian “lyuboz- Medicine. For the discovery of a new cell world, revealing nanie” - “lyubov”, love, “znanie”, knowledge) led to the membrane-bound organelles (mitochondria, endoplasmic re- whish to “see inside” the body of organisms. Initially, this ticulum, Golgi complex, lysosomes, caveolae) and cytoskel- was achieved by the dissection of human cadavers performed etal elements (filaments and microtubules). by the pioneer anatomist Andreas Vesalius. Later on the mi- The plasma membrane (plasmalemma, cell surface) is a croscope was invented. In 1609, Galileo was among the first complex lipoprotein structure surrounding the cells in all to use a telescope as an instrument to observe stars and plan- living organisms. Cells have constant need for the build- ets. The names „telescope“ and „microscope“ were coined for ing components of life: amino acids, lipids, carbohydrates, Galileo‘s instrument, in 1611. Illustrations of insects made and nucleic acids. -
Cell Secretion and Membrane Fusion: Highly Significant Phenomena in the Life of a Cell
DISCOVERIES 2014, Jul -Sep, 2(3): e30 DOI: 10.15190/d.2014.22 Cell Secretion and Membrane Fusion EDITORIAL Cell secretion and membrane fusion: highly significant phenomena in the life of a cell Mircea Leabu 1,2,3,*, Garth L. Nicolson 4,* 1University of Medicine and Pharmacy “Carol Davila”, Department of Cellular and Molecular Medicine, 8, Eroilor Sanitari Blvd., 050474, Bucharest, Romania 2 “Victor Babes” National Institute of Pathology, 99101, Splaiul Independentei, 050096, Bucharest, Romania 3University of Bucharest, Research Center for Applied Ethics, 204, Splaiul Independentei, 060024, Bucharest, Romania 4Department of Molecular Pathology, Institute for Molecular Medicine, Huntington Beach, California, 92647 USA *Corresponding authors: Mircea Leabu, PhD , “Victor Babes” National Institute of Pathology, 99-101, Splaiul Independentei, 050096, Bucharest, Romania; E-mail: [email protected]; Garth L. Nicolson, Ph.D , The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, CA 92652 USA. Email: [email protected] Submitted: Sept. 10, 2014; Revised: Sept. 14, 2014; Accepted: Sept. 17, 2014; Published: Sept. 18, 2014; Citation : Leabu M, Nicolson GL. Cell Secretion and membrane fusion: highly significant phenomena in the life of a cell. Discoveries 2014, Jul-Sep; 2(3): e30. DOI: 10.15190/d.2014.22 Keywords : cell secretion, membrane fusion, every cell’s existence, and they must be very well porosome, exosomes, electron microscopy, cancer, coordinated and controlled. Membrane trafficking, mathematical approach, secretory vesicle, science which involves vesicular budding of the source history membrane, directed transport and eventually fusion with the target membrane is a very specific process. All of these processes depend, in particular, on Introduction basic principals of biological membrane structure Is there any cell that does not secrete something and dynamics, a topic that was reviewed recently in necessary for maintenance of the organism? this journal 1. -
Ams 3 2009.Qxp
Review paper Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unstable membranes? Glyn Wainwright1, Luca Mascitelli2, Mark R. Goldstein3 1Independent Reader of Research, Leeds, United Kingdom Corresponding author: 2Medical Service, Comando Brigata Alpina “Julia”, Udine, Italy Luca Mascitelli, MD 3Fountain Medical Court, Bonita Springs, FL, USA Comando Brigata Alpina “Julia” Medical Service Submitted: 15 April 2009 8 Via S. Agostino Accepted: 4 May 2009 Udine 33100, Italy Phone: +39 0432584044 Arch Med Sci 2009; 5, 3: 289-295 Fax: +390432584053 Copyright © 2009 Termedia & Banach E-mail: [email protected] Abstract Current guidelines encourage ambitious long term cholesterol lowering with statins, in order to decrease cardiovascular disease events. However, by regulating the biosynthesis of cholesterol we potentially change the form and function of every cell membrane from the head to the toe. As research into cell morphology and membrane function realises more dependencies upon cholesterol rich lipid membranes, our clinical understanding of long term inhibition of cholesterol biosynthesis is also changing. This review of non- cardiovascular research concerning such membrane effects raises important new issues concerning the clinical advantages and disadvantages of the long term use, and broadening criteria, of cholesterol reductions. Key words: cholesterol, exocytosis, lipid, membrane, statin. Introduction The undoubted commercial success story in modern medicine has been the creation of that infamous household dietary and medical obsession: ‘Cholesterol’. Over the past decade researchers have achieved new insight into the regulatory relationship between cholesterol and the world of lipid transport. A persuasive association of statistics about cardiovascular outcomes and levels of blood plasma lipids has created a sophisticated range of therapeutic targets for cholesterol lowering therapies [1]. -
BIOLOGYGAMSAT-Prep.Com
GAMSAT C M Y CM MY CY CMY K BIOLOGYGAMSAT-prep.com GENERALISED EUKARYOTIC CELL Chapter 1 Memorise Understand Importance * Structure/function: cell/components * 1st year university level info* High level: 15% of GAMSAT Biology * Components and function: cytoskeleton * Membrane transport questions released by ACER are related to * DNA structure and function * Hyper/hypotonic solutions content in this chapter (in our estimation). * Transmission of genetic information * Saturation kinetics: graphs * Note that approximately of the * Mitosis, events of the cell cycle * Unique features of eukaryotes 75% questions in GAMSAT Biology are related * Basics: Cell junctions, microscopy to just 7 chapters: 1, 2, 3, 4, 7, 12, and 15. Introduction Cells are the basic organisational unit of living organisms. They are contained by a plasma membrane and/or cell wall. Eukaryotic cells (eu = true; karyote refers to nucleus) are cells with a true nucleus found in all multicel- lular and nonbacterial unicellular organisms including animal, fungal and plant cells. The nucleus contains ge- netic information, DNA, which can divide into 2 cells by mitosis. Get ready to waste some time! Glad to have your attention! Our experience is that most students ‘overstudy’ Biol- ogy and underperform in Biology when they see the types of questions that are asked on the GAMSAT. Please do not get trapped in details. We’ll guide you as much as we can but in the end, it’s up to you: colour-coded table of contents, yellow highlighter, underline, foundational and GAMSAT-level practice questions at the end of the chapter, etc. For now, enjoy the story that you are expected to be exposed to for the GAMSAT, but generally the content will likely be more helpful to you in medical school. -
Snapshot: Actin Regulators II Anosha D
SnapShot: Actin Regulators II Anosha D. Siripala and Matthew D. Welch Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA Representative Proteins Protein Family H. sapiens D. melanogaster C. elegans A. thaliana S. cerevisiae Endocytosis and Exocytosis ABP1/drebrin mABP1, drebrin, drebrin- †Q95RN0 †Q9XUT0 Abp1 like EPS15 EPS15 Eps-15 EHS-1 †Q56WL2 Pan1 HIP1R HIP1R †Q8MQK1 †O62142 Sla2 Synapsin synapsin Ia, Ib, IIa, IIb, III Synapsin SNN-1 Plasma Membrane Association Anillin anillin Scraps ANI-1, 2, 3 Annexins annexin A1–11, 13 (actin Annexin B9-11 NEX-1–4 ANN1-8 binding: 1, 2, 6) ERM proteins ezrin, radixin, moesin DMoesin ERM-1 MARCKS MARCKS, MRP/ Akap200 MACMARCKS/F52 Merlin *merlin/NF2 Merlin NFM-1 Protein 4.1 4.1R, G, N, B Coracle Spectrin α-spectrin (1–2), β-spectrin α-spectrin, β-spectrin, β heavy- SPC-1 (α-spectrin), UNC-70 (1–4), β heavy-spectrin/ spectrin/Karst (β-spectrin), SMA-1 (β heavy- karst spectrin) Identifi ed Cellular Role: X Membrane traffi cking and phagocytosis Cell-Cell Junctions X Cytokinesis α-catenin α-catenin 1–3 α-catenin HMP-1 X Cell surface organization and dynamics X Cell adhesion Afadin afadin/AF6 Canoe AFD-1 X Multiple functions ZO-1 ZO-1, ZO-2, ZO-3 ZO-1/Polychaetoid †Q56VX4 X Other/unknown Cell-Extracellular Matrix Junctions †UNIPROT database accession number *Mutation linked to human disease Dystrophin/utrophin *dystrophin, utrophin/ Dystrophin DYS-1 DRP1, DRP2 LASP LASP-1, LASP-2, LIM- Lasp †P34416 nebulette Palladin palladin Parvin α-, β-, χ-parvin †Q9VWD0 PAT-6 -
Identification of Endogenous Adenomatous Polyposis Coli Interaction Partners 1 and Β-Catenin-Independent Targets by Proteomics
Author Manuscript Published OnlineFirst on June 3, 2019; DOI: 10.1158/1541-7786.MCR-18-1154 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. 1 Identification of endogenous Adenomatous polyposis coli interaction partners 2 and E-catenin-independent targets by proteomics 3 4 Olesja Popow1,2, João A. Paulo2, Michael H. Tatham3, Melanie S. Volk5, Alejandro 5 Rojas-Fernandez4, Nicolas Loyer5, Ian P. Newton5, Jens Januschke5, Kevin M. 6 Haigis1,6, Inke Näthke5* 7 8 1Cancer Research Institute and Department of Medicine, Beth Israel Deaconess 9 Medical Center, Boston, MA 02215, United States 10 2Department of Cell Biology, Harvard Medical School, Boston, MA 02115, United States 11 3Centre for Gene Regulation and Expression, School of Life Sciences, University of 12 Dundee, Dundee, DD1 5EH, Scotland UK 13 4Center for Interdisciplinary Studies on the Nervous System (CISNe) and Institute of 14 Medicine, Universidad Austral de Chile, Valdivia, Chile 15 5Cell and Developmental Biology, School of Life Sciences, University of Dundee, 16 Dundee, DD1 5EH, Scotland UK 17 6Harvard Digestive Disease Center, Harvard Medical School, Boston, MA 02215, United 18 States 19 20 Running title: The APC interactome and its E-catenin-independent targets. 21 22 Keywords: Adenomatous polyposis coli, destruction complex, colorectal cancer, 23 proteomics, Misshapen-like kinase 1. 1 Downloaded from mcr.aacrjournals.org on October 3, 2021. © 2019 American Association for Cancer Research. Author Manuscript Published OnlineFirst on June 3, 2019; DOI: 10.1158/1541-7786.MCR-18-1154 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.