Nancy M. Bonini
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CPI Newsletter – June 2018
Mail Stop 2404 • College Station, TX 77843-2404 • (979) 862-9166 • [email protected] ------------------------------------------------------------------------------------ CPI Newsletter – June 2018 ------------------------------------------------------------------------------------ Included in this issue: ⎯ Update from the CPI Chair ⎯ Huffines Faculty Research Seed Grants – Deadline June 15, 2018 ⎯ Potential Opportunity for NSF and NIH Supplements to Existing Grants ⎯ Export Controls Designated Liaison Network ⎯ 3rd Annual Postdoctoral Research Symposium – September 19, 2018 ⎯ Sign Up for Notifications about Limited Submission Proposal Opportunities ⎯ Bulletin for Principal Investigators 2017-18 CPI roster: Chair — Penny Riggs , COALS ● Vice Chair — David Threadgill , Veterinary Medicine ● AgriLife Extension — Craig Carpenter, Gaylon Morgan ● AgriLife Research — Michael Brewer, Ambika Chandra, Fugen Dou, Lee Tarpley ● Architecture — Ergun Akleman ● Bush School — Kent Portney ● COALS — Fuller Bazer, Russell Cross, Martin Dickman, Micky Eubanks, Elizabeth Pierson, David Stelly ● Education – Oi-Man Kwok, Jeffrey Liew ● Engineering — Jorge Alvarado, Ulisses Braga-Neto, Zachary Grasley, Melissa Grunlan, Tony Hsieh Sheng-Jen, Daniel Jiménez, Jodie Lutkenhaus, Ramesh Talreja ● Geosciences — Alejandro Orsi, Pamela Plotkin, Brendan Roark ● IBT/PHARM/RCHI — Julian Hurdle ● Law – Susan Fortney ● Liberal Arts — Sandra Braman, Steve Maren, Harland Prechel ● Mays — Korok Ray ● Medicine —Vytas Bankaitis, Kayla Bayless ● Science — Darren DePoy, Michael Hall, -
Twists and Turns in Protein Assembly
Twists and Turns in Protein Assembly Professor Robert Fairman TWISTS AND TURNS IN PROTEIN ASSEMBLY In nerve cells, the accumulation of protein into bundles of insoluble fibres is the underlying cause of a number of neurodegenerative diseases. Professor Robert Fairman and his team at Haverford College are developing cutting edge techniques to unravel this process. Proteins are the building blocks of life. The leads to the death of particularly vulnerable genetic code within each cell of our bodies cells such as neurones – the elaborate and controls the sequence of molecules called sensitive cells in our brain. This is the basic amino acids, which assemble together mechanism that causes the debilitating and to form each protein. But this is only the currently untreatable neurological disorder first step. Amino acids are small charged Huntington’s disease, which is characterised molecules that interact with one another as by a disruption of normal movements and they join together to form strings of peptides a decline in mental ability, resulting in (polypeptides), which spontaneously develop dementia. into different structures known as secondary structures. This can involve the formation ‘The relationship of this aggregation to of sheets or helical spirals following certain disease is poorly understood, and differences rules determined by the order of the amino in protein structure may underlie differences acids. These secondary structures then in toxicity,’ Professor Fairman admits. ‘Many interact with one another to form larger neurodegenerative diseases (Alzheimer’s, tertiary structures of proteins that control Huntington’s, Parkinson’s) have a similar and mediate every aspect of cell function. underlying molecular mechanism of protein aggregation, involving the formation of ‘Ever since I was an undergraduate student, an extended polypeptide chain that can I’ve always been fascinated with a chemical aggregate through ß-sheet formation.’ view of biology,’ Professor Fairman tells As such, it is vital to understand how Scientia. -
From the President's Desk
Sept | Oct 2009 From the President’s desk: The Increasing Importance of Model Organism Research I’m sure you know this scenario: You’re at a party, and someone hears you’re a biologist, and asks, “What do you work on?” When this happens to me, and I respond that I study yeast, I frequently get the follow-up question that you have probably already anticipated: “Are you learning how to make better beer?” At that point, I offer my explanation about the value of studying model organisms, which in cludes the statement that my daughter, now 17, learned to repeat with me by the time she was 3: “Yeast are actually a lot like people.” If you study a model organism, whether it’s yeast, bacteria, phage, flies, worms, fish, plants, or something else, you probably have been in Fred Winston a similar situation when talking to someone who is not a scientist. There GSA President is little understanding among the general public about the value of studying a model organism. This is also true among some who we might think would better understand this issue. While you wouldn’t be surprised to learn that the person at this party was a lawyer or a businessperson, you might also not be too surprised if that person turned out to be a physician, or even a human biologist. Even among some biologists who understand the history of model organisms, there may be a lack of appreciation for what model organism research can contribute to future scientific understanding. For these scientists, model organi sms appear to be in the twilight of their usefulness with the advent of new sequencing technologies and other genome-wide, high-throughput approaches that can be used in human studies. -
'Epigenetic Landscape' Is Protective in Normal Aging, Impaired in Alzheimer's Disease 5 March 2018
'Epigenetic landscape' is protective in normal aging, impaired in Alzheimer's disease 5 March 2018 compaction of chromosomes in the nucleus (called acetylation of lysine 16 on histone H4, or H4K16ac for short). Changes to the way H4K16ac is modified along the genome in disease versus normal aging brains may signify places for future drug development. Because changes in H4K16ac govern how genes are expressed, the location and amount of epigenetic alterations is called the "epigenetic landscape." "This is the first time that we have been able to look at these relationships in human tissue by using donated postmortem brain tissue from the Penn Brain Bank," said Shelley Berger, PhD, a professor of Cell and Developmental Biology in the Perelman School of Medicine and a professor of Biology in the School of Arts and Sciences. "Our results Coronal section of human brain indicating the lateral establish the basis for an epigenetic link between temporal lobe (red circle) used in this study. Credit: aging and Alzheimer's disease." Coronal section of human brain indicating The lab of Shelley Berger, PhD, Perelman School of Medicine, Berger, also the director of the Penn Epigenetics University of Pennsylvania Institute, Nancy Bonini, PhD, a professor of Biology, and Brad Johnson, MD, PhD, an associate professor of Pathology and Laboratory Medicine, are co-senior authors of the new study. Although certain genetic variants increase the risk of Alzheimer's disease (AD), age is the strongest H4K16ac is a key modification in human health known risk factor. But the way in which molecular because it regulates cellular responses to stress processes of aging predispose people to AD, or and to DNA damage. -
Plant Biology '99
THE NEWSLETTER OF THE AMERICAN SOCIETY OF PLANT PHYSIOLOGISTS Volume 26, Number 1 January/February 1999 Plant Biology '99 III Plant lobs Grab Crabs: Chesapeake Boy Crabs Await You 01 Plant Biology '99! Photo courtesy of Baltimore Areo Convention &Visitors Association. Join your colleagues in celebrating ASPP's SYMPOSIA 75th Anniversary at Plant Biology '99 in Baltimore, Maryland, on July 24-28! Auxin Biology Organizers: Mark Estelle and Ottaline Leyser ASPP's 75th Anniversary Meeting Events: Cell Cycle Regulation Organizer: Tom Jacobs Special President's Symposium functional Plant Genomics Banquet Honoring Past Officers, Award Winners, & Organizer: JeffBennetzen ASPP Traditions Biochemical Genetics Organizer: Dean Della Penna Chesapeake Bay Crab & Chicken Feast President's Symposium: Global Issues in Plant Biology ASPP Family Tree Organizer: Brian Larkins Speakers: Peter Raven, Lester Brown, and Extended Poster Sessions Robert Fraley INSIDE ... i T ASPP-Sponsored Workshop in Greece . ' '~. I' T Novartis, UC-Berkeley Plant Scientists Reach $25 Million Research Collaboration T Call for Nominations for Officers and Awards ASPP Future ASPP Annual Meetings OFFICERS & STAFF .CONTENTS flresident Brian A. Larkins .".""""""" """.. 520·621·9958 1 flresident·Elect .·Plant Biology '99 Deborah Delmer """"""" .."""""""""""""""",,, 530·752·7561 1999 Immediate flost flresident ·3 '" . Ken Keegstra .."""""""""""" ..""""""""""""",517·353·2770 Saturday, July 24, through Secretory . ASPP-Sponsored Workshop in Greece Daniel R. Bush ""......,.."""""""""", ..,..""""""", 217·333·6109 Wednesday, July 28 Treasurer ;MbnagingEditor of Plant Physiology Terri Lomax ."""" .."........."""""""""""."""""", 541·737·5278 .Resigns ' Baltimore, Maryland Choir, Boord of Trustees Douglas D. Randall .........".""""""....."..."""""" 573·882·4847 ASPP's 75th anniversary Choir, flublications Committee 4 . Rebella Chasan .."""""""..."......."""""""""""" 202·628·1500 Public Affairs .' '. meeting Choir, Committee on the -NSF's $85 Millibn in Awards Status of Women in fllont flhysio/ogy Ann M. -
Annual Report Fy 2018 Human Frontier Science Program Organization
APRIL 2017 APRIL 2018 — MARCH 2019 ANNUAL REPORT FY 2018 HUMAN FRONTIER SCIENCE PROGRAM ORGANIZATION The Human Frontier Science Program Organization (HFSPO) is unique, supporting international collaboration to undertake innovative, risky, basic research at the frontier of the life sciences. Special emphasis is given to the support and training of independent young investigators, beginning at the postdoctoral level. The Program is implemented by an international organisation, supported financially by Australia, Canada, France, Germany, India, Italy, Japan, the Republic of Korea, New Zealand, Norway, Singapore, Switzerland, the United Kingdom of Great Britain and Nothern Ireland, the United States of America, and the European Commission. Since 1990, over 7000 researchers from more than 70 countries have been supported. Of these, 28 HFSP awardees have gone on to receive the Nobel Prize. 2 The following documents are available on the HFSP website www.hfsp.org: Joint Communiqués (Tokyo 1992, Washington 1997, Berlin 2002, Bern 2004, Ottawa 2007, Canberra 2010, Brussels 2013, London 2016): https://www.hfsp.org/about/governance/membership Statutes of the International Human Frontier Science Program Organization: https://www.hfsp.org/about/governance/hfspo-statutes Guidelines for the participation of new members in HFSPO: https://www.hfsp.org/about/governance/membership General reviews of the HFSP (1996, 2001, 2006-2007, 2010, 2018): https://www.hfsp.org/about/strategy/reviews Updated and previous lists of awards, including titles and abstracts: -
St. Geme Symposium Pediatrics, University of Sponsored by the Colorado, AMC Section of Developmental Biology
Department of St. Geme Symposium Pediatrics, University of Sponsored by the Colorado, AMC Section of Developmental Biology September 10, 2020 2:00pm-4:00pm Speaking Schedule Introduction by Dr. Bruce Appel, Section Head, The St. Geme Symposium Developmental Biology will be held this year in association with the St. 2:00 Caleb Doll, PhD – Fragility in specification; roles for Geme Lectureship, an the RNA binding protein FMRP in gliogenesis annual event in honor of 2:15 Agnese Kocere – RBM8A deficiency in TAR syndrome Dr. Joseph St. Geme, a impacts the lateral plate mesoderm former Dean of the 2:30 Julia Derk, PhD – A critical role for Wnt suppression in School of Medicine. The the development of the arachnoid barrier of the purpose of the meninges Symposium is to 2:45 Kelly Sullivan, PhD – Normalization of Interferon introduce research Receptor Gene Dosage in Mouse Model of Down performed in the Section Syndrome of Developmental Biology 3:00 Yunus Ozekin – Exploring the Effects of Prenatal to our St. Geme Lecturer, ECigarette Exposure on Craniofacial Development Dr. Nancy Bonini, 3:15 Jessica Warns, PhD – Does NF‐Y regulate cilia gene members of the St. Geme networks? family and the Anschutz 3:30 Kayt Scott – Prdm8 regulates pMN progenitor Medical Campus specification for motor neuron and oligodendrocyte community. fates by modulating Shh signaling response 3:45 Peter Dempsey, PhD ‐ Cellular Plasticity of Intestinal Secretory Progenitors in Response to Injury Zoom link https://ucdenver.zoom.us/j/921 40407653 Developmental Biology faculty, post-doctoral fellows About the Section of and student’s biographical information: Developmental Biology: Dempsey, Peter, PhD - Associate Professor Dr. -
Temporal Patterns of Short Non-Coding Rna Modifications And
TEMPORAL PATTERNS OF SHORT NON-CODING RNA MODIFICATIONS AND EXPRESSION by AMMAR S. NAQVI A dissertation submitted to the Graduate School – Camden Rutgers, The State University of New Jersey In partial fulfillment of the requirements For the degree of Doctor of Philosophy Graduate Program in Computational and Integrative Biology Written under the direction of Dr. Andrey Grigoriev And approved by ________________________ Andrey Grigoriev ________________________ Jongmin Nam ________________________ Nancy Bonini Camden, New Jersey May 2015 ABSTRACT OF THE DISSERTATION Temporal Patterns of non-coding RNA Modifications and Expression by AMMAR S. NAQVI Dissertation Director: Dr. Andrey Grigoriev We investigated the function and properties of small RNAs, particularly microRNAs and tRNA-derived fragments (tRFs) with age. We report the characterization of a novel 3'-to- 5' exonuclease, Nibbler (Nbr), that generates differing isoforms of miRNAs in Drosophila. We developed a robust approach to help identify and characterize 3' heterogeneity in microRNAs controlled by Nbr, which assisted in identifying age- associated traits, including neurodegeneration and lifespan. Subsequently, given the fact Nbr interacts with Ago1 and not Ago2, we observed an accumulation of certain isoforms, which lead us to ask if there were particular patterns and trends that were Ago-specific. Interestingly, we report a novel age-associated change of select isoforms with age that is Ago2 specific. RNA deep-sequencing analysis coupled with experimental evidence reflected an increased loading of miRNA isoforms into Ago2 with age. Essentially, the loss of methylated miRNAs led to accelerated brain degeneration and shortened lifespan. Intriguingly, we also observed and identified Ago-loaded tRFs, which appear to have properties similar to those of miRNAs. -
TFEB/Mitf Links Impaired Nuclear Import to Autophagolysosomal
RESEARCH ARTICLE TFEB/Mitf links impaired nuclear import to autophagolysosomal dysfunction in C9- ALS Kathleen M Cunningham1, Kirstin Maulding1, Kai Ruan2, Mumine Senturk3, Jonathan C Grima4,5, Hyun Sung2, Zhongyuan Zuo6, Helen Song2, Junli Gao7, Sandeep Dubey2, Jeffrey D Rothstein1,2,4,5, Ke Zhang7, Hugo J Bellen3,6,8,9,10, Thomas E Lloyd1,2,5* 1Cellular and Molecular Medicine Program, School of Medicine, Johns Hopkins University, Baltimore, United States; 2Department of Neurology, School of Medicine, Johns Hopkins University, Baltimore, United States; 3Program in Developmental Biology, Baylor College of Medicine (BCM), Houston, United States; 4Brain Science Institute, School of Medicine, Johns Hopkins University, Baltimore, United States; 5Solomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, United States; 6Department of Molecular and Human Genetics, BCM, Houston, United States; 7Department of Neuroscience, Mayo Clinic, Jacksonville, United States; 8Department of Neuroscience, BCM, Houston, United States; 9Jan and Dan Duncan Neurological Research Institute, Texas Children’s Hospital, Houston, United States; 10Howard Hughes Medical Institute, Houston, United States Abstract Disrupted nucleocytoplasmic transport (NCT) has been implicated in neurodegenerative disease pathogenesis; however, the mechanisms by which disrupted NCT causes neurodegeneration remain unclear. In a Drosophila screen, we identified ref(2)P/p62, a key regulator of autophagy, as a potent suppressor of neurodegeneration caused by the GGGGCC hexanucleotide repeat expansion (G4C2 HRE) in C9orf72 that causes amyotrophic lateral sclerosis *For correspondence: [email protected] (ALS) and frontotemporal dementia (FTD). We found that p62 is increased and forms ubiquitinated aggregates due to decreased autophagic cargo degradation. Immunofluorescence and electron Competing interest: See microscopy of Drosophila tissues demonstrate an accumulation of lysosome-like organelles that page 18 precedes neurodegeneration. -
Polyq Expansions in Ataxin-2—A Risk Factor for Amyotrophic Lateral Sclerosis?
RESEARCH HIGHLIGHTS MOTOR NEURON DISEASE PolyQ expansions in ataxin-2—a risk factor for amyotrophic lateral sclerosis? ntermediate-length polyglutamine (polyQ) expansions in the ataxin-2 I(ATXN2) gene could confer an increased risk of developing amyotrophic lateral sclerosis (ALS), according to research from a team led by Aaron Gitler and Nancy Bonini at the University of Pennsylvania, USA. Their findings indicate that ataxin-2 enhances the toxicity of TAR DNA-binding protein 43 (TDP-43)—a molecule that has already been strongly implicated in ALS pathogenesis—and the interaction between these two proteins could A combination of approaches involving yeast cells (left), Drosophila (center) and human motor neurons (right) has identified a provide a lead for the development of role for ataxin-2 in amyotrophic lateral sclerosis. Images provided by Professor Nancy Bonini and Professor Aaron Gitler. much-needed new therapies for ALS. Permission obtained from Nature Publishing Group © Elden, A. C. et al. Nature 466, 1069–1075 (2010). Long polyQ expansions (>34 glutamines) in the ATXN2 gene have overexpressed, increased TDP-43 toxicity. degradation, thereby increasing its previously been shown to cause the One of these genes was PBP1, the yeast concentration in the cell. hereditary neurodegenerative disease ortholog of ATXN2. These new findings identify ATXN2 spinocerebellar ataxia type 2 (SCA2). To examine the effects of the ATXN2– as a susceptibility gene for ALS, as well Gitler, Bonini and colleagues measured TDP-43 interaction in the context of as providing a number of avenues for ATXN2 polyQ repeat lengths in 915 the nervous system, the researchers further investigation of the underlying patients with sporadic or familial ALS, switched their attention to a Drosophila disease mechanisms. -
NEWSLETTER VOLUME 35, NUMBER 6 Student/Postdoc- Led Local Meetings NIH Working Group Proposes Page 3 Training Changes More ASCB Award the Recommendations of a U.S
ASCB J U L Y 2 0 1 2 NEWSLETTER VOLUME 35, NUMBER 6 Student/Postdoc- Led Local Meetings NIH Working Group Proposes Page 3 Training Changes More ASCB Award The recommendations of a U.S. National Institutes of Health (NIH) Working Group on the Announcements biomedical research workforce include changes in the programs offered by academic institutions, Page 8 limits on NIH support for graduate students, and changes in the way graduate students and postdocs are supported. The Working Group, a subcommittee of the Advisory Committee to An Innovative the NIH Director, was formed in January 2011 by NIH Director Francis Collins to examine Approach to Dual- the state of the biomedical research workforce and make recommendations to ensure the future Career Support competitiveness of the U.S. biomedical research enterprise. Page 11 The Biomedical Research Workforce Working Group was co-chaired by Shirley Tilghman and Sally Rockey, NIH Deputy Director for Extramural Research, and included ASCB members Leemor Joshua-Tor and Keith Yamamoto. In June 2012, the Working Group sent its report, with a series of recommendations, to Collins for his review and consideration. Inside Despite low unemployment for biomedical PhDs, the percentage of PhDs who move into President’s Column 3 tenured or tenure-track positions has declined by 8% since 1993. In contrast, science-related Did You Know? 6 occupations that do not involve the conduct of research or do not require graduate training WICB Junior, Senior Awards 8 are seeing increases in employment. According to -
Current Positions
Jay Shendure, MD, PhD Updated December 31, 2020 Current Positions Investigator, Howard Hughes Medical Institute Professor, Genome Sciences, University of Washington Director, Allen Discovery Center for Cell Lineage Director, Brotman Baty Institute for Precision Medicine Contact Information E-mail: [email protected] Lab website: http://krishna.gs.washington.edu Office phone: (206) 685-8543 Education • 2007 M.D., Harvard Medical School (Boston, Massachusetts) • 2005 Ph.D. in Genetics, Harvard University (Cambridge, Massachusetts) Research Advisor: George M. Church Thesis entitled “Multiplex Genome Sequencing and Analysis” • 1996 A.B., summa cum laude in Molecular Biology, Princeton University (Princeton, NJ) Research Advisor: Lee M. Silver Professional Experience • 2017 – present Scientific Director Brotman-Baty Institute for Precision Medicine • 2017 – present Scientific Director Allen Discovery Center for Cell Lineage Tracing • 2015 – present Investigator Howard Hughes Medical Institute • 2015 – present Full Professor (with tenure) Department of Genome Sciences, University of Washington, Seattle, WA • 2010 – present Affiliate Professor Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA • 2011 – 2015 Associate Professor (with tenure) Department of Genome Sciences, University of Washington, Seattle, WA • 2007 – 2011 Assistant Professor Department of Genome Sciences, University of Washington, Seattle, WA • 1998 – 2007 Medical Scientist Training Program (MSTP) Candidate Department of Genetics, Harvard Medical School, Boston, WA • 1997 – 1998 Research Scientist Vaccine Division, Merck Research Laboratories, Rahway, NJ • 1996 – 1997 Fulbright Scholar to India Department of Pediatrics, Sassoon General Hospital, Pune, India 1 Jay Shendure, MD, PhD Honors, Awards, Named Lectures • 2019 Richard Lounsbery Award (for extraordinary scientific achievement in biology & medicine) National Academy of Sciences • 2019 Jeffrey M. Trent Lectureship in Cancer Research National Human Genome Research Institute, National Institutes of Health • 2019 Paul D.