Chemistry News
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Springer A++ Viewer
PublisherInfo PublisherName : BioMed Central PublisherLocation : London PublisherImprintName : BioMed Central Ira Herskowitz dies ArticleInfo ArticleID : 4766 ArticleDOI : 10.1186/gb-spotlight-20030506-01 ArticleCitationID : spotlight-20030506-01 ArticleSequenceNumber : 118 ArticleCategory : Research news ArticleFirstPage : 1 ArticleLastPage : 4 RegistrationDate : 2003–5–6 ArticleHistory : OnlineDate : 2003–5–6 ArticleCopyright : BioMed Central Ltd2003 ArticleGrants : ArticleContext : 130594411 Brendan Maher Email: [email protected] Ira Herskowitz, professor of genetics at the University of California, San Francisco (UCSF), died at home on April 28 of pancreatic cancer. He was 56. Remembered for clarity of mind, exceptional science, enthusiastic teaching, and a love of music, his death sent a shock throughout the yeast community this week, where Herskowitz made many great contributions and friends. "It's a great loss to us all," said Paul Nurse, Nobel Laureate and new president of The Rockefeller University. "Ira Herskowitz had a huge influence on the yeast field and on me personally." Laureate Leland Hartwell, president of Fred Hutchinson Cancer Research Center told us in an e-mail, "I'll bet there are few scientists in genetics, molecular and cell biology who were not personally affected by him." Born in Brooklyn, NY, Herskowitz moved with his family about the country as father Irwin, a Drosophilageneticist, took various academic positions. Herskowitz received a bachelor's degree in science from the California Institute of Technology in 1967 and a PhD in microbiology from the Massachusetts Institute of Technology (MIT) in 1971. After a short postdoctoral stint there, he assumed an assistant professor position at the University of Oregon. Moving in 1982 to UCSF, he immediately revamped the genetics program there, chaired the department of biochemistry and biophysics from 1990 to 1995, and co-directed the program in human genetics from 1997. -
Curriculum Vitae Jasper Rine Address: Work Home Department of Molecular and Cellular Biology 400 Western Drive Division of Genet
Curriculum Vitae Jasper Rine Address: Work Home Department of Molecular and Cellular Biology 400 Western Drive Division of Genetics Richmond, California 94801 California Institute for Quantitative Biosciences 374A Stanley Hall 510-232-4293 University of California Birth Date: October 16, 1953 Berkeley, CA 94720-3202 Tel: 510-642-7047 Fax: 510-666-2768 Higher Education Post-doctoral Fellow 1980-1982 Stanford University School of Medicine Advisor: Ronald W. Davis University of Oregon, Ph.D. 1975-1979 Molecular Genetics Advisor: Ira Herskowitz State University of New York at Albany 1971-1975 B.S. Biological Sciences, Magna Cum Laude Professional Experience Professor of Genetics Division of Genetics, Genomics and Development Department of Molecular and Cell Biology University of California, Berkeley 1990-Present Director, Human Genome Center Lawrence Berkeley Labs Berkeley, California 1991-1994 Associate Professor of Genetics Division of Genetics Department of Molecular and Cell Biology University of California, Berkeley 1989-1990 Assistant Professor of Biochemistry Department of Biochemistry University of California, Berkeley 1982-1988 Honors/Awards N.I.H. Postdoctoral Fellowship 1980-1982 The Camille and Henry Dreyfus Teacher Scholar Award 1986 Miller Research Professor, UC Berkeley 1993 Philips Distinguished Lecturer, Haverford College 1993 American Academy of Microbiology – Fellow Election 1993 Streisinger Lecturer, University of Oregon 1993 UCB Distinguished Teaching Award 1997 Richard & Rhoda Goldman Distinguished Professor of Biology -
Leo Szilard in Physics and Information By
Leo Szilard in Physics and Information by Richard L. Garwin IBM Fellow Emeritus IBM Thomas J. Watson Research Center P.O. Box 218, Yorktown Heights, NY 10598 www.fas.org/RLG/ Email: [email protected] Presented in the invited APS session R17 “The Many Worlds of Leo Szilard” Savannah, Georgia April 7, 2014 at 11:21 AM _04/07/2014 Leo Szilard in Physics and Information.doc 1 Abstract: The excellent biography1 by William Lanouette, ``Genius in the Shadows,'' tells it the way it was, incredible though it may seem. The 1972 ``Collected Works of Leo Szilard: Scientific Papers,'' Bernard T. Feld and Gertrud W. Szilard, Editors, gives the source material both published and unpublished. Szilard's path-breaking but initially little-noticed 1929 paper, ``On the Decrease of Entropy in a Thermodynamic System by the Intervention of Intelligent Beings'' spawned much subsequent research. It connected what we now call a bit of information with a quantity k ln 2 of entropy, and showed that the process of acquiring, exploiting, and resetting this information in a one-molecule engine must dissipate at least kT ln 2 of energy at temperature T. His 1925 paper, ``On the Extension of Phenomenological Thermodynamics to Fluctuation Phenomena,'' showed that fluctuations were consistent with and predicted from equilibrium thermodynamics and did not depend on atomistic theories. His work on physics and technology, demonstrated an astonishing range of interest, ingenuity, foresight, and practical sense. I illustrate this with several of his fundamental contributions to nuclear physics, to the neutron chain reaction and to nuclear reactors, and also to electromagnetic pumping of liquid metals. -
From Controlling Elements to Transposons: Barbara Mcclintock and the Nobel Prize Nathaniel C
454 Forum TRENDS in Biochemical Sciences Vol.26 No.7 July 2001 Historical Perspective From controlling elements to transposons: Barbara McClintock and the Nobel Prize Nathaniel C. Comfort Why did it take so long for Barbara correspondence. From these and other to prevent her controlling elements from McClintock (Fig. 1) to win the Nobel Prize? materials, we can reconstruct the events moving because their effects were difficult In the mid-1940s, McClintock discovered leading up to the 1983 prize*. to study when they jumped around. She genetic transposition in maize. She What today are known as transposable never had any inclination to pursue the published her results over several years elements, McClintock called ‘controlling biochemistry of transposition. and, in 1951, gave a famous presentation elements’. During the years 1945–1946, at Current understanding of how gene at the Cold Spring Harbor Symposium, the Carnegie Dept of Genetics, Cold activity is regulated, of course, springs yet it took until 1983 for her to win a Nobel Spring Harbor, McClintock discovered a from the operon, François Jacob and Prize. The delay is widely attributed to a pair of genetic loci in maize that seemed to Jacques Monod’s 1960 model of a block of combination of gender bias and gendered trigger spontaneous and reversible structural genes under the control of an science. McClintock’s results were not mutations in what had been ordinary, adjacent set of regulatory genes (Fig. 2). accepted, the story goes, because women stable alleles. In the term of the day, they Though subsequent studies revealed in science are marginalized, because the made stable alleles into ‘mutable’ ones. -
2020 Online Session Descriptions
Thursday, April 16 2:00 pm - 6:00 pm Mammalian Trainee Symposium Session Chairs: Fernando Pardo-Manuel de Villena, UNC Chapel Hill Linda Siracusa, Hackensack Meridian School of Medicine at Seton Hall University 538A 2:00 pm No more paywalls: cost-benefit analysis across scRNA-seq platforms reveals biological insight is reproducible at low sequencing depths. Kathryn McClelland, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK/NIH) 882C 2:15 pm Control of target gene specificity in Wnt signaling by transcription factor interactions. Aravindabharathi Ramakrishnan, University of Michigan, Ann Arbor 2217C 2:30 pm Evolutionary genomics of centromeric satellites in House Mice (Mus). Uma Arora, The Jackson Laboratory 2:45 pm Reference quality mouse genomes reveal complete strain-specific haplotypes and novel functional loci. Mohab Helmy, EMBL-EBI 887B 3:00 pm Divergence in KRAB zinc finger proteins is associated with pluripotency spectrum in mouse embryonic stem cells. Candice Byers Jackson Laboratory 531C 3:15 pm Replicability and reproducibility of genetic analysis between different studies using identical Collaborative Cross inbred mice. UNC CHAPEL HILL 3:30 pm Proteomics reveals the role of translational regulation in ES cells. Selcan Aydin, The Jackson Laboratory for Mouse Genetics 563B 3:45 pm Super-Mendelian inheritance mediated by CRISPR–Cas9 in the female mouse germline. Hannah Grunwald, University of California San Diego 2103C 4:00 pm Gene Editing ELANE in Human Hematopoietic Stem and Progenitor Cells Reveals Variant Pathogenicity and Therapeutic Strategies for Severe Congenital Neutropenia. Shuquan Rao, Boston Childrens Hospital 4:15 pm Phase separation of YAP reorganizes genome topology for long-term YAP target gene expression. -
Cold Spring Harbor Symposia on Quantitative Biology
COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY VOLUME XLV---PART 1 COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY VOLUME XLV MOVABLE GENETIC ELEMENTS COLD SPRING HARBOR LABORATORY 1981 COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY VOLUME XLV 1981 by The Cold Spring Harbor Laboratory International Standard Book Number 0-87969-044-5 Library of Congress Catalog Card Number 34-8174 Printed in the United States of America All rights reserved COLD SPRING HARBOR SYMPOSIA ON QUANT1TA T1VE BIOLOGY Founded in 1933 by REGINALD G. HARRIS Director of the Biological Laboratory 1924 to 1936 Previous Symposia Volumes I (1933) Surface Phenomena XXIII (1958) Exchange of Genetic Material: Mechanism I1 (1934) Aspects of Growth and Consequences Ili (1935) Photochemical Reactions XX1V (1959) Genetics and Twentieth Century Darwinism IV (1936) Excitation Phenomena XXV (1960) Biological Clocks V (1937) Internal Secretions XXV1 (I 961) Cellular Regulatory Mechanisms VI (1938) Protein Chemistry XXVll (1962) Basic Mechanisms in Animal Virus Biology VII (1939) Biological Oxidations XXVIlI (1963) Synthesis and Structure of Macromolecules VIII (1940) Permeability and the Nature of Cell Mem- XXIX (1964) Human Genetics branes XXX (1965) Sensory Receptors 1X (1941) Genes and Chromosomes: Structure and Organi- XXXI (1966) The Genetic Code zation XXXII (1967) Antibodies X (1942) The Relation of Hormones to Development XXXIlI (1968) Replication of DNA in Microorganisms XI (1946) Heredity and Variation in Microorganisms. XXX1V (1969) The Mechanism of Protein -
Volume I - Science
THE COLLECTED ORKS OF LEO SZILARD VOLUME I - SCIENCE Edited by Bernard T. Feld and Gertrud Weiss Szilar d with the assistance of Kathleen R. Winsor -I \t ( I ( {/ r Introductory Essays by Carl F . :Jrokart Bernard T. Feld Maurice Ooldhaber Aaron Noviok. Julius Ta.bin M. I . T. Press, Cambridge ,Mass. t I I II{ n ( 0 .!.;t-- Ct((cl L (r- u [ ( ~ A [1· {r I "1 (1 - ' ch ~Y. ,, • l It I I { . ( J L L· I u( I Jacques Honod Professor, College de France Director of Pasteur Institute Paris, France Carl H. Eckart Professor of Geophysics University of California, San Diego Bernard T. Feld Professor of Physics Massachusetts Institute of Technology Boston, Hassachusetts Haurice Goldhaber Director, Brookhaven National Laboratory Upton, Long Island, New York Aaron Novick Professor of Biology Institute of Molecular Biology University of Oregon Eugene, Oregon Julius Tabin Patent Attorney Chicago, Illinois Gertrud Weiss Szilard, M. D. School of Medicine University of California, San Diego Kathleen R. Winsor Librarian University of California, San Diego TABLE OF CONTENTS 1 I ( l C { ForewoJl to Collected Works ( f') Preface ( --Oart_rud_ Weiss Szilard) rriculum Vitae by Leo Szilard (From Grant Application) ~ ~ )) '> tA.t..c( SECTION I. PU:BLISHED PAPERS IN PHYSICS tq• (..~ 1939 Bibliography A. Thermodynamics ,\ Introdu. ctory :&:~say by Carl H. Eokart ~ _ f-lr I/ c 1 -• B. Expel'imenta.l work with x-rays ~ ) :, , 0 ( c. Nuclear Physi s Introductory Es y by Maurice Goldhaber ~ f·- ;-:. J SECTION II. UNPUBLISHED PAPERS AND REPORTS IN PHYSICS, ETALLURGY AND ENGINEERING, \, (- Declassified documents from Manhatta.nProject) ( 1940- 1945J Bibliography I. -
2000 Highlights
from the 2000 Annual Report HIGHLIGHTS OF THE YEAR The research and education programs at the Laboratory continue their strong momentum. The Watson School of Biological Sciences recruited its second class of students this year, and the DNA Learning Center underwent extensive renovations that will further its educa- tional objectives. The Meetings and Courses program and Banbury Center continue to be invaluable resources for scientific information, and the Cold Spring Harbor Laboratory Press added new projects and properties to its long list of titles. In this, the year of the Human Genome, Cold Spring Harbor Laboratory was a bustling center of scientific activity. Research Cancer Malignant melanoma is an aggressive, deadly cancer that does not respond to conventional chemotherapy. Other aggressive, chemoresistant can- cers—and approximately half of all cancers—are characterized by muta- tions in the p53 tumor suppressor gene. Malignant melanomas, however, do not typically display mutations in the p53 gene. To explore alternative explanations for the origins and properties of malignant melanoma, and to identify potential targets and strategies for therapy, Scott Lowe and his colleagues have examined the status of other genes known to function downstream from p53 in a pathway leading to Scott Lowe “apoptosis” or “programmed cell death.” When intact, this pathway rids the body of abnormal, precancerous cells by triggering a cellular self-destruct mechanism. When this pathway is disrupted (by the loss of p53 function, for example), precancerous cells sur- vive and proliferate, resulting in cancer. This year, Scott and postdoctoral fellow Marisol Soengas found that malignant melanomas often lose a key trigger of programmed cell death, a protein called Apaf-1 (apop- tosis activation factor-1). -
Leo Szilard Papers
http://oac.cdlib.org/findaid/ark:/13030/tf0z09n7k3 No online items Leo Szilard Papers Mandeville Special Collections Library Mandeville Special Collections Library The UCSD Libraries 9500 Gilman Drive University of California, San Diego La Jolla, California 92093-0175 Phone: (858) 534-2533 Fax: (858) 534-5950 URL: http://orpheus.ucsd.edu/speccoll/ Copyright 2005 The Regents of the University of California. All rights reserved. Leo Szilard Papers MSS 0032 1 Descriptive Summary Creator: Szilard, Leo Title: Leo Szilard Papers, Date (inclusive): 1898-1998 Extent: 47.30 linear feet(112 archives boxes, 1 records carton, 2 card file boxes, 18 oversize folders) Abstract: Papers of a nuclear physicist, biologist, and advocate of global arms control. Born in Budapest, Hungary in 1898, Szilard moved to Berlin in 1919, where he studied engineering and physics and received his doctorate under Max von Laue at the University of Berlin. He migrated to England in 1933 where he made important discoveries relating to the nuclear chain-reaction. After moving to the United States in the late 1930s, he worked on the Manhattan Project and made significant contributions to the development of the atomic bomb. After World War II he concentrated on the field of biology and became one of the world's leading advocates of global cooperation and arms control. He was associated with many universities, including Oxford, Columbia, and Chicago. In 1951 he married Dr. Gertrude Weiss. In 1963 he became a fellow of the Salk Institute for Biological Studies. He died in San Diego, California, in 1964. The majority of the materials in the Szilard papers date from the late 1930s to the early 1960s -- the period following Szilard's move to the U.S. -
Flexibility of the Yeast A2 Repressor Enables It to Occupy the Ends of Its Operator, Leaving the Center Free
Downloaded from genesdev.cshlp.org on September 29, 2021 - Published by Cold Spring Harbor Laboratory Press Flexibility of the yeast a2 repressor enables it to occupy the ends of its operator, leaving the center free Robert T. Sauer,* Dana L. Smith, and Alexander D. Johnson Departments of Microbiology and Biochemistry/Biophysics, University of California, San Francisco, California 94143 USA The yeast a2 protein, the product of the MATal gene, is a regulator of yeast cell type; it turns off transcription of the a-specific genes by binding to an operator located upstream of each gene. In this paper we describe the domain structure, subunit organization, and some unusual features of the way this protein contacts its operator. We show that the protein is folded into two domains. The carboxy-terminal domain binds specifically to the operator; the amino-terminal domain contains dimerization contacts. The a2 dimer differs from those of the phage repressors in that it is flexible and therefore is able to bind tightly to differently spaced operator half-sites. In the natural operator, the centers of the operator half-sites are two and one-half turns of DNA apart, exposing them on opposite sides of the DNA helix. We show that the design of a2 allows a dimer to reach across its operator such that it occupies the two half-sites but leaves the middle of the operator available to other proteins. [Key Words: DNA-protein interaction; repressor; gene expression; homeo domain] Received March 29, 1988; revised version accepted May 13, 1988. The yeast a2 protein is related by sequence (and presum of 24,000, its amino-terminal sequence is Met-Asn-Lys- ably structure) and by function (the determination of Ile..., and the purified protein exhibits the expected cell type) to a large group of proteins that contain the amino acid composition (see Methods). -
A Yeast Model of FUS/TLS-Dependent Cytotoxicity
A Yeast Model of FUS/TLS-Dependent Cytotoxicity The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Ju, Shulin et al. “A Yeast Model of FUS/TLS-Dependent Cytotoxicity.” Ed. Jonathan S. Weissman. PLoS Biology 9.4 (2011) : e1001052. As Published http://dx.doi.org/10.1371/journal.pbio.1001052 Publisher Public Library of Science Version Final published version Citable link http://hdl.handle.net/1721.1/65580 Terms of Use Creative Commons Attribution Detailed Terms http://creativecommons.org/licenses/by/2.5/ A Yeast Model of FUS/TLS-Dependent Cytotoxicity Shulin Ju1,2, Daniel F. Tardiff3,4, Haesun Han3,4, Kanneganti Divya1, Quan Zhong5,6, Lynne E. Maquat7, Daryl A. Bosco8, Lawrence J. Hayward8, Robert H. Brown Jr.8, Susan Lindquist3,4, Dagmar Ringe1,2*, Gregory A. Petsko1,2* 1 Department of Biochemistry and Chemistry, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, United States of America, 2 Department of Neurology and Center for Neurologic Diseases, Harvard Medical School and Brigham & Women’s Hospital, Cambridge, Massachusetts, United States of America, 3 Whitehead Institute for Biomedical Research, Cambridge, Massachusetts, United States of America, 4 Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 5 Department of Cancer Biology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America, 6 Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America, 7 Department of Biochemistry and Biophysics and Center for RNA Biology, School of Medicine and Dentistry, University of Rochester, Rochester, New York, United States of America, 8 Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America Abstract FUS/TLS is a nucleic acid binding protein that, when mutated, can cause a subset of familial amyotrophic lateral sclerosis (fALS). -
Role of the Casein Kinase I Isoform, Hrr25, and the Cell Cycle-Regulatory
Proc. Natl. Acad. Sci. USA Vol. 94, pp. 581–586, January 1997 Genetics Role of the casein kinase I isoform, Hrr25, and the cell cycle-regulatory transcription factor, SBF, in the transcriptional response to DNA damage in Saccharomyces cerevisiae (DNA repairytranscriptionycell cycle) YUEN HO*, STEPHEN MASON*†,RYUJI KOBAYASHI‡,MERL HOEKSTRA§, AND BRENDA ANDREWS*¶ *Department of Molecular and Medical Genetics, University of Toronto, Toronto, ON Canada M5S 1A8; ‡Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724; and §ICOS Corporation, 22021-20th Avenue SE, Bothell, WA 22021 Communicated by Ira Herskowitz, University of California, San Francisco, CA, November 1, 1996 (received for review July 31, 1996) ABSTRACT In the budding yeast, Saccharomyces cerevi- agents such as methyl methanesulfonate (MMS) and UV siae, DNA damage or ribonucleotide depletion causes the irradiation. Recent studies have delineated a pathway by which transcriptional induction of an array of genes with known or the damage signal is transduced to the checkpoint and tran- putative roles in DNA repair. The ATM-like kinase, Mec1, and scriptional response apparatus. The kinases, Mec1 (4, 17) and the serineythreonine protein kinases, Rad53 and Dun1, are Rad53 (6, 17), are required for both responses, whereas the required for this transcriptional response. In this paper, we Dun1 kinase, believed to act downstream of Mec1 and Rad53, provide evidence suggesting that another kinase, Hrr25, is is only required for the transcriptional induction response (16). also involved in the transcriptional response to DNA damage Mutations in another kinase, Hrr25, were identified as causing through its interaction with the transcription factor, Swi6. hypersensitivity to double-stranded DNA breaks induced by The Swi6 protein interacts with Swi4 to form the SBF complex endonuclease expression, x-irradiation, or continuous exposure and with Mbp1 to form the MBF complex.