Making the Right Movesa Practical Guide to Scientifıc Management for P
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Regulation of Recombination and Genomic Maintenance
Downloaded from http://cshperspectives.cshlp.org/ on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press Regulation of Recombination and Genomic Maintenance Wolf-Dietrich Heyer1,2 1Department of Microbiology and Molecular Genetics, University of California, Davis, Davis, California 95616-8665 2Department of Molecular and Cellular Biology, University of California, Davis, Davis, California 95616-8665 Correspondence: [email protected] Recombination is a central process to stably maintain and transmit a genome through somatic cell divisions and to new generations. Hence, recombination needs to be coordi- nated with other events occurring on the DNA template, such as DNA replication, transcrip- tion, and the specialized chromosomal functions at centromeres and telomeres. Moreover, regulation with respect to the cell-cycle stage is required as much as spatiotemporal coor- dination within the nuclear volume. These regulatory mechanisms impinge on the DNA substrate through modifications of the chromatin and directly on recombination proteins through a myriad of posttranslational modifications (PTMs) and additional mechanisms. Although recombination is primarily appreciated to maintain genomic stability, the process also contributes to gross chromosomal arrangements and copy-number changes. Hence, the recombination process itself requires quality control to ensure high fidelity and avoid genomic instability. Evidently, recombination and its regulatory processes have significant impact on human disease, specifically cancer and, possibly, -
Simon W.-L Chan Full CV
Simon W.-L. Chan University of California, Davis Department of Plant Biology 1 Shields Ave. Davis, CA 95616 (530) 754 9652 [email protected] Education and Research Experience July 2006- University of California, Davis, Davis, CA Assistant Professor 2002-2006 University of California, Los Angeles, Los Angeles, CA Postdoctoral fellowship Advisor: Dr. Steven E. Jacobsen 1996-2002 University of California, San Francisco, San Francisco, CA Ph.D. in Cell Biology. Advisor: Dr. Elizabeth H. Blackburn 1992-1995 University of Auckland, Auckland, New Zealand Bachelor of Science (with Honours) in Biochemistry. Advisor: Dr. Nigel P. Birch Awards 2010 Basil O’Connor Starter Scholar Award, March of Dimes 2006 American Society of Plant Biologists Early Career Award 2004 UCLA Boyer-Parvin Postdoctoral Award 2003-2006 Life Sciences Research Foundation Postdoctoral Fellowship (sponsored by the U.S. Department of Energy, Energy BioSciences division) 1997-2002 Howard Hughes Medical Institute Predoctoral Fellowship Advanced Coursework 2008 National Academies Education Fellow in the Life Sciences (attended The National Academies Summer Institute on Undergraduate Education in Biology). 2003 QB3 Microarray Course at UC Santa Cruz (taught by Dr. Joseph Derisi and colleagues). Publications Marimuthu, M.P.A.*, Jolivet, S.*, Ravi, M.*, Pereira, L., Davda, J.N., Cromer, L., Wang, L., Nogué, F., Chan, S.W.L.#, Siddiqi, I.# & Mercier, R.# Synthetic clonal reproduction through seeds Science in press * co-first authors, # corresponding authors Greenberg, M.V.C., Ausin, I., Chan, S.W.L, Cokus, S.J., Cuperus, J.T., Feng, S., Law, J.A., Chu, C., Pellegrini, M., Carrington, J.C. and Jacobsen, S.E. Identification of genes required for de novo DNA methylation in Arabidopsis Epigenetics 6, 344-354 (2011) Chan, S.W.L. -
Alex Greninger [email protected] 415-439-3448 Nominator Information
Nominee Information: Alex Greninger [email protected] 415-439-3448 Nominator Information: Keith Jerome [email protected] (206) 667-6793 Award: Young Investigator Award Statement of Recommendation January 5, 2017 To the selection committee: It gives me great pleasure to nominate Dr. Alex Greninger, a resident physician at the University of Washington, for an ASM/PASCV Young Investigator Award. Alex is an exceptional young scientist, and committed to a career in diagnostic virology. I hope I am able to convey the reasons behind my enthusiastic endorsement. Alex joined our laboratory 18 months ago, coming to us out of an MD/PhD program at UCSF, where he had worked with Drs. Joe DeRisi and Charles Chiu. Alex was remarkably productive during his graduate training, publishing approximately 40(!) papers in the peer-reviewed literature. His main focus was the use of unbiased technologies such as next-generation sequencing and mass spectrometry with an emphasis on viral illnesses. His first first-author paper detailed the discovery of salivirus, a new picornavirus that is associated with up to 4% of pediatric diarrhea. He then went on to perform an affinity purification mass-spectrometry screen of all culturable picornaviruses to find novel host protein interactors. This work culminated in the discovery of a new host protein ACBD3 that acts as a hub for PI4KB recruitment by a wide-array picornavirus 3A proteins, including the enteroviruses and rhinoviruses. Four years later, the crystal structures of these complexes are just being completed and forming the basis for the development of broadly-active 3A inhibitors against enteroviruses and other picornaviruses, similar to the NS5A inhibitors for hepatitis C virus. -
2010 Program Meeting Schedule
Vision Sciences Society 10th Annual Meeting, May 7-12, 2010 Naples Grande Resort & Club, Naples, Florida Program Contents Board, Review Committee & Staff . 2 Satellite Events. 22 Keynote Address . 3 Club Vision Dance Party. 22 Meeting Schedule . 4 Open House . 23 Schedule-at-a-Glance . 6 Member-Initiated Symposia . 24 Poster Schedule . 8 Friday Sessions . 29 Talk Schedule . 10 Saturday Sessions . 33 Young Investigator Award . 11 Sunday Sessions . 43 Abstract Numbering System. 11 Monday Sessions . 53 VSS Dinner and Demo Night . 12 Tuesday Sessions . 58 VSS Public Lecture . 15 Wednesday Sessions . 68 VSS at ARVO . 15 Topic Index. 71 Attendee Resources . 16 Author Index . 74 Exhibitors . 19 Hotel Floorplan . 86 Travel Awards . 21 Advertisements. 89 Board, Review Committee & Staff Board of Directors Abstract Review Committee Tony Movshon (2011), President David Alais Laurence Maloney New York University Marty Banks Ennio Mingolla Pascal Mamassian (2012), President Elect Irving Biederman Cathleen Moore CNRS & Université Paris 5 Geoff Boynton Shin’ya Nishida Eli Brenner Tony Norcia Bill Geisler (2010), Past President Angela Brown Aude Oliva University of Texas, Austin David Burr Alice O’Toole Marisa Carrasco (2012), Treasurer Patrick Cavanagh John Reynolds New York University Marvin Chun Anna Roe Barbara Dosher (2013) Jody Culham Brian Rogers University of California, Irvine Greg DeAngelis Jeff Schall James Elder Brian Scholl Karl Gegenfurtner (2013) Steve Engel David Sheinberg Justus-Liebig Universität Giessen, Germany Jim Enns Daniel Simons -
2019 Annual Report
BECKMAN CENTER 279 Campus Drive West Stanford, CA 94305 650.723.8423 Stanford University | Beckman Center 2019 Annual Report Annual 2019 | Beckman Center University Stanford beckman.stanford.edu 2019 ANNUAL REPORT ARNOLD AND MABEL BECKMAN CENTER FOR MOLECULAR AND GENETIC MEDICINE 30 Years of Innovation, Discovery, and Leadership in the Life Sciences CREDITS: Cover Design: Neil Murphy, Ghostdog Design Graphic Design: Jack Lem, AlphaGraphics Mountain View Photography: Justin Lewis Beckman Center Director Photo: Christine Baker, Lotus Pod Designs MESSAGE FROM THE DIRECTOR Dear Friends and Trustees, It has been 30 years since the Beckman Center for Molecular and Genetic Medicine at Stanford University School of Medicine opened its doors in 1989. The number of translational scientific discoveries and technological innovations derived from the center’s research labs over the course of the past three decades has been remarkable. Equally remarkable have been the number of scientific awards and honors, including Nobel prizes, received by Beckman faculty and the number of young scientists mentored by Beckman faculty who have gone on to prominent positions in academia, bio-technology and related fields. This year we include several featured articles on these accomplishments. In the field of translational medicine, these discoveries range from the causes of skin, bladder and other cancers, to the identification of human stem cells, from the design of new antifungals and antibiotics to the molecular underpinnings of autism, and from opioids for pain -
Daniel Griffith Anderson
DAVID H. KOCH INSTITUTE FOR INTEGRATIVE DANIEL G. ANDERSON CANCER RESEARCH MASSACHUSETTS INSTITUTE OF TECHNOLOGY [email protected] 500 MAIN STREET, BUILDING 76 ROOM 653 CAMBRIDGE, MA 02139 (617) 258-6843 EDUCATION Ph.D. Molecular Genetics. University of California at Davis, CA, December 1997 Dissertation: Biochemical characterization of the initiation of homologous recombination in Escherichia coli. Advisor: Prof. Stephen Kowalczykowski. MS Molecular Genetics. University of California at Davis, CA, June 1995 B.A. Math and Biology double major, University of California at Santa Cruz, September 1992 COLLEGE HONORS Graduate Jastro-Shields Fellowship National Institute of Health Biotechnology Fellowship National Science Foundation Honors University of California at Davis Graduate Fellowship Sigma Xi Biology Honors Society Membership Undergraduate College Honors Highest Honors, Biology Honors in the Senior Requirement in Biology PROFESSIONAL EXPERIENCE Associate Professor, Chemical Engineering, Health Science Technology, David H. Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 2010- Associate Member, Ragon Institute 2015- Associate Member, Broad Institute 2011- Adjunct Investigator, Joslin Institute 2010- Associate Scientific Staff Member, Department of Anesthesiology, Children’s Hospital, Harvard, Boston, MA 2007- Goldblith Associate Professor, 2012-2015 Research Associate. David H. Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 2006 – 2010 Research Associate. Prof. Robert Langer, Mentor. Department of Chemical Engineering, MIT, Cambridge, MA 2003 - 2006 Postdoctoral Fellow. Prof. Robert Langer, Mentor. Department of Chemical Engineering, MIT, Cambridge, MA 1999 - 2003 Postdoctoral Researcher. Prof. Stephen Kowalczykowski, Mentor. Department of Microbiology, UCD, Davis, CA. 1998-1999 Graduate Student. Prof. Stephen Kowalczykowski, Mentor. Department of Microbiology, UCD, Davis, CA. 1992-1997. Undergraduate Researcher. Prof. Jerry Feldman, Mentor. -
Viral Outbreak: the Science of Emerging Disease Lecture 4 – Solving SARS and Other Viral Mysteries Joe Derisi, Ph.D
Viral Outbreak: The Science of Emerging Disease Lecture 4 – Solving SARS and other Viral Mysteries Joe Derisi, Ph.D. 1. Begin of Lecture 4 (0:16) [ANNOUNCER:] From the Howard Hughes Medical Institute. The 2010 Holiday Lectures on Science. This year's lectures, "Viral Outbreak: The Science of Emerging Disease", will be given by Dr. Joseph DeRisi, Howard Hughes Medical Institute investigator at the University of California, San Francisco, and by Dr. Eva Harris, Professor of Infectious Diseases at the University of California, Berkeley. The fourth lecture is titled Solving SARS and Other Viral Mysteries. And now to introduce our program, the President of the Howard Hughes Medical Institute, Dr. Robert Tjian 2. Welcome by HHMI President Dr. Robert Tjian (01:07) [DR. TJIAN:] Welcome back to this final presentation of this year's Holiday Lectures on Science. It's a great pleasure once again to introduce Joe DeRisi to give our fourth and last lecture in the series. Previously, Joe told us about how using bioengineering, computers, and molecular biology, he has been able to combine these tools for a potent approach to hunt for new viruses. In this lecture, Joe is going to show you how he can use his Virochip in real-time and in real life situations to discover and quickly diagnosis new viral outbreaks. Joe will also, I think, give us a glimpse of what the future in biotechnology holds towards the end of his talk. And now a brief video about Joe. 3. Profile of Dr. Joseph DeRisi (02:07) [DR. DERISI:] Science as we know it now is a highly interdisciplinary endeavor. -
Biochemistry of Recombinational DNA Repair
BiochemistryBiochemistry ofof RecombinationalRecombinational DNADNA Repair:Repair: CommonCommon ThemesThemes StephenStephen KowalczykowskiKowalczykowski UniversityUniversity ofof California,California, DavisDavis •Overview of genetic recombination and its function. •Biochemical mechanism of recombination in Eukaryotes. •Universal features: steps common to all organisms. HomologousHomologous RecombinationRecombination AB ab+ Ab aB+ Genesis:Genesis: ScienceScience andand thethe BeginningBeginning ofof TimeTime How does recombination occur? And why? DNADNA ReplicationReplication CanCan ProduceProduce dsDNAdsDNA BreaksBreaks andand ssDNAssDNA GapsGaps RepairRepair ofof DNADNA BreaksBreaks Non-Homologous Homologous End-Joining (NHEJ) Recombination (HR) (error-prone) (error-free) dsDNA Break-Repair Synthesis-Dependent ssDNA Annealing (DSBR) Strand-Annealing (SSA) (SDSA) DoubleDouble--StrandStrand DNADNA BreakBreak RepairRepair 5' 3' 3' 5' + 3' 5' 5' 3' Initiation 1 5' 3' Helicase and/or 3' 5' nuclease 2 5' 3' 3' 3' 3' 5' Homologous Pairing & DNA Strand 3 Exchange 3' 5' 5' 3' RecA-like protein 5' 3' Accessory proteins 3' 3' 5' 4 3' 5' 5' 3' 5' 3' 3' 5' DNA Heteroduplex 5 Branch migration Extension proteins 3' 5' 5' 3' 5' 3' 3' 5' Resolution 6 Resolvase Spliced Patched ProteinsProteins InvolvedInvolved inin RecombinationalRecombinational DNADNA RepairRepair E. coli Archaea S. cerevisiae Human Initiation RecBCD -- -- -- SbcCD Mre11/Rad50 Mre11/Rad50/Xrs2 Mre11/Rad50/Nbs1 RecQ Sgs1(?) Sgs1(?) RecQ1/4/5 LM/WRN(?) RecJ -- ExoI ExoI UvrD -- Srs2 -- Homologous Pairing RecA RadA Rad51 Rad51 & DNA Strand SSB SSB/RPA RPA RPA Exchange RecF(R) RadB/B2/B3(?) Rad55/57 Rad51B/C/D/Xrcc2/3 RecO -- Rad52 Rad52 -- -- Rad59 -- -- Rad54 Rad54/Rdh54 Rad54/54B Brca2 DNA Heteroduplex RuvAB Rad54 Rad54 Rad54 Extension RecG -- -- RecQ Sgs1(?) RecQL/4/5 LM/WRN(?) Resolution RuvC Hjc/Hje -- -- -- -- Mus81/Mms4 Mus81/Mms4 ProteinsProteins InvolvedInvolved inin RecombinationalRecombinational DNADNA RepairRepair 5' 3' E. -
How DNA Finds Its Match
7/3/13 4:47 PM Web address: http://www.sciencedaily.com/releases/2012/02/ 120208132309.htm How DNA Finds Its Match Feb. 8, 2012 — It's been more than 50 years since James Watson and enlarge Francis Crick showed that DNA is a double helix of two strands that complement each other. But how does a short piece of DNA find its match, out of the millions of "letters" in even a small genome? New work by researchers at the University of California, Davis, handling and observing single molecules of DNA, shows how it's done. The results are published online Feb. 8 by the journal Nature. Defects in DNA repair and copying are strongly linked to cancer, birth Part of DNA matchup. (Credit: Image courtesy of defects and other problems. University of California - Davis) "This is a real breakthrough," said Stephen Kowalczykowski, professor of microbiology and co-author of the paper with postdoctoral researcher Anthony Forget. "This is an issue that has been outstanding in the field for more than 30 years." "It's the solution of one of the greatest needle-in-the-haystack problems in biology," said Professor Wolf-Dietrich Heyer, a UC Davis molecular biologist who also studies DNA repair but was not involved in this research. "How can one double-stranded DNA break find its match in an entire genome, five billion base pairs in humans? Now we know the fundamental mechanism," Heyer said. Forget and Kowalczykowski used technology developed in Kowalczykowski's lab over the past 20 years to trap lengths of DNA and watch, in real time, as the proteins involved in copying and repairing DNA do their work. -
Biochemical Basis of SOS-Induced Mutagenesis In
Proc. Natl. Acad. Sci. USA Vol. 95, pp. 9755–9760, August 1998 Biochemistry Biochemical basis of SOS-induced mutagenesis in Escherichia coli: Reconstitution of in vitro lesion bypass dependent on the UmuD2*C mutagenic complex and RecA protein i MENGJIA TANG†,IRINA BRUCK†‡,RAMON ERITJA§,JENNIFER TURNER¶,EKATERINA G. FRANK , i ROGER WOODGATE ,MIKE O’DONNELL¶, AND MYRON F. GOODMAN†** †Department of Biological Sciences, Hedco Molecular Biology Laboratories, University of Southern California, Los Angeles, CA 90089-1340; §European Molecular Biology Organization, Heidelberg 69012, Germany; ¶Rockefeller University and Howard Hughes Medical Institute, New York, NY 10021; and iSection on DNA Replication, Repair and Mutagenesis, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-2725 Communicated by I. Robert Lehman, Stanford University School of Medicine, Stanford, CA, June 26, 1998 (received for review May 12, 1998) ABSTRACT Damage-induced SOS mutagenesis requir- that together with UmuD9 and RecA*, DNA pol III was able ing the UmuD*C proteins occurs as part of the cells’ global to facilitate limited translesion DNA synthesis of a synthetic response to DNA damage. In vitro studies on the biochemical abasic site (16). We recently have succeeded in purifying the 9 basis of SOS mutagenesis have been hampered by difficulties native UmuD2C complex directly, in soluble form (17). We in obtaining biologically active UmuC protein, which, when showed that this complex binds cooperatively to single- overproduced, is insoluble in aqueous solution. We have stranded DNA (17), having similar affinities to damaged and * circumvented this problem by purifying the UmuD2C complex undamaged DNA, and effectively blocks recombinational in soluble form and have used it to reconstitute an SOS lesion strand exchange in vitro (W. -
Consciousness, Accessibility, and the Mesh Between Psychology and Neuroscience
BEHAVIORAL AND BRAIN SCIENCES (2007) 30, 481–548 Printed in the United States of America doi: 10.1017/S0140525X07002786 Consciousness, accessibility, and the mesh between psychology and neuroscience Ned Block Department of Philosophy, New York University, New York, NY 10003 [email protected] Abstract: How can we disentangle the neural basis of phenomenal consciousness from the neural machinery of the cognitive access that underlies reports of phenomenal consciousness? We see the problem in stark form if we ask how we can tell whether representations inside a Fodorian module are phenomenally conscious. The methodology would seem straightforward: Find the neural natural kinds that are the basis of phenomenal consciousness in clear cases – when subjects are completely confident and we have no reason to doubt their authority – and look to see whether those neural natural kinds exist within Fodorian modules. But a puzzle arises: Do we include the machinery underlying reportability within the neural natural kinds of the clear cases? If the answer is “Yes,” then there can be no phenomenally conscious representations in Fodorian modules. But how can we know if the answer is “Yes”? The suggested methodology requires an answer to the question it was supposed to answer! This target article argues for an abstract solution to the problem and exhibits a source of empirical data that is relevant, data that show that in a certain sense phenomenal consciousness overflows cognitive accessibility. I argue that we can find a neural realizer of this overflow if we assume that the neural basis of phenomenal consciousness does not include the neural basis of cognitive accessibility and that this assumption is justified (other things being equal) by the explanations it allows. -
Sources of DNA Double-Strand Breaks and Models of Recombinational DNA Repair
Downloaded from http://cshperspectives.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Sources of DNA Double-Strand Breaks and Models of Recombinational DNA Repair Anuja Mehta and James E. Haber Rosenstiel Basic Medical Sciences Research Center, MS029 Rosenstiel Center, Brandeis University, Waltham, Massachusetts 02454-9110 Correspondence: [email protected] DNA is subject to many endogenous and exogenous insults that impair DNA replication and proper chromosome segregation. DNA double-strand breaks (DSBs) are one of the most toxic of these lesions and must be repaired to preserve chromosomal integrity. Eukaryotes are equipped with several different, but related, repair mechanisms involving homologous re- combination, including single-strand annealing, gene conversion, and break-induced rep- lication. In this review, we highlight the chief sources of DSBs and crucial requirements for each of these repair processes, as well as the methods to identify and study intermediate steps in DSB repair by homologous recombination. EXOGENOUS AND ENDOGENOUS Some well-known exogenous DNA damag- SOURCES OF DNA DOUBLE-STRAND ing agents (clastogens) are anticancer chemo- BREAKS therapeutic drugs and ionizing radiation (IR). Chemotherapeutic drugs include DNA-alkyl- NA damage can occur as a result of en- ating agents such as methyl methanosulfo- Ddogenous metabolic reactions and replica- nate and temozolomide, cross-linking agents tion stress or from exogenous sources like radi- such as mitomycin C and cisplatin, and radio- ation and chemotherapeutics. Damage comes mimetic compounds such as bleomycin or in several different varieties: base lesions, intra- phleomycin (Chen and Stubbe 2005; Wyrobek and interstrand cross-links, DNA-protein cross- et al.