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Thomas E. Johnson

Bio: Thomas E. Johnson is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Caenorhabditis elegans & Quantitative trait locus. The author has an hindex of 69, co-authored 265 publications receiving 20013 citations. Previous affiliations of Thomas E. Johnson include University of Texas at San Antonio & Cornell University.


Papers
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Journal ArticleDOI
Gary A. Churchill, David C. Airey1, Hooman Allayee2, Joe M. Angel3, Alan D. Attie4, Jackson Beatty5, Willam D. Beavis6, John K. Belknap7, Beth Bennett8, Wade H. Berrettini9, André Bleich10, Molly A. Bogue, Karl W. Broman11, Kari J. Buck12, Edward S. Buckler13, Margit Burmeister14, Elissa J. Chesler15, James M. Cheverud16, Steven J. Clapcote17, Melloni N. Cook18, Roger D. Cox19, John C. Crabbe12, Wim E. Crusio20, Ariel Darvasi21, Christian F. Deschepper22, Rebecca W. Doerge23, Charles R. Farber24, Jiri Forejt25, Daniel Gaile26, Steven J. Garlow27, Hartmut Geiger28, Howard K. Gershenfeld29, Terry Gordon30, Jing Gu15, Weikuan Gu15, Gerald de Haan31, Nancy L. Hayes32, Craig Heller33, Heinz Himmelbauer34, Robert Hitzemann12, Kent W. Hunter35, Hui-Chen Hsu36, Fuad A. Iraqi37, Boris Ivandic38, Howard J. Jacob39, Ritsert C. Jansen31, Karl J. Jepsen40, Dabney K. Johnson41, Thomas E. Johnson8, Gerd Kempermann42, Christina Kendziorski4, Malak Kotb15, R. Frank Kooy43, Bastien Llamas22, Frank Lammert44, J. M. Lassalle45, Pedro R. Lowenstein5, Lu Lu15, Aldons J. Lusis5, Kenneth F. Manly15, Ralph S. Marcucio46, Doug Matthews18, Juan F. Medrano24, Darla R. Miller41, Guy Mittleman18, Beverly A. Mock35, Jeffrey S. Mogil47, Xavier Montagutelli48, Grant Morahan49, David G. Morris50, Richard Mott51, Joseph H. Nadeau52, Hiroki Nagase53, Richard S. Nowakowski32, Bruce F. O'Hara54, Alexander V. Osadchuk, Grier P. Page36, Beverly Paigen, Kenneth Paigen, Abraham A. Palmer, Huei Ju Pan, Leena Peltonen-Palotie55, Leena Peltonen-Palotie5, Jeremy L. Peirce15, Daniel Pomp56, Michal Pravenec25, Daniel R. Prows28, Zonghua Qi1, Roger H. Reeves11, John C. Roder17, Glenn D. Rosen57, Eric E. Schadt58, Leonard C. Schalkwyk59, Ze'ev Seltzer17, Kazuhiro Shimomura60, Siming Shou61, Mikko J. Sillanpää55, Linda D. Siracusa62, Hans-Willem Snoeck40, Jimmy L. Spearow24, Karen L. Svenson, Lisa M. Tarantino63, David W. Threadgill64, Linda A. Toth65, William Valdar51, Fernando Pardo-Manuel de Villena64, Craig H Warden24, Steve Whatley59, Robert W. Williams15, Tom Wiltshire63, Nengjun Yi36, Dabao Zhang66, Min Zhang13, Fei Zou64 
Vanderbilt University1, University of Southern California2, University of Texas MD Anderson Cancer Center3, University of Wisconsin-Madison4, University of California, Los Angeles5, National Center for Genome Resources6, Portland VA Medical Center7, University of Colorado Boulder8, University of Pennsylvania9, Hannover Medical School10, Johns Hopkins University11, Oregon Health & Science University12, Cornell University13, University of Michigan14, University of Tennessee Health Science Center15, Washington University in St. Louis16, University of Toronto17, University of Memphis18, Medical Research Council19, University of Massachusetts Medical School20, Hebrew University of Jerusalem21, Université de Montréal22, Purdue University23, University of California, Davis24, Academy of Sciences of the Czech Republic25, University at Buffalo26, Emory University27, University of Cincinnati28, University of Texas Southwestern Medical Center29, New York University30, University of Groningen31, Rutgers University32, Stanford University33, Max Planck Society34, National Institutes of Health35, University of Alabama at Birmingham36, International Livestock Research Institute37, Heidelberg University38, Medical College of Wisconsin39, Icahn School of Medicine at Mount Sinai40, Oak Ridge National Laboratory41, Charité42, University of Antwerp43, RWTH Aachen University44, Paul Sabatier University45, University of California, San Francisco46, McGill University47, Pasteur Institute48, University of Western Australia49, Yale University50, University of Oxford51, Case Western Reserve University52, Roswell Park Cancer Institute53, University of Kentucky54, University of Helsinki55, University of Nebraska–Lincoln56, Harvard University57, Merck & Co.58, King's College London59, Northwestern University60, Shriners Hospitals for Children61, Thomas Jefferson University62, Novartis63, University of North Carolina at Chapel Hill64, Southern Illinois University Carbondale65, University of Rochester66
TL;DR: The Collaborative Cross will provide a common reference panel specifically designed for the integrative analysis of complex systems and will change the way the authors approach human health and disease.
Abstract: The goal of the Complex Trait Consortium is to promote the development of resources that can be used to understand, treat and ultimately prevent pervasive human diseases. Existing and proposed mouse resources that are optimized to study the actions of isolated genetic loci on a fixed background are less effective for studying intact polygenic networks and interactions among genes, environments, pathogens and other factors. The Collaborative Cross will provide a common reference panel specifically designed for the integrative analysis of complex systems and will change the way we approach human health and disease.

1,040 citations

Journal ArticleDOI
08 May 1998-Science
TL;DR: Three biodemographic insights--concerning the correlation of death rates across age, individual differences in survival chances, and induced alterations in age patterns of fertility and mortality--offer clues and suggest research on the failure of complicated systems, on new demographic equations for evolutionary theory, and on fertility-longevity interactions.
Abstract: Old-age survival has increased substantially since 1950 Death rates decelerate with age for insects, worms, and yeast, as well as humans This evidence of extended postreproductive survival is puzzling Three biodemographic insights—concerning the correlation of death rates across age, individual differences in survival chances, and induced alterations in age patterns of fertility and mortality—offer clues and suggest research on the failure of complicated systems, on new demographic equations for evolutionary theory, and on fertility-longevity interactions Nongenetic changes account for increases in human life-spans to date Explication of these causes and the genetic license for extended survival, as well as discovery of genes and other survival attributes affecting longevity, will lead to even longer lives

974 citations

Journal ArticleDOI
01 Jan 1988-Genetics
TL;DR: Evidence that longer life results from a mutation in a single gene that increases the probability of survival at all chronological ages is presented and it is likely that the action of age-1 in lengthening life results not from eliminating a programmed aging function but rather from reduced hermaphrodite self-fertility or from some other unknown metabolic or physiologic alteration.
Abstract: age-1(hx546) is a recessive mutant allele in Caenorhabditis elegans that results in an increase in mean life span averaging 40% and in maximal life span averaging 60% at 20 degrees; at 25 degrees age-1(hx546) averages a 65% increase in mean life span (25.3 days vs. 15.0 days) and a 110% increase in maximum life span (46.2 days vs. 22.0 days for wild-type hermaphrodites). Mutant males also show extended life spans. age-1(hx546) is associated with a 75% decrease in hermaphrodite self-fertility as compared to the age-1+ allele at 20 degrees. Using two novel strategies for following the segregation of age-1, we present evidence that longer life results from a mutation in a single gene that increases the probability of survival at all chronological ages. The long-life and reduced-fertility phenotypes cosegregate and are tightly linked to fer-15, a locus on linkage group II. age-1(hx546) does not affect the timing of larval molts, the length of embryogenesis, food uptake, movement, or behavior in any way tested. Although age-1(hx546) lowers hermaphrodite self-fertility, it does not markedly affect the length of the reproductive period with all the increase in life expectancy due to an increase in the length of postreproductive life. In so far as we are aware, this mutant in age-1 is the only instance of a well-characterized genetic locus in which the mutant form results in lengthened fife. It is likely that the action of age-1 in lengthening life results not from eliminating a programmed aging function but rather from reduced hermaphrodite self-fertility or from some other unknown metabolic or physiologic alteration.

945 citations

Journal ArticleDOI
TL;DR: It is suggested that changes in the subcellular localization of DAF-16 by environmental cues allows for rapid reallocation of resources in response to a changing environment at all stages of life.

852 citations

Journal ArticleDOI
TL;DR: The results suggest that ability to respond to stress limits the life expectancy of C. elegans and might do so in other metazoa as well, and the relationship between increased thermotolerance and increased life-span is investigated.
Abstract: We have discovered that three longevity mutants of the nematode Caenorhabditis elegans also exhibit increased intrinsic thermotolerance (Itt) as young adults. Mutation of the age-1 gene causes not only 65% longer life expectancy but also Itt. The Itt phenotype cosegregates with age-1. Long-lived spe-26 and daf-2 mutants also exhibit Itt. We investigated the relationship between increased thermotolerance and increased life-span by developing conditions for environmental induction of thermotolerance. Such pretreatments at sublethal temperatures induce significant increases in thermotolerance and small but statistically highly significant increases in life expectancy, consistent with a causal connection between these two traits. Thus, when an animal's resistance to stress is increased, by either genetic or environmental manipulation, we also observe an increase in life expectancy. These results suggest that ability to respond to stress limits the life expectancy of C. elegans and might do so in other metazoa as well.

827 citations


Cited by
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Journal ArticleDOI
09 Nov 2000-Nature
TL;DR: Evidence that the appropriate and inappropriate production of oxidants, together with the ability of organisms to respond to oxidative stress, is intricately connected to ageing and life span is reviewed.
Abstract: Living in an oxygenated environment has required the evolution of effective cellular strategies to detect and detoxify metabolites of molecular oxygen known as reactive oxygen species. Here we review evidence that the appropriate and inappropriate production of oxidants, together with the ability of organisms to respond to oxidative stress, is intricately connected to ageing and life span.

8,665 citations

Journal ArticleDOI
TL;DR: TASSEL (Trait Analysis by aSSociation, Evolution and Linkage) implements general linear model and mixed linear model approaches for controlling population and family structure and allows for linkage disequilibrium statistics to be calculated and visualized graphically.
Abstract: Summary: Association analyses that exploit the natural diversity of a genome to map at very high resolutions are becoming increasingly important. In most studies, however, researchers must contend with the confounding effects of both population and family structure. TASSEL (Trait Analysis by aSSociation, Evolution and Linkage) implements general linear model and mixed linear model approaches for controlling population and family structure. For result interpretation, the program allows for linkage disequilibrium statistics to be calculated and visualized graphically. Database browsing and data importation is facilitated by integrated middleware. Other features include analyzing insertions/deletions, calculating diversity statistics, integration of phenotypic and genotypic data, imputing missing data and calculating principal components. Availability: The TASSEL executable, user manual, example data sets and tutorial document are freely available at http://www. maizegenetics.net/tassel. The source code for TASSEL can be found at http://sourceforge.net/projects/tassel.

5,460 citations

20 Jan 2017
TL;DR: The Grounded Theory: A Practical Guide through Qualitative Analysis as mentioned in this paper, a practical guide through qualitative analysis through quantitative analysis, is a good starting point for such a study.
Abstract: การวจยเชงคณภาพ เปนเครองมอสำคญอยางหนงสำหรบทำความเขาใจสงคมและพฤตกรรมมนษย การวจยแบบการสรางทฤษฎจากขอมล กเปนหนงในหลายระเบยบวธการวจยเชงคณภาพทกำลงไดรบความสนใจ และเปนทนยมเพมสงขนเรอยๆ จากนกวชาการ และนกวจยในสาขาสงคมศาสตร และศาสตรอนๆ เชน พฤตกรรมศาสตร สงคมวทยา สาธารณสขศาสตร พยาบาลศาสตร จตวทยาสงคม ศกษาศาสตร รฐศาสตร และสารสนเทศศกษา ดงนน หนงสอเรอง “ConstructingGrounded Theory: A Practical Guide through Qualitative Analysis” หรอ “การสรางทฤษฎจากขอมล:แนวทางการปฏบตผานการวเคราะหเชงคณภาพ” จะชวยใหผอานมความรความเขาใจถงพฒนาการของปฏบตการวจยแบบสรางทฤษฎจากขอมล ตลอดจนแนวทาง และกระบวนการปฏบตการวจยอยางเปนระบบ จงเปนหนงสอทควรคาแกการอานโดยเฉพาะนกวจยรนใหม เพอเปนแนวทางในการนำความรความเขาใจไประยกตในงานวจยของตน อกทงนกวจยผเชยวชาญสามารถอานเพอขยายมโนทศนดานวจยใหกวางขวางขน

4,417 citations

Journal ArticleDOI
12 Jun 1992-Cell
TL;DR: Results indicate that while a 3-fold reduction in levels of genomic m5C has no detectable effect on the viability or proliferation of ES cells in culture, a similar reduction of DNA methylation in embryos causes abnormal development and embryonic lethality.

3,994 citations

Journal ArticleDOI
25 Feb 2005-Cell
TL;DR: The evidence is reviewed that both supports and conflicts with the free radical theory of aging and the growing link between mitochondrial metabolism, oxidant formation, and the biology of aging is examined.

3,870 citations