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Supported by an IDeA grant from the National Center
for Research Resources, NIH
Joerg Bewersdorf, Ph.D.
Research Scientist
The Jackson Laboratory
joerg.bewersdorf@jax.org
http://research.jax.org/faculty/joerg_bewersdorf.html
BS, University of Glasgow, U.K., 1995, Physics
PhD, Max Planck Institute for Biophysical Chemistry, 2002Towards Molecular Resolution in Light Microscopy
Biological systems are both three-dimensional (3D) and dynamic. Visualizing the 3D structure and dynamics at the molecular scale is a current and critical need in biomedical research. Unfortunately, current microscopic techniques cannot resolve 3D cellular sub-structures, such as chromatin in interphase nuclei, at the nanometer level on a millisecond time scale. Thus, radically enhancing the 3D spatial and temporal resolution is essential for new breakthroughs in biomedical research and a seminal challenge in modern light microscopy.
The Bewersdorf group is developing and applying new fluorescence (far-field) microscopy techniques with spatial and/or temporal resolutions far exceeding current technology. They focus especially on the 3D aspect of imaging and its application to biological questions.
The laboratory houses the only 4Pi Microscope in the United States. 4Pi Microscopy provides the highest 3D resolution currently available in fluorescence microscopy. By utilizing two opposing high-numerical aperture objective lenses, 4Pi Microscopy increases the axial resolution of laser scanning microscopy ~6-fold. With 100-nm resolution along the optic axis (z axis), it allows far more defined images of cellular structures than conventional (confocal) microscopy. Recently, DR. Bewersdorfhas expanded the field of 4Pi Microscopy applications to cell nuclei and even tissue sections several tens of microns thick.R. Khanna, Q. Li, J. Bewersdorf, E.F. Stanley. 2007. “The presynaptic CaV2.2 channel-transmitter release site core complex”, Eur. J. Neurosci. 26: 547-559.
N. Lue, J. Bewersdorf, M.D. Lessard, K. Badizadegan, R.R. Dasari, M.S. Feld, G. Popescu. 2007. “Tissue refractometry using Hilbert phase microscopy”, Opt. Lett. 32(24): 3522-3524.
L.B. Caddle, JL Grant, J. Szatkiewicz, J. von Hase, G. Kreth, J. Denegre, B. Shirley, J. Bewersdorf, C. Cremer, A. Arneodo, A. Khalil, K.D. Mills. 2007. “Heterologous chromosome territory neighborhoods promote translocation susceptibility in primary lymphocyte”, Chromosome Res. 15:1061-1073.
M.F. Juette, T.J. Gould, M.D. Lessard, M.J. Mlodzianoski, B.S. Nagpure, B.T. Bennett, S.T. Hess, J.Bewersdorf. “Three-Dimensional sub-100 nm Resolution Fluorescence Microscopy of Thick Samples”, Nature Methods, published online 11 May 2008; DOI:10.1038/NMETH.1211.
T.J. Gould, J. Bewersdorf, S.T. Hess. 200_. “A Quantitative Comparison of the Photophysical Properties of Select Quantum Dots and Organic Fluorophores”, Z. Phys. Chem., in press.
L. Plecitá-Hlavatá, M.D. Lessard, J. Šantorováa, J. Bewersdorf, P. Ježek. 200_. “Mitochondrial oxidative phosphorylation and energetic status are reflected by morphology of mitochondrial network in INS-1E and HEP-G2 cells viewed by 4Pi microscopy”, Biophys. Biochim. Acta, in press.
Carol J. Bult, Ph.D.
Associate Professor
The Jackson Laboratory
carol.bult@jax.org
http://research.jax.org/faculty/carol_bult.html
BS, George Mason University, 1984, Biology
PhD, The University of New Hampshire, GeneticsProfessor Bult’s program focuses on two major areas: bioinformatics and developmental genomics. In the area of bioinformatics she focuses on building information systems that can facilitate the use of the laboratory mouse as a model system for understanding normative biology and disease processes in humans. Her group are members of the Mouse Genome Informatics (MGI) consortium and work collaboratively with other investigators at The Jackson Laboratory to build and maintain databases that contain the most comprehensive collection of integrated functional genetic and genomic data for the laboratory mouse available in the public domain. In addition to the MGI information system, they also maintain the Mouse Phenome Database, which contains baseline phenotype measurement for hundreds of traits across scores of inbred lines of mice. Recent projects include the release of a comprehensive gene catalog for the reference mouse genome assembly and the release of MouseCyc, a database of curated biochemical pathways in the laboratory mouse. In the area of developmental genomics, she is working in collaboration with Dr. Isaac Kohane (Children's Hospital Boston) to use an understanding of the molecular genetics of normal lung development in mouse as a framework for identifying key genes and pathways in lung diseases such as cancer and pulmonary fibrosis. Recent projects include generating an integrated data set of mRNA and microRNA profiles over several key developmental time points in murine lung development.
Maeda N, Kasukawa T, Oyama R, Gough J, Frith M, Engström PG, Lenhard B, Aturaliya RN, Batalov S, Beisel KW, Bult CJ, et al. 2006. Transcript annotation in FANTOM3: mouse gene catalog based on physical cDNAs. PLoS Genet. 2(4):e62.
Bogue MA, Grubb SC, Maddatu TP, Bult CJ. 2007. Mouse Phenome Database (MPD). Nucleic Acids Res. 35(Database ):D643-9.
Bouma GJ, Affourtit JP, Bult CJ, Eicher EM. 2007. Transcriptional profile of mouse pre-granulosa and Sertoli cells isolated from early-differentiated fetal gonads. Gene Expr Patterns. 7(1-2):113-23.
Peters LL, Robledo RF, Bult CJ, Churchill GA, Paigen BJ, Svenson KL. 2007. The mouse as a model for human biology: a resource guide for complex trait analysis. Nat Rev Genet 8(1):58-69.
Bult CJ, Eppig JT, Kadin JA, Richardson JE, Blake JA; Mouse Genome Database Group. 2008. The Mouse Genome Database (MGD): mouse biology and model systems. Nucleic Acids Res. 36(Database):D724-8.
Krupke DM, Begley DA, Sundberg JP, Bult CJ, Eppig JT. 2008. The Mouse Tumor Biology database. Nat Rev Cancer 8(6):459-65.
Robert Burgess, Ph.D.
Staff Scientist
The Jackson Laboratory
robert.burgess@jax.org
http://research.jax.org/faculty/robert_burgess.html
BS, Michigan State University, 1990, Biochem/Physiology
PhD, Stanford University, 1996, NeuroscienceDr. Burgess studies the molecular events of synapse formation and maintenance in the nervous system. At the neuromuscular junction, the point of contact between spinal motor neurons and skeletal muscle fibers, the protein agrin provides an essential signal for the differentiation of cells on the muscle side of the junction. He is continuing to identify new functions of agrin, both at the neuromuscular junction and in other sites such as the vasculature of the brain, where agrin may contribute to the blood-brain-barrier and influence the accumulation of beta-amyloid, a pathological marker of Alzheimer's Disease. He is also examining the requirements of maintaining neuromuscular junctions in a number or genetic models of motor neuron diseases (ALS), and peripheral neuropathies (Charcot-Marie-Tooth). Finally, the lab is working to find mechanisms in central nervous system development that parallel those we have studied at the neuromuscular junction. Using the retina as our experimental system, he has identified Dscam as an adhesion molecule that provides an essential label for cells to recognize one another as neuronal circuits in the retina form.
Burgess RW, Jucius TJ, Ackerman SL. 2006. Motor axon guidance of the mammalian trochlear and phrenic nerves: dependence on the netrin receptor Unc5c and modifier loci. J Neurosci 26:5756-5766.
Seburn KL, Nangle LA, Cox GA, Schimmel P, and Burgess RW. 2006. An active dominant mutation of Glycyl-tRNA synthetase causes neuropathy in a Charcot Marie Tooth 2D mouse model. Neuron 51(6):715-26.
Fuerst PG, Rauch SM, and Burgess RW. 2007. Defects in eye development in transgenic mice overexpressing the heparan sulfate proteoglycan agrin. Dev Biol 303(12):165-180.
Harvey SJ, Jarad G, Cunningham J, Rops AL, van der Vlag J, Berden JH, Moeller MJ, Holzman LB, Burgess RW, Miner JH. 2007. Disruption of Glomerular Basement Membrane Charge through Podocyte-Specific Mutation of Agrin Does Not Alter Glomerular Permselectivity. Am J Pathol Jul;171(1):139-52.
Misgeld T, Kerschensteiner M, Bareyre FM, Burgess RW, Lichtman JW. 2007. Imaging axonal transport of mitochondria in vivo. Nat Methods Jul;4(7):559-61.
Fuerst PG, Koizumai A, Masland R, Burgess RW. 2008. Neurite arborization and mosaic spacing in the mouse retina requires DSCAM. Nature Jan 24;451(7177) 2470-2474.
Patton BL, Wang B, Tarumi YS, Seburn KL, Burgess RW. 2008. A single point mutation in the LN domain of LAMA2 causes muscular dystrophy and peripheral amyelination. J. Cell Sci. May 22;121(10): 1593-1604.
Gary A. Churchill, Ph.D.
Staff Scientist
The Jackson Laboratory
gary.churchill@jax.org
http://research.jax.org/faculty/gary_churchill.html
BS, Mass. Institute of Technology, 1983, Mathematics
PhD, University of Washington-Seattle, 1988, BiostatisticsDr. Churchill is actively applying a new “systems” approach to studying the genetics of health and disease, incorporating new statistical methods for the investigation of complex disease-related traits in the mouse. He employs a combination of strategies using standard genotype and phenotype data obtained from mouse crosses together with data from high-throughput gene expression arrays to investigate the genetic basis of these complex traits. He has developed new methods that improve the power of gene expression analysis and has also developed methods to establish relational networks among traits using genetically randomized populations of mice.
Svenson KL, Von Smith R, Magnani PA, Suetin HR, Paigen B, Naggert JK, Li R, Churchill GA, Peters LL. 2007. Multiple trait measurements in 43 inbred mouse strains capture the phenotypic diversity characteristic of human populations. J Appl Physiol 102(6):2369-2378.
The International Stem Cell Initiative. 2007. Characterization of human embryonic stem cell lines by the International Stem Cell Initiative. Nat Biotechnol 25(7):803-816.
Yang H, Bell TA, Churchill GA, Pardo-Manuel de Villena F. 2007. On the subspecific origin of the laboratory mouse. Nat Genet 39(9):1100-1107.
Churchill GA, Doerge RW. 2008. Naive application of permutation testing leads to inflated type I error rates. Genetics 178(1):609-610.
Li R, Svenson KL, Donahue LR, Peters LL, Churchill GA. 2008. Relationships of dietary fat, body composition, and bone mineral density in inbred mouse strain panels. Physiol Genomics 33(1):26-32.
Stylianou IM, Affourtit JP, Shockley KR, Wilpan RY, Abdi FA, Bhardwaj S, Rollins J, Churchill GA, Paigen B. 2008. Applying gene expression, proteomics and single-nucleotide polymorphism analysis for complex trait gene identification. Genetics 178(3):1795-1805.
Szatkiewicz JP, Beane GL, Ding Y, Hutchins L, Pardo-Manuel de Villena F, Churchill GA. 2008. An imputed genotype resource for the laboratory mouse. Mamm Genome 19(3):199-208.
Janan T. Eppig, Ph.D.
Professor
The Jackson Laboratory
jte@informatics.jax.org
http://research.jax.org/faculty/janan_eppig.html
BS, University of Washington, 1975, Mathematics
PhD, The University of Maine, 1982,ZoologyThe mouse is a key model organism for the understanding of mammalian biology because it has been well studied and is genetically and physiologically similar to humans. To utilize mouse data to its fullest, Dr. Eppig led the development of an integrated database of mouse genetic, genomic and biological data. The Mouse Genome Informatics Database (MGI) is used by the international scientific community as its primary resource for mouse information and as a tool for new biological discovery. The database contains a wide variety of data pertaining to genes, their DNA and protein sequences, and the phenotypes that result from mutations in different genes. The three central components of MGI are the Mouse Genome Database (MGD), an internationally recognized database for the laboratory mouse, the Mouse Tumor Biology (MTB) database, which facilitates the selection of experimental models for cancer research, and the International Mouse Strain Resource (IMSR), a searchable online database cataloging mouse stocks available worldwide. The database continues to expand to keep abreast of new technologies and to grow with our expanding knowledge of how the genetic blueprint of DNA manifests in traits of a living individual.
Eppig JT, Bult CJ, Kadin JA, Richardson JE, Blake JA and the Mouse Genome Database Group. 2005. The Mouse Genome Database (MGD): From Genes to Mice, A Community Resource for Mouse Biology. Nucleic Acids Research 33: D471-5.
Krupke DM, Naf D, Vincent MJ, Allio T, Mikaelian I, Sunderg JP, Bult CJ, Eppig JT. 2005. The Mouse Tumor Biology Database: integrated access to mouse cancer biology data. Exp Lung Res 31: 259-270.
Smith CL, Goldsmith CA, Eppig JT. 2005. The Mammalian Phenotype Ontology as a tool for annotating, analyzing, and comparing phenotypic information. Genome Biology 6(1): R7.
Blake JA, Eppig JT, Bult CJ, Kadin JA, Richardson JE. 2006. The Mouse Genome Database (MGD): updates and enhancements. Nucleic Acids Research 34: D562-D567.
Begley DA, Krupke DM, Vincent MJ, Sundberg JP, Bult CJ, Eppig JT. 2007. Mouse Tumor Biology Database (MTB): status update and future directions. Nucleic Acids Res. 35: D638-D642.
Eppig JT, Blake JA, Bult CJ, Kadin JA, Richardson JE, and the Mouse Genome Database Group. 2007. The Mouse Genome Database (MGD): new features facilitating a model system. Nucleic Acids Res. 35: D630-D637.
Smith CM, Finger JH, Hayamizu TF, McCright IJ, Eppig JT, Kadin JA, Richardson JE, Ringwald M. 2007. The Mouse Gene Expression Database (GXD): 2007 update. Nucleic Acids Res. 35: D618-D623.
Joel Graber, Ph.D.
Assistant Professor
The Jackson Laboratory
joel.graber@jax.org
http://research.jax.org/faculty/joel_graber.html
BS, Michigan Technological University, 1987, Physics
BS, Michigan Technological University, 1987, Computer Science
PhD, Cornell University, 1993, PhysicsA mammalian genome comprises some tens of thousands of genes, and an equal or greater number of additional functional elements. The Graber group’s studies center on an improved understanding of the interactions between these elements and how modification or disruption of the interactions can lead to developmental problems or genetic disease. He conducts research at both a global level, characterizing complex interactive networks, and at smaller scales, studying the specific interactions that regulate specific genes or groups of genes. In collaboration with several other Jackson Laboratory researchers, hehelped establish the Center for Genome Dynamics, which seeks to better understand chromosome evolution, organization and function through a systems genetics approach. His analysis of gene regulation is focused on the post-transcriptional stage of expression, where the information has been transcribed to RNA, but not yet translated to protein. Studies are aimed towards the identification and characterization of sequence elements embedded within the RNA transcript that control its lifetime, localization and translation to protein.
Graber JH, Churchill GA, Dipetrillo KJ, King BL, Petkov PM, Paigen K. 2006. Patterns and mechanisms of genome organization in the mouse. J Exp Zoolog 305A(9):683-688.
Liu D, Graber JH. 2006. Quantitative comparison of EST libraries requires compensation for systematic biases in cDNA generation. BMC Bioinformatics 7:77.
Salisbury J, Hutchison KW, Graber JH. 2006. A multispecies comparison of the metazoan 3'-processing downstream elements and the CstF-64 RNA recognition motif. BMC Genomics 7:55.
Graber JH, Salisbury J, Hutchins LN, Blumenthal T. 2007. C. elegans sequences that control trans-splicing and operon pre-mRNA processing. RNA 13(9):1409-1426.
Liu D, Brockman JM, Dass B, Hutchins LN, Singh P, McCarrey JR, MacDonald CC, Graber JH. 2007. Systematic variation in mRNA 3'-processing signals during mouse spermatogenesis. Nucleic Acids Res 35(1):234-246.
Petkov PM, Graber JH, Churchill GA, DiPetrillo K, King BL, Paigen K. 2007. Evidence of a large-scale functional organization of mammalian chromosomes. PLoS Biol 5(5):e127.
Thomas Gridley, Ph.D.
Senior Staff Scientist
The Jackson Laboratory
tom.gridley@jax.org
http://research.jax.org/faculty/thomas_gridley.html
BS, State University of New York, 1976, Biology
PhD, Massachusetts Institute of Technology, BiologyThe Gridley laboratory studies genes important for embryonic development of mice, and the connections between mutations in these genes and congenital human disease syndromes. Analyses focus on the Notch pathway, an evolutionarily conserved cell communication and signaling system, and on genes of the Snail superfamily, which encode transcriptional repressor proteins. The lab has created and analyzed numerous genetically engineered mouse models to understand the essential functions of individual components of these pathways, and have generated models for inherited human disease syndromes such as Alagille syndrome.
Gridley T (2007) Notch signaling in vascular development and physiology. Development 134:2709-2718.
Kiernan AE, Li R, Hawes NL, Churchill GA, Gridley T (2007) Genetic background modifies inner ear and eye phenotypes of Jag1 heterozygous mice. Genetics 177:307-311. PMCID: PMC2013712
Rodriguez S, Sickles HM, DeLeonardis C, Alcaraz A, Gridley T, Lin DM (2008) Notch2 is required for maintaining sustentacular cell function in the adult mouse main olfactory epithelium. Dev Biol 314:40-58.
Lozier J, McCright B, Gridley T (2008) Notch signaling regulates bile duct morphogenesis in mice. PLoS One 3:e1851. PMCID: PMC2266994
Escriva M, Peiró S, Herranz N, Villagrasa P, Dave N, Montserrat-Sentís B, Murray SA, Francí C, Gridley T, Virtanen I, García de Herreros A (2008) Repression of PTEN phosphatase by Snail1 transcriptional factor during gamma radiation-induced apoptosis. Mol Cell Biol 28:1528-1540.
Gridley T (200_) Arteriovenous patterning in the vascular system. In Heart Development and Regeneration, N. Rosenthal and R. Harvey, eds. Academic Press, New York. In press.
Robert-Moreno A, Ruiz-Herguido C, Guiu J, López ME, Inglés-Esteve J, Riera L, Tipping A, Enver T, Dzierzak E, Gridley T, Espinosa L, Bigas A (200_) Impaired embryonic hematopoiesis yet normal arterial development in the absence of the Notch ligand Jagged1. EMBO J. In press.
Mary Ann Handel, Ph.D.
Senior Scientist
The Jackson Laboratory
maryann.handel@jax.org
http://research.jax.org/faculty/mary_ann_handel.html
BA, Goucher College, 1965, Biology
PhD, Arizona State University, 1970, ZoologyThe laboratory investigates the genetic regulation of spermatogenesis and male fertility. She studies the mechanisms by which germ cells form condensed chromosomes as they enter the meiotic division phase. Appropriate dynamics and behavior of chromosomes during meiosis is of crucial importance for the formation of gametes, ensuring the haploid chromosome content of the future gamete, as well as genetic integrity and reproductive success. Studies are providing significant new information about assembly of mammalian meiotic chromosomes, and ultimately will help us understand how errors in these meiotic mechanisms cause aneuploidy, or inappropriate chromosome number, in offspring. Additionally, she takes an unbiased genetic approach to identify new mutations that affect meiotic processes, spermatogenic differentiation, and male fertility. Because the traits she studies, spermatogenic "maturation arrest" and fertilization failure, occur in many unexplained cases of human male infertility and reproductive toxicity, this approach can shed light on infertility, and possibly identify potential targets for contraception.
Davisson M, Akeson E, Schmidt C, Harris B, Farley J, Handel MA. 2007. Impact of trisomy on fertility and meiosis in male mice. Hum Reprod 22:468-476.
Lessard C, Lothrop H, Schimenti JC, Handel MA. 2007. Mutagenesis-generated mouse models of human infertility with abnormal sperm. Hum Reprod 22:159-166.
Good JM, MA Handel, MW Nachman. 2008. Asymmetry and polymorphism of hybrid male sterility during the early stages of speciation in house mice. Evolution 62:50-65.
Ryu KW, SA Sinnar, LG Reinholdt, S Vaccari, S Hall, MA Garcia, TS Zaitseva, DM Bouley, K Boekelheide, MA Handel, M Conti, RR Kopito. 2008. The mouse polyubiquitin gene Ubb is essential for meiotic progression. Mol Cell Biol 28:1136-1146.
La Salle S, F Sun, MA Handel. 2008. Isolation and Short-tem culture of mouse spermatocytes for analysis of meiosis. In: Methods in Molecular Biology, Molecular Medicine and Biotechnology (Series Editor: J. N. Walker), Meiosis Protocols (Ed. S. Keeney). Humana Press. In press.
Philipps, D., Wigglesworth, K., Hartford, S., Sun, F., Pattabiraman, S., Schimenti, K., Handel, M.A., Eppig, J.J. and Schimenti, J. The dual bromodomain and WD repeat-containing mouse protein BRWD1 is required for normal spermiogenesis and the oocyte-embryo transition. Devel. Biol. 317:72-82.
David Harrison, Ph.D.
Professor
The Jackson Laboratory
david.harrison@jax.org
http://research.jax.org/faculty/david_harrison.html
BS, Bates College, 1964, Chemistry
PhD, Stanford University, 1969, Inorganic ChemistryThe Harrison research group investigates aging in mouse models, focusing on processes that have the potential to retard aging and prolong health. For example, one line of research investigates mutations that reduce IGF-1 and insulin function. He has shown that such mutations can increase life span and delay certain aspects of aging, especially development of cancer. Now the lab is developing models that combine multiple mutations. They will use these models to define additional aging phenotypes and to test effects of these mutations on molecular pathways critical to aging processes. This research could lead to clinical treatments that delay endocrine-driven aging. Another line of research involves hematopoietic (blood system) stem cells. The focus is on adult stem cells, which constantly proliferate and differentiate to maintain tissue functions throughout life. If aging exhausts the function of adult stem cells, the balance between damage and repair is disrupted and tissue functions become defective. The group has found that genetic mechanisms protect hematopoietic stem cells from exhaustion in some mouse strains. This research may suggest clinical treatments to retard the aging of stem cells and thus delay aging of tissue functions.
Flurkey K, Brandvain Y, Klebanov SE, Austad SN, Miller RA, Yuan R, Harrison DE. 2007. PohnB6F1: a cross of wild and domestic mice that is a new model of extended female reproductive life span. J Gerontol Biol Sci Nov;62(11):1187-1198.
Miller RA, Harrison DE, Astle CM, Floyd RA, Flurkey K, Hensley KL, Javors MA, Leeuwenburgh C, Nelson JF, Ongini E, Nadon NL, Warner HR, Strong R. 2007. An Aging Interventions Testing Program: study design and interim report. Aging Cell 6:565-575.
Sharma Y, Astle CM, Harrison DE. 2007. Heterozygous kit mutants with little or no apparent anemia exhibit large defects in overall hematopoietic stem cell function. Exp Hematol 35(2):214-220.
Ertl RP, Chen J, Astle CM, Duffy TM, Harrison DE. 2008. Effects of dietary restriction on hematopoietic stem cell aging are genetically regulated. BLOOD 111(3):1709-1716.
Nadon NL, Strong R, Miller RA, Nelson J, Javors M, Sharp ZD, Peralba JM, Harrison DE. 2008. Design of Aging Intervention Studies: the NIA Interventions Testing Program. AGE onlinehttp://dx.doi.org/10.1007/s11357-008-9048-1.
Strong R, Miller RA, Astle CM, Floyd RA, Flurkey K, Hensley KL, Javors MA, Leeuwenburgh C, Nelson JF, Ongini E, Nadon NL, Warner HR, Harrison DE. 200_. Nordihydroguaiaretic acid and aspirin increase lifespan of genetically heterogeneous male mice. Aging Cell (in press)
BS, Bucknell University, 1988, Biology
PhD, Cornell University, 1996, BiochemistryGenes are activated and repressed within the cell nucleus, an organelle with a complex three dimensional structure. Along with changes in gene expression, changes to gene positions within the nucleus also occur during normal development and in some genetic diseases, particularly in cancers. To better understand the relationship between gene expression and nuclear organization, DR. Shopland is carefully mapping the nuclear locations of several genes that are activated during very early stages of normal mammalian development and in embryonic stem cells. These include genes in a region of mouse chromosome 14 that shows great similarity to human chromosome 13. These genes are organized near the nuclear periphery, a nuclear compartment that plays a role in chromosome structure and gene regulation. Sheis investigating how gene positioning at the nuclear periphery is related to gene regulation during development. This compartment also is implicated in a number of human genetic diseases, including muscular dystrophies, lipodystrophies, and premature aging. In addition, she is testing how the nuclear organization of genes goes awry in cancer (lymphoma) cells, where chromosome sequences have been rearranged. These studies will help to elucidate the ways in which genes work together during normal development, as well as how gene regulation can go wrong in cancer and other human genetic diseases.
Shopland LS, Byron M, Stein JL, Lian JB, Stein GS, Lawrence JB. 2001. Replication-dependent histone gene expression is related to Cajal body (CB) associated but does not require sustained CB contact. Mol Biol Cell 12:565-576.
Shopland LS, Johnson CV, Lawrence JB. 2002. Evidence that all SC-35 domains contain mRNAs and that transcripts can be structurally constrained within these domains. J Struct Biol 140:131-139.
Shopland LS, Johnson CV, Byron M, McNeil J, Lawrence JB. 2003. Clustering of multiple specific genes and gene-rich R-bands around SC-35 domains: Evidence for local euchromatic neighborhoods. J Cell Biol 162:981-990.
Moen PT, Johnson CV, Byron M, Shopland LS, de la Serna I, Imbalzano A, Lawrence JB. 2004. Repositioning of muscle-specific genes to the periphery of SC-35 domains during skeletal myogenesis. Mol Biol Cell 15:197-206.
Shopland, LS, Lynch CR, Peterson K, Thornton K, Kepper N, Stein S, Vincent S, Molloy K, Kreth G, Cremer C, Bult CJ, O’Brien, TP. 2006. Folding and organization of a contiguous chromosome region according to the gene distribution pattern in primary genomic sequence, J. Cell Biol 174: 27-38.