Previous Seminars

Information on up coming seminars
 

Monday, October 06, 2008 Cancelled
Dr. Dmitri Zaykin  NIEHS
"Haplotype association methods"
CANCELLED

Wednesday, September 24, 2008 Completed
Dr. Douglas Portman more info University of Rochester, School of Medicine and Dentistry
"Sex and the Single worm: Sex differences in C. elegans behavior and development"
What effect does the sexual “status” of a cell have on its development and function? Using the nematode C. elegans, we have found two cases in which “cellular sex” plays a critical role in biology. In the nervous system, the sex of shared neurons has profound effects on behavior, and in the epidermis, the sex of tail tip cells controls their morphogenesis. The mechanisms regulating these processes are likely to have importance for disorders such as autism whose incidence is highly sex-biased. This seminar will be held at the Waksman Institute Rm 1001.

Monday, September 15, 2008 Completed
Dr. Tara Matise more info Associate Professor, Department of Genetics, Rutgers University
"Take a Left at Chromosome 14"
My lab conducts research on projects that span statistical genetics, computer science, and bioinformatics. In this presentation I will describe my efforts in three areas. I will focus on the construction and evaluation of linkage maps, including development of the most comprehensive linkage maps available, and comparison of distribution of recombination between males and females and across different populations. I will also present my work on characterization of schizophrenia candidate gene regions, and on a study of the genetics of female reproductive aging.

Wednesday, September 10, 2008 Completed
Dr. Michael A. Miller more info Dept. of Cell Biology, University of Alabama at Birmingham, AL
"Worm and Sex and Amyotrophic Lateral Sclerosis: A basic connection?"
I will discuss how our studies of sperm and egg communication are providing insight into the biological functions of VAPB genes, which when mutated in humans causes ALS.

Tuesday, September 09, 2008 Completed
Dr. Kim McKim more info Department of Genetics/Waksman Institute of Microbiology, Rutgers University
"Flying through meiosis to segregate chromosomes"
Meiosis is an essential part of gametogenesis and in its essence is composed of two phases. First, during prophase double strand breaks are made in the DNA which, when repaired, form exchanges between homologous chromosomes. Second, these exchanges physically link homologous chromosomes together, directing their segregation at metaphase I and anaphase I. The result of these two phases is the precise splitting of the diploid genetic content into the gametes.

Wednesday, August 13, 2008 Completed
Dr. Hee-Sup  Center for Neural Science, Korea Institute of Science and Technology, Seoul Korea
"T-type Calcium channels in thalamic sensory gating and other brain functions: from genes to behavior"
The thalamus is actively engaged in shaping and modulating the afferent signals from the periphery to relay to the cortex. The intrinsic properties of thalamocortical relay (TC) neurons play an important role in this ‘sensory gating’ process. For example, burst spike activities of TC neurons that are driven by low threshold Ca2+ currents mediated by α1G T-type channels appear to set the ‘closed gate’ state. Thus, mice lacking the thalamic burst firing due to a deletion of the α1G T-type channel show hyperalgesic responses to persistent pain, accompanied by an increase in pain-encoding tonic spikes in TC neurons. Furthermore, the mutant mice show resistance to the development of absence seizures and sleep disturbances. These phenotypes can all be attributed to the impairment of the mutant mice in the sensory gating function of the thalamus. In addition to the role in the sensory signaling process, the thalamus is also involved in other brain functions. Recently, we have been studying the role of the thalamus in modulation of memory. These results together suggest that burst firings in the thalamus may be involved in the `control of information transfer at different levels. I will briefly review the roles of the thalamocortical circuit and discuss new findings that are relevant to the issue.

Monday, August 04, 2008 Completed
Dr. Ning Sun  Biostatistics Division, Yale School of Public Health, Yale University School of Medicine
"Regression Models for Dissecting Transcriptional Regulatory Network "
Dissecting transcriptional regulatory network is an important issue in biology. With the availability of many types of large-scale genomic data, various statistical modeling approaches have been proposed to integrate different genomic data for network reconstruction. Regression models are commonly used in this context to relate the observed gene expression data with their underlying regulations. However, different regression models make different assumptions and contain different covariates and their interactions. This talk will discuss the performance of different regression models on learning transcription regulatory network.

Thursday, July 24, 2008 Completed
Dr. Jarema Malicki more info Harvard Medical School, Boston, MA
"Ciliogenesis, Nuclear Positioning, and Other Aspects of Cell Polarity in the Vertebrate Embryo"
Polarity is an essential feature of most living cells. In the vertebrate embryo, polarity is particularly obvious in epithelial structures, which range in complexity from relatively simple protective cell layers on the body surface to architecturally complex tissues, such as the retina. In many of these contexts, polarity is apparent at the level of individual cells as the compartmentalization of their membranes, polar orientation of cytoskeletal components, as well as an asymmetric distribution of organelles.

Monday, July 21, 2008 Completed
Dr. Sandhya Koushika 
"Regulating mitochondrial transport in C. elegans neurons"
Mitochondrial transport in neurons is an essential and regulated process. Transport of this organelle is controlled by molecular motors, one amongst these is the Kinesin-I protein. The Kinesin-I motor is present in a complex with multiple proteins such as UNC-16/JIP3, UNC-51, UNC-76/Fez1. We are attempting to understand the role of these proteins on mitochondrial transport. We find that in unc-16 mutants there is an increase mitochondrial numbers in axons while mutants in other molecules associated with the Kinesin-I motor reduce the number of mitochondria at synapses. The increase in numbers of mitochondria in unc-16 mutants occurs through an effect on both anterograde and retrograde transport pathways. However the anterograde changes in transport are all mediated in a Kinesin-I independent manner. Our data predict the recruitment of an alternate motor to mitochondria in the absence of UNC-16 whose identity remains to be clearly identified.

Wednesday, June 04, 2008 Completed
Dr. Mark Mayford more info University of California, San Diego
"Genetic Dissection of Memory Circuits"
We have recently developed a genetic technique that allows us to specifically introduce genetic changes into neurons that are activated by behavioral stimuli. By introducing a visible marker protein we can permanently tag activated subsets of neurons creating a precise record of the activity pattern at a specific point in time. We used this approach to address questions regarding learning and memory

Wednesday, May 14, 2008 Completed
Dr. Hongyu Zhao more info Professor, Yale School of Pubic Health/Director, Yale Center for Statistical Genomics and Proteomics
"Incorporating Prior Biological Knowledge in Genome-Wide Association Studies "
The last four years have seen great successes in many Genome-Wide Association Studies (GWAS) which have identified numerous genetic variants underlying complex traits. The analysis and interpretation of data from GWAS presents great statistical and computational challenges, especially after the initial discoveries of variants carrying relatively large effects. Although various statistical approaches have been or are being developed to better analyze GWAS data, it has become apparent that the incorporation of information from prior studies and other sources is indispensable. In this presentation, we discuss our recently developed statistical methods and bioinformatics tools that are designed to more effectively integrate diverse types of prior biological information in analyzing GWAS data. The usefulness of these methods will be illustrated through their applications to some recent large scale GWAS data.

Monday, May 12, 2008 Completed
Dr. Sylvia Lee-Huang  Dept. Biochem., NYU Medical Center, New York, NY
"Novel Anti-HIV Agents from Natural Products"
Ole, HT, MAP30 and GAP31 are novel anti-HIV agents from natural products, effective against multiple stages of viral life cycle, blocking viral entry and integration. Molecular modeling and structure/activity mapping reveal distinct antiviral mechanisms. Ole and HT interact with HIV-gp41 and integrase whereas MAP30 and GAP31 act on HIV-LTR DNA.

Monday, May 05, 2008 Completed
Dr. Mark Van Doren  Dept. of Biology, Johns Hopkins Univ., Baltimore, MD
"Vive la Difference: The creation of sexual dimorphism in the soma and germline"

Monday, April 28, 2008 Completed
Dr. Stephanie Sherman more info Dept. Human Genetics, Emory University., School of Medicine
"Trisomy 21: Causes and consequences"
Human chromosome errors of segregation during gamete formation are the leading cause of pregnancy loss and birth defects. We have investigated trisomy 21, or Down syndrome, as a model to understand the chromosome nondisjunction and its phenotype consequences. Our current research results will be presented.

Monday, April 21, 2008 Completed
Dr. San Ming Wang more info EHN Research Institute, Feinberg School of Medicine, Northwestern University, Evanston, IL
"Studying Human Genome Structure at Kilobase Resolution"
Normal genome variation and pathogenic genome alteration frequently affect small regions in the genome. We have developed the DGS (Ditag Genome Scanning) platform for kilobase-resolution analysis of genome structure. Analyzing five normal and cancer genomes using this platform reveals new patterns of normal genome variation and cancer genome mutation.

Monday, March 31, 2008 Completed
Dr. Carol Wise more info Texas Scottish Rite Hospital, Dallas TX
"Genetics of idiopathic scoliosis: Insights into a common and complex disease of childhood"
Idiopathic scoliosis (IS) is a spinal deformity affecting 2-3% of children, and its etiology is unknown. Clinical management poses a public health burden costing billions of U.S. dollars each year. The recent identification of a candidate gene for IS, and its overall strong genetic underpinnings, suggest the potential for large-scale studies to identify additional susceptibility risk factors. Such studies may also provide insights into disease variability.

Friday, March 21, 2008 Completed
Dr. Keiji Wada more info National Center of Neurology and Psychiatry, Tokyo, Japan
"Essential players in neuro-gliology: GPCRs and deubiquitinating enzymes"
Recent studies indicate that glia play essential roles in the regulation of neural transmission. At the seminar, I introduce an idea on neuro-gliology and present our data on deubiquitinating enzymes and GPCRs to show that the molecules play important roles in the neuron-glia interaction.

Monday, March 17, 2008 Completed
Dr. Lu Chen more info Dept. of Molecular and Cell Biology, University of California, Berkeley, CA
"Translational regulation in homeostatic synaptic plasticity"
Normal functions of the nervous system require that neurons maintain their activity in an optimal range. When membrane and synaptic activity are blocked, the neuron scales up the strengths of all its excitatory synapses, a phenomenon known as synaptic scaling. This process has been shown to involve local protein synthesis. Our work revealed a messenger molecule that turns on local protein translation upon activity blockade.

Monday, March 10, 2008 Completed
Dr. Rajesh Ranganathan more info Novartis Institutes for Biomedical Research, Inc
"Putting patients first: Meeting the drug discovery challenge"
This seminar will begin by discussing the current scientific, regulatory, social, and financial environment in which drug discovery operates and outline the challenges that need to be overcome. A general overview of the canonical drug discovery process will be presented to serve as a baseline. One particular approach to addressing these challenges will be presented as a launch pad to catalyze further discourse about potential paths forward.

Monday, March 03, 2008 Completed
Dr. Maurice Kernan more info Dept. Neurobiology and Center for Developmental Genetics, SUNY, Stony Brook, NY
"Ciliary mechanisms and mechanosensory cilia in Drosophila"
Most sensory signal transduction takes place in cilia, ancient cellular extensions that use a conserved intraflagellar transport (IFT) pathway for their assembly. Drosophila mechanosensory mutations affecting IFT and IFT-associated proteins show how they have adapted for sensory ends, and shed new light on both IFT function and mechanotransduction.

Monday, February 25, 2008 Completed
Dr. Prakash Gorroochurn more info Dept. Biostatistics, Columbia Univ. New York, NY
"Non-replication of association studies: “pseudo-failures” to replicate?"
Recently, serious doubts have been cast on the usefulness of association studies because most initial findings fail to replicate in subsequent studies. The reasons usually invoked are population stratification, genetic heterogeneity, and inflated Type I errors. I will argue that, even when these problems are addressed, the scientific community usually has unreasonably high expectations on replication success, based on initial low P values. Because many initially significant findings result in low replication power, replication failure should not be surprising or be interpreted as necessarily refuting the initial findings.

Monday, February 11, 2008 Completed
Dr. Robert Gatenby  Departments of Radiology and Applied Mathematics, University of Arizona, Tuscon, Arizona
"The Darwinian Dynamics of Cancer"
Invasive cancer emerges following a complex, multistep process often described as “somatic evolution.” Models of carcinogenesis are typically based on the Darwinian principle that evolution requires genetic and/or epigenetic changes that generate new phenotypes. However, the models do not typically address why these specific phenotypic/genotypic changes are necessary for carcinogenesis or why they occur in the observed sequence. I propose carcinogenesis is a sequence of successful adaptations to six distinct microenvironmental proliferation barriers that arise in the adaptive landscapes generated by normal and premalignant populations growing on epithelial surfaces. The genotypic and phenotypic heterogeneity of cancer populations is explained by an “ecological equivalence” in which multiple strategies can successfully adapt to the same barrier. This model provides a theoretical framework in which the diverse cancer geno-/phenotypes to be understood according to their roles in overcoming specific microenvironmental growth constraints.

Monday, February 04, 2008 Completed
Dr. Peter Tolias more info Institute of Genomic Medicine, UMDNJ-NJMS, Newark, NJ
"Enabling the era of personalized medicine through translational research"
UMDNJ has established the Institute of Genomic Medicine (IGM), a personalized medicine and translational research center as a valuable resource for academic researchers as well as biotechnology, pharmaceutical and diagnostic companies. Activities include complete genomic and proteomic biomarker discovery and assay development and operation of three CLIA-certified diagnostic reference labs and a genetic outpatient clinic serving seven major hospitals in NJ. IGM is the first academic medical center in the world to offer mass spec immunoassay (MSIA) technology which couples automated antibody affinity capture to mass spectrometry allowing determination in one platform of both sensitive quantification as well as qualitative changes in proteins arising from amino acid substitutions, RNA splice variants, posttranslational modifications and proteolytic processing.

Monday, January 28, 2008 Completed
Dr. Derek SantAngelo more info Division of Immunology, MSKCC, New York
"A BTB-ZF transcriptional repressor controls innate versus conventional T cell development"
Differentiation of thymocytes into functionally distinct lineages of T cells is fundamental for successful immunity. One lineage of T cells, the invariant Natural Killer T cell (iNKT cell), is of particular interest due to its innate immunity-like rapidity of response to antigen and its capacity to modulate effector functions of other cells. Here we show that the BTB-ZF transcriptional regulator, PLZF (promyelocytic leukemia zinc finger protein), is essential for the innate-like function of iNKT cells since iNKT cells lacking PLZF develop into conventional, naïve CD4 T cells. Furthermore, ectopic expression of PLZF in developing thymocytes is sufficient to transfer innate-like characteristics to conventional CD4 and CD8 T cells. Therefore, PLZF is the master regulator of innate T cell effector functions of iNKT cells.

Monday, December 10, 2007 Completed
Dr. Frank McNally  Molecular & Cellular Biology, University of California, Davis
"The Asymmetry of Female Meiosis"
In oocytes, female meiotic spindles attach to the cell cortex where they mediate expulsion of three fourths of the maternal chromosomes in highly asymmetric cell divisions. In C. elegans, a complex of proteins that include kinesin 1 mediate the initial movement of the spindle to the cortex, and the microtubule-severing ATPase, katanin, regulates spindle size and the asymmetry of cytokinesis.

Monday, December 03, 2007 Completed
Dr. Susan Bergeson  Pharmacology & Neuroscience, Texas Tech University Health Science Center
"Towards understanding the molecular mechanisms of alcoholism"
Global transcriptional analyses of several genetic mouse models of alcohol drinking and dependence have uncovered new genes and biological pathways not previously known to be involved in alcohol-related responses. Further, chromatin remodeling and miRNA expression may play a role in the differential transcriptional response seen in an adolescent mouse model of high drinking.

Monday, November 19, 2007 Completed
Dr. Zhiyuan Shen more info Dept. of Radiation Oncology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ
"Roles of a BRCA2 Interacting Protein (BCCIP) in Maintenance of Genomic Stability"
BCCIP is a BRCA2 and CDKN1A (p21) interacting protein. Our studies have suggested critical roles of BCCIP in multiple pathways required for the protection of genomic integrity, including DNA repair, cell cycle regulation, and mitosis. Furthermore, alternations of BCCIP has been implicated in multiple human cancer.

Monday, November 12, 2007 Completed
Dr. Hal Broxmeyer more info Walther Oncology Center, Indiana University, School of Medicine, Indianapolis, IN
"Regulation of Hematopoietic and Embryonic Stem Cells"
Hematopoietic Stem Cells (HSC) have been used to treat and cure a large number of malignant and non-malignant disorders. There is still much to be learned regarding the regulation of HSC proliferation, self-renewal, survival, differentiation, migration/homing for optimal HSC transplantation. Embryonic Stem Cells (ESC) have extensive proliferative, self-renewal and differentiation activity. However, these cells are not yet ready for use in regenerative clinical medicine. Understanding the regulation of HSC and ESC function could accelerate the use of both cell types for clinical advantage. This presentation focuses on HSC and ESC regulation.

Monday, October 22, 2007 Completed
Dr. Ray Birge more info Dept. of Biochemistry and Molecular Biology, New Jersey Medical School, UMDNJ, Newark, NJ
"Cyclophilins"
Physiological cell death is a process whose purpose is the elimination of functionally inappropriate cells in a manner that does not elicit an inflammatory response. The process of specific apoptotic cell recognition represents a ubiquitous and unconventional innate immunity that discriminates effete from viable cells and that potently suppresses inflammation. A variety of data implicate the presence, on the apoptotic cell surface, of specific evolutionarily conserved recognition determinants that elicit innate anti-inflammatory responses. Arguably, the best understood of these “eat-me” signals results from the exposure of the anionic lipid phosphatidylserine (PS) on the outer surface of the plasma membrane. PS is normally restricted to the inner leaf of the plasma membrane, but becomes externalized to the outer leaflet of the membrane as an early event associated with apoptosis. In doing so, it signals to an evolutionarily conserved anti-inflammation pathway characterized by active production of anti-inflammatory cytokines such as TGF-β and IL-10, and the down-modulation of pro-inflammatory cytokines such as TNF-α,IL-1β, and IL-12. MFG-E8 and Gas-6 are two of the principal PS binding proteins that function to bridge PS on the apoptotic cell to receptors on phagocytes during engulfment. Mice deficient in MFG-E8 or Gas6 signaling pathways develop splenomegaly, form numerous germinal centers, and develop age-dependent autoimmune disease with antibodies towards self-components highly reminiscent of SLE. In this talk, I will discuss mechanisms by which PS is recognized and processed by phagocytic cells, as well as offer insights as to how apoptotic cell mimetics may be harnessed as anti-inflammatory therapeutics.

Monday, October 15, 2007 Cancelled
Dr. Gary Chase more info Public Health Sciences, Penn State College of Medicine, Hershey, PA
"Genetic Factors in Nicotine Dependence"
Recently a case-control study was performed using the outcome of nicotine dependence as defined by the Fagerstrom test; controls were required to have been exposed to 100 cigarettes and to remain non-dependent. A whole genome scan as well as a detailed analysis of thousands of SNPs was done. Results showed a strong indication of susceptibility genes for nicotine dependence.

Monday, October 01, 2007 Completed
Dr. Stephen Finch  Dept. of Applied Math and Statistics, Stony Brook University, Stony Brook, NY
"A mixture based test for case-control association studies with copy number polymorphisms."
Measurements of copy number polymorphisms (CNPs )are based on a quantitative measurement that is modeled by a mixture of component distributions with possibly different mixing proportions. The likelihood ratio (LRTS) that these proportions are equal in cases and controls is derived and shown to be better than the chi-squared test in an important class of studies.

Monday, September 24, 2007 Completed
Dr. Veronica Vieland more info Center for Quantitative and Computational Biology, Ohio State University, Columbus, OH
"More is known than is: How what we know (about gene mapping for complex diseases) can hurt us."
The contemporary literature on methods for gene mapping in human genetics tends to take certain established, agree-upon “facts” as a starting point for further development. These include, among other things, the shared knowledge that linkage analysis does not work well for complex disorders; that association analysis is more powerful than linkage analysis for complex disorders; and that “genetic architecture” (including modeling of multi-locus pathways) can be done on the basis of case-control data without the need for families. Using analysis of a real data set to illustrate, I will show that these things may be known, but they are not true. In the process, I will describe methods for successful elucidation of genetic architecture in realistic human data sets.

Monday, September 17, 2007 Completed
Dr. Terry McGuire  Genetics Department, Rutgers University, Piscataway, NJ
"From the Scholarship of Discovery to the Scholarship of Learning and Teaching"
I have been working with the Scholarship of Teaching and Learning (SOTL) within Genetics. Geneticists in our Department are probably more familiar with the Scholarship of Discovery. Discovery is the discipline research we do. SOTL is an evidence-based approach for understanding how others comprehend and construct information with a discipline. SOTL connects and encompasses all other forms of scholarship and ensures their perpetuation (Boyer, 1990). SOTL is discipline-specific. Effective research in SOTL for Genetics is best done by geneticists. I will discuss my work with three NSF-funded dissemination projects, the Carnegie Academy and several of my research projects.

Wednesday, September 12, 2007 Completed
Dr. Chi-hua Chiu  Department of Genetics, Rutgers University, Piscataway, NJ
"Hox gene regulation and evolution in chordates"
Research in my lab integrates molecular and developmental evolution, the two most recent, and now widely recognized, fields of study centered on evolution and its mechanisms at the genetic level. My lab focuses on the Hox family of transcriptional regulator proteins that play an essential role in pattern formation of muscular, skeletal, and nervous system tissues and higher level structures such as limbs, vertebral column, and spinal cord. We have pioneered the use of ‘comparative genomics’, i.e. comparing genomic sequences across species to identify regulatory sequences in chordate Hox clusters and draw two major conclusions. One, Hox clusters of jawed vertebrates exhibit a striking degree of conservation of cluster architecture and blocks of noncoding known and putative cis-regulatory sequences. Two, Hox cluster evolution in ray-finned fishes demonstrates a dynamicism unique amongst the jawed vertebrates. These unexpected results open up new avenues of investigation that we are pursuing and that I will discuss.

Monday, July 30, 2007 Completed
Dr. Simon Gregory more info Duke University Center for Human Genetics
"Determining the underlying genetic architecture of coronary artery disease"
We are utilizing an approach that incorporates genome-wide analyses, such as transcription factor mapping, methylation profiling and linkage scans, in addition to differential gene expression and candidate gene association analysis to identify genes implicated in the development of coronary artery disease.

Monday, June 04, 2007 Completed
Dr. Pablo Gejman  Dept. of Psychiatry, Feinberg School of Medicine, Northwestern University, Illinois
"Perspectives of the Genetics of Schizophrenia"
The history of the genetics of schizophrenia has been characterized by false starts and intense strategic debate. The results of many experiments (and then, the status of the field) have been difficult to interpret. A myriad of explanations have been offered to explain the slow progress but each remains highly hypothetical. We are testing the hypothesis that samples with sufficient statistical power will be critical to the solution of the schizophrenia conundrum and are currently finalizing the collection of 3000 schizophrenia cases and 3000 control of European ancestry (EA), and 1,300 cases and 1,100 controls of African-American (AA) ancestry. The sample is been utilized for comprehensive candidate gene association experiments and the systematic follow-up genetic linkage experiments. Whole genome association (GWA) experiments conducted by us and by others are also undergoing. The field, collectively, has access to data from very large samples by combination of existing resources. The results of the current wave of experiments will have major influence on the strategic stage.

Monday, May 21, 2007 Completed
Dr. Louis B. Hersh more info Dept. of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine
"Peripheral Expression of the peptidase Neprilysin as a way to treat and prevent Alzheimer’s disease. "
Peripherally administered antibodies can reduce brain amyloid burden without the antibody entering the brain. We have exploited this finding using the Aβ degrading peptidase neprilysin. Peripheral expression of neprilysin leads to a significant reduction in brain Aβ levels, opening up a new approach for the treatment and prevention of AD.

Monday, May 14, 2007 Completed
Dr. Elizabeth Engle more info Dept. of Neurology, Children's Hospital / Harvard Medical School, Boston, MA
"Genetics of the congenital cranial dysinnervation disorders"
I will present my labs ongoing investigation into the genetic bases of both complex and common strabismus. The genetic analysis of complex strabismus disorders has led to the identification of a series of disparate genes, including PHOX2A, SALL4, KIF21A, ROBO3, and HOXA1, each of which appears to play an essential role in the normal development and/or connectivity of cranial motoneurons.

Wednesday, May 09, 2007 Completed
Dr. Michael Novacek (seminar at Alampi Room, Institute of Marine & Coastal Sciences, Cook)  Division of Paleontology, American Museum of Natural History
"The Evolution of Dinosaurs and Mammals"
TBA

Monday, May 07, 2007 Completed
Dr. Alcino J. Silva more info Depts. of Neurobiology, Psychiatry and Biobehavioral Sciences, etc., UCLA
"Molecular and cellular cognition: memory and how it fails"
TBA

Monday, April 30, 2007 Completed
Dr. Samuel Wilson  Deputy Director: National Institute of Environmental Health Sciences/ National Institutes of Health
"Temporal and Spatial Relationships Governing Chemistry within a DNA Polymerase Active Site"

Wednesday, April 25, 2007 Completed
Dr. Joanna Mountain (seminar at Waksman Auditorium)  Departments of Anthropological Sciences and Genetics, Stanford University
"Human Genetic Differences of the Past, Present and Future"
TBA

Monday, April 23, 2007 Completed
Dr. Ju Chen  University of California at San Diego
"Scaffold LIM Domain Proteins in Cardiac Function & Disease"
I will discuss our up-to-date results on the role of two LIM domain containing cytoskeletal/scaffold proteins, Cypher and FHL1 in cardiac function and human cardiomyopathy and hypertrophy. I will also discuss the potential mechanism by which mutations in cipher result in cardiomyopathy.

Monday, April 09, 2007 Completed
Dr. Janet Sinsheimer more info University of California at Los Angeles, Department of Human Genetics
"Mother and Child Reunion: Maternal-Fetal Gene Interactions"
Biological mechanisms involving a combination of genetic and environmental factors have been hypothesized to explain susceptibility to complex familial disease. I will present our efforts to detect interactions between mother’s and child’s genes that can create adverse prenatal environments and increase susceptibility to diseases such as schizophrenia and rheumatoid arthritis.

Monday, April 02, 2007 Completed
Dr. Qingshen Gao more info ENH Research Institute, Northwestern University Feinberg School of Medicine
"BRCA2-interacting proteins and their roles in DNA damage repair."
Germ line mutations in BRCA2 gene predispose women to early-onset familial breast and ovarian cancer. BRCA2 has been found to play an important role in homologous recombinational repair of DNA double strand breaks via its interaction with rad51. While BRCA2 binds to rad51 mainly via its conserved brc repeats, the most conserved region of BRCA2, the C-terminal region, binds a number of proteins, including DSS1 and MAGE-D1. These BRCA2 interacting proteins also play a role in DNA damage repair.

Monday, March 26, 2007 Completed
Dr. Suzie Chen  Susan Lehman Cullman Laboratory for Cancer Research, Ernesto Mario School of Pharmacy
"Aberrant Expression of Metabotropic Glutamate Receptor 1 in Melanoma"
We have showed and confirmed the ectopic expression of metabotropic glutamate receptor 1 (Grm1), a member of the G-protein-coupled-seven-transmembrane-domain-receptor family to be sufficient in inducing melanoma development in vivo. We also have demonstrated that ectopic expression of GRM1 in a subset of human melanoma cell lines and biopsies. The possibilities of using GRM1 as a target for therapy will be discussed.

Monday, March 19, 2007 Completed
Dr. Marcella Devoto  Dept. of Ped. & Dept. of Biostats. and Epidemiology, The Children's Hospital of Phila. and Univ. of Penn. School of Medicine
"Identification of susceptibility loci for osteoporosis by genetic analysis of bone mineral density"
I will describe our studies on families with recurrence of low bone mineral density (BMD), a risk factor for osteoporosis. Following a genome wide scan, we identified a BMD QTL on 1p36. We are now working on fine mapping the critical region by genotyping SNPs across 11 Mb in 1p36, as well as SNPs from candidate genes.

Monday, March 05, 2007 Completed
Dr. Yufang Shi  Robert Wood Johnson Medical School, Department of Molecular Genetics, Microbiology and Immunology
"Roads to the grave: How do T-cells choose?"
T lymphocytes possess a great potential to proliferate upon receiving antigenic stimulation. In order to keep lymphocyte homeostasis, most activated lymphocytes are eliminated through a process called activation-induced cell death (AICD). In this seminar, recent data regarding the death pathways of different T cell subsets will be presented.

Monday, February 26, 2007 Completed
Dr. Francesco Ramirez more info Child Health Institute, UMDNJ-RWJMS
"Marfan Syndrome and related disorders; complex mechanism of pathogenesis involving structural and signaling molecules."
Marfan syndrome (MFS) is a connective tissue disorder with abnormalities that predominantly involve the ocular, musculoskeletal, and cardiovascular systems. Pleiotropic manifestations in MFS are accounted for by mutations in fibrillin-1, the major constituent of extracellular microfibrils that impart structural properties to the connective tissue. Significant progress using mouse models of the disease has helped delineate the pathological events responsible for the manifestations of MFS. These studies have revealed that fibrillin-1 microfibrils participate in regulating extracellular availability of active transforming growth factor-B (TGF-B and implicitly, that dysregulated TGF-B signaling is a major determinant of MFS pathogenesis. Consistent with these findings, a new syndrome with overlapping MFS-like manifestations has been identified that is caused by mutations in TGF-B receptor types I and II. Collectively these studies indicate that MFS is part of a larger group of developmental disorders with broad and complex effects on the morphogenesis, homeostasis and function of multiple organ systems. Importantly, they have also identified anti-TGF-B therapeutic agents as productive treatment strategies in MFS and potentially related disorders.

Thursday, February 22, 2007 Completed
Dr. Sarah Tishkoff more info Department of Biology, University of Maryland, College Park, MD
"Genetic Variation and Adaptation in Africa: Implications for Human Evolution and Human Disease"
Africa contains the greatest levels of human genetic variation and is the source of the worldwide range expansion of all modern humans. Knowledge of the genetic population boundaries within Africa has important implications for the design and implementation of disease association studies in Africans and African Americans, and for reconstructing modern human origins. Additionally, studies of genetic adaptation in Africa have important implications for identifying genes that play an important role in human evolution and disease. In this talk I will discuss results of analyses of a large dataset consisting of ~1200 genome-wide markers genotyped in ~3,200 Africans and 118 African Americans. I will also discuss the results of our study of the genetic basis of lactase persistence in Africa and identification of regulatory mutations that have evolved independently in Africans and Europeans.

Monday, February 12, 2007 Completed
Dr. Elof A.Carlson  Dept. of Biochemistry and Cell Biology, Stony Brook University
"Darwin: Used, Abused, And Necessary"
Darwin’s theory of natural selection is the basis for today’s evolutionary theory. Darwin’s work is essential for modern biology. His theory continues to be the most important interpretation of how evolution works every prediction of similarity from classical methods borne out by molecular analysis. Darwin’s scientific theory has been abused by those fostering bigotry, racism, class discrimination, rationalizing exploitation, and promoting spurious eugenic movements.

Tuesday, February 06, 2007 Completed
Dr. Cory Teuscher  University of Vermont , Burlington, VT
"Madam, I’m Adam or Evidence that the Y-Chromosome Influences Susceptibility of Female Mice to Autoimmune Disease of the CNS "
Experimental allergic encephalomyelitis (EAE), an autoimmune model of multiple sclerosis, is a complex disease influenced by genetic, intrinsic, and environmental factors. In a series of studies, we provide evidence for the existence of a Y-chromosome polymorphism capable of modifying susceptibility to EAE in male mice, and leading to the organizational masculinzation of EAE in their female littermates.

Monday, February 05, 2007 Completed
Dr. Yibin Kang more info Molecular Biology Dept., Princeton University
"Genomic Analysis of Breast Cancer Metastasis"
Metastasis is the most dreadful development of neoplastic diseases. Although metastasis contributes to over 90% of human cancer mortality, the molecular mechanism of this process remains largely unknown. In this talk, I will discuss our recent study of breast cancer metastasis using a multidisciplinary approach that combines molecular biology, genomics and computational biology tools with animal models and advanced in vivo imaging technologies.

Monday, January 29, 2007 Completed
Dr. Michael Boehnke more info Department of Biostatistics, University of Michigan
"Efficient Design and Analysis of Genome-Wide Association Studies with Application to Type 2 Diabetes"
Genome wide association studies in which hundreds of thousands of genetic markers are genotyped on hundreds or thousands of subjects are now a practical approach to study the genetic basis of complex human diseases. In this talk, I will discuss optimal experimental design and analysis methods for two-stage genome wide association studies in which a subset of samples is genotyped on all genetic markers in stage 1, and the remaining samples are genotyped on the most interesting markers in stage 2. I will illustrate these methods with application to data from stage 1 of a genome wide association study of type 2 diabetes from the Finland-United States Investigation of NIDDM Genetics (FUSION) study.

Friday, January 26, 2007 Completed
Dr. Joann Sweasy  Therapeutic Radiology and Genetics, Yale University School of Medicine, New Haven, CT
"Cancer-Associated Mutants of DNA Polymerase Beta"
Approximately 30% of tumors studied possess DNA polymerase beta (Pol ß) variants. We have found that these variants exhibit functional phenotypes including mutator activity and that they induce cellular transformation. Because Pol ß functions in base excision repair, our results suggest that this repair system is a tumor suppressor.

Monday, January 22, 2007 Completed
William T. Adams, J.D., L.L.M., Christopher G. Izzo, J.D., Kathleen D. Rigault, Ph.D., J.D.  Office of Corporate Liaison and Technology Transfer, Rutgers, New Brunswick
"Introduction to Patents and Intellectual Property"
The Office of Corporate Liaison and Technology Transfer negotiates contracts between members of the Rutgers faculty and industrial research sponsors, as well as oversees all aspects of the protection and licensing of intellectual property. Some of the following topics will be addressed: what is a patent, benefits to faculty, how to a new discovery, how to get a patent, are there restrictions on publication, biological materials transfer agreements, and others. Opportunities to answer questions will be available after the seminar.

Monday, December 18, 2006 Completed
Dr. Ted Abel more info University of Pennsylvania, Department of Biology, Director, Biological Basis of Behavior Program
"Molecular Mechanisms of Transcriptional Regulation During Long-Term Memory Storage "
Transcriptional activation is thought to be a key process in long-lasting forms of memory and synaptic plasticity. This activation is directed by transcription factors and their coactivators, which regulate gene expression via chromatin remodeling, histone modification and interactions with the basal transcription machinery. One type of histone modification associated with transcriptional activation is acetylation, which is regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs) that add or remove acetyl groups from histones, respectively. Recently, we and others have demonstrated that the transcriptional coactivator CREB-binding protein (CBP), a potent HAT, is involved in specific forms of long-term memory and synaptic plasticity.. A complementary method to study the role of histone acetylation in synaptic plasticity and memory is to examine the effects of HDAC inhibitors, which increase the level of histone acetylation that correlates with transcriptional activation. We found that increasing histone acetylation using the HDAC inhibitor TSA enhances long-term contextual memory and facilitates synaptic plasticity via the transcription factor CREB. In summary, these results support the idea that histone acetyltransferases and histone acetylation are critical to mechanisms of long-term memory storage. Histone acetylation may provide an epigenetic mechanism for establishing gene-specific modifications that result in the coordinate expression of genes required for long-term memory storage.

Monday, December 11, 2006 Completed
Dr. Valerie Reinke  Dept. of Genetics, Yale University School of Medicine
"Germ cell specification and proliferation in C. elegans"
I will present global gene expression profiling data that identified critical components regulating germline stem cell proliferation and differentiation, as well as factors controlling inheritance of germline-specific organelles in the embryonic germ lineage.

Monday, December 04, 2006 Completed
Dr. Victoria Prince more info University of Chicago, Dept. of Organismal Biology and Anatomy
"Using the zebrafish to understand pancreas development"
We are using the advantages of the zebrafish model to gain insights into the earliest steps in pancreas cell specification. In particular, we are focused on the cellular and molecular interactions necessary to specify the insulin-secreting beta cell.

Wednesday, November 29, 2006 Completed
Dr. Douglas Erwin (seminar at Waksman Auditorium)  National Museum of Natural History, Smithsonian Institute
"Developmental Invention and Ecological Innovation during the Cambrian Metazoan Radiation"
TBA

Monday, November 27, 2006 Completed
Dr. Michael Levine  University of California at Berkeley, Department of Molecular and Cell Biology
"Gene networks for animal development and evolution."
I will discuss the use of gene networks to understand the evolutionary origins of the multi-chambered heart of vertebrates and the diversity of the insect ventral midline. ChIP-chip assays help illuminate these networks and provide insights into the mechanisms of gene regulation.

Monday, November 13, 2006 Completed
Dr. Jane Hubbard more info New York University, Dept. of Biology
"New perspectives on the control of germline proliferation in C. elegans"
New perspectives on the control of germline proliferation in C. elegans During organogenesis, cells must decide when, where and how fast to proliferate. Improper control of cell proliferation can lead to developmental defects and cancer. We are focusing on the relatively unexplored area of the control of pattern and extent of germline proliferation in C. elegans as a model for this process, especially as controlled by signaling between the somatic gonad and the germ line during their co-development.

Wednesday, November 08, 2006 Completed
Dr. J. Peter Gogarten (seminar at Alampi Room, Institute of Marine & Coastal Sciences, Cook )  Department of Molecular and Cell Biology, University of Connecticut
"Organismal Evolution: Tree-of-Life or Tangled Web"
TBA

Monday, November 06, 2006 Completed
Dr. Shridar Ganesan  The Cancer Institute of New Jersey
"BRCA1 and the Biology of Basal-like Breast Cancer"
Basal-like breast cancer is a subtype of human breast cancer identified by gene expression profiling and accounts for approximately 15% of sporadic breast cancer cases. These tumors are high grade, poorly differentiated ductal carcinomas that do not express the estrogen receptor, or the progesterone receptor and do not harbor HER2 amplifications. They have a poor clinical outcome, and there is no targeted therapy for these tumors. Breast cancers that arise in women with germ line BRCA1 mutations tend to have morphological, IHC and gene expression profiles similar to sporadic Basal-like breast cancers (BLC). This raises the possibility that sporadic basal-like breast cancers may be phenocopies of BRCA1 -/- tumors. As BRCA1 -/- tumors have characteristic abnormalities in DNA repair, and in maintenance of X chromosome inactivation, we explored these parameters in sporadic basal-like breast cancers. We found that most sporadic BLC, unlike other high grade non-BLC have X chromosome abnormalities similar to that seen in BRCA1 -/- tumors. This was associated with up regulation of a small set of X chromosome genes. Preliminary clinical studies have been initiated to explore the possibility that BLC also have defects in DNA repair that may render them sensitive to certain classes of DNA damaging agents.

Monday, October 30, 2006 Completed
Dr. Todd Lamitina  Dept. of Physiology, University of Pennsylvania
"Compartment specific protein damage as a regulator of osmosensitive gene expression"
The mechanisms that animals use to sense and adapt to osmotic stress are are poorly understood. Using RNAi screening, we identified >100 genes that regulate osmosensitive gene expression in C. elegans. Most of these genes regulate protein folding, biogenesis, and degradation, suggesting the novel hypothesis that accumulation of damaged/misfolded proteins may be a mechanisms for osmosensation in animals.

Monday, October 16, 2006 Cancelled
Dr. Michael Miller more info University of Alabama at Birmingham, Cell Bio Dept.
"Molecular communication between the sexes: a case study"
I will present research from my lab on intercellular signaling mechanisms used by Caenorhabditis elegans sperm and oocytes to prepare for fertilization.

Monday, October 02, 2006 Completed
Dr. Bill Mohler more info Dept. of Genetics and Dev. Biology, U. of Conn. Health Center
"Making giant cells: Somatic cell fusion in C.elegans development"
Many animal tissues include multinucleated cells form by cell membrane fusion. In no system, however, is a clear molecular mechanism for this process known. In the nematode C. elegans, the gene eff-1 encodes an integral membrane protein that appears required and sufficient for the recognition and fusion of partner cells

Wednesday, September 27, 2006 Completed
Dr. Daniel L. Hartl (seminar at Waksman Auditorium) more info Harvard University
"Genetics and evolution of drug resistance in malaria"
Malaria accounts for one death every 10 seconds, primarily African children under the age of five, and drug therapy has been compromised owing to the evolution of parasite resistance. New approaches based on population genetics are being used to identify the genetic basis of drug resistance and establish a framework of detecting new drug resistance mutants as they arise.

Friday, September 22, 2006 Completed
Dr. Wendy Hanna-Rose more info Dept. of Biochem & Molecular Biology, Penn State University
"A little late, a deadly fate? Temporal mis-coordination of organogenesis within the C. elegans egg laying apparatus"
I use uterine and vulval development in C. elegans as a model to elucidate mechanisms directing organ formation and specifically aim to understand how connections form between lumens of two different organs during development. My talk will focus on our analysis of a new gene called cog-3, which has highlighted the importance of temporal regulation in promoting correct spatial development.

Wednesday, July 05, 2006 Completed
Dr. Shiaw-Min Hwang  Bioresource Collection and Research Center (BCRC), Food Industry Research and Development Institute (FIRDI)
"Disparate differentiation potential of human mesenchymal stem cells "
Mesenchymal stem cells (MSCs) are a population of multipotent cells with the capacity for self-renewal and differentiation potentials into various lineages including osteoblasts, chondrocytes, adipocytes, smooth muscle cells and even hepatocytes and neuronal cells. MSCs can be isolated from many tissues. This has raised the new strategies for cell therapy and regeneration. Some reports mentioned that MSCs isolated by different protocols from bone marrow were virtually indistinguishable on their cell surface markers and differentiation potentials. However, MSCs isolated from different tissues by the same protocol did show a significant difference in the capacity of differentiation. In this presentation, I’ll discuss the disparate characteristics of MSCs from human adult bone marrow, umbilical cord blood, and amniotic fluid based on different developmental stages. Cell surface marker analysis reveals that these MSCs were positive for SH2, SH3, SH4 (mesenchymal markers), CD13, CD29, CD44, CD90 (adhesion markers), HLA-A,B,C (HLA class I) and negative for CD34, CD45 (hematopoietic markers), HLA-DR, DP, DQ (HLA class II). However, amniotic fluid-derived MSCs possess both markers of mesenchymal and neural stem cells. Umbilical cord blood-derived MSCs have the strongest osteogenic potential. Bone marrow-derived MSCs showed a highest capacity of adipogenesis. The telomere lengths and growth potentials of MSCs are sequential reduced from amniotic fluid to umbilical cord blood and adult bone marrow. These data were consistent with the development of tissues and suggested that MSCs from different tissues should be considered in further applications as the best strategy.

Wednesday, May 24, 2006 Completed
Dr. Wanjin Hong more info Institute of Molecular and Cell Biology
"Membrane traffic in mammalian cells: role of SNAREs and GTPases"
It is becoming clearer that subcellular location of a protein is key to its function and regulation. The secretory and endocytic pathways play vital role in many cellular and physiological processes. I will describe the molecular machineries (particular the SNAREs, GTPases, PX domain proteins) that govern membrane traffic in the secretory and endocytic pathways of mammalian cells.

Friday, May 19, 2006 Completed
Dr. Kiley P-H Miller more info Schreiner University
"Molecular Recognition of Chlorine-Doped Polypyrrole"
Numerous processes have accomplished tissue platforms by non-specific protein adsorption, covalent attachment, biomolecule entanglement, and synthesis of new polymers with the desired functionality. The focus of this work is to modify the polymer’s binding capability to cells while not altering the bulk properties. Phage display and yeast surface display were used to modify the chlorine-doped polypyrrole (PPyCl) surface to facilitate binding of neuronal phenotype cells.

Monday, May 15, 2006 Completed
Dr. Paul Lasko more info McGill University, Montreal, Quebec
"Translational regulation in the Drosophila germ line"
Translational control is critical to establishing axial patterning in the one-cell Drosophila embryo. I will discuss the roles of Vasa, a DEAD-box RNA helicase, in regulating the translation of target RNAs involved in oogenesis and axial patterning. The seminar will also include information about how 4E-HP, a translational repressor that interacts with the 5' mRNA cap structure, regulates caudal and hunchback mRNAs and helps establish their spatially graded distribution

Thursday, May 11, 2006 Completed
Dr. Matthew State  Child Study Center & Dept. of Genetics, Yale Univ. School of Medicine, New Haven, CT
"Cherish the exceptions: outlier approaches to the genetics of Tourette syndrome"
Tourette syndrome (TS) is a highly heritable disorder characterized by vocal and motor tics. This seminar will discuss gene discovery efforts in TS. Particular attention will be paid to molecular cytogenetic approaches and the identification of SLITRK1 as a candidate gene in a small percentage of patients with TS.

Monday, May 08, 2006 Completed
Dr. Paul Sternberg more info Cal Tech
"Genomic control of organogenesis"
We use C. elegans vulval development to elucidate the signaling and transcriptional regulatory networks that underlie organogenesis. I will discuss how we use various bioinformatic and comparative genomic approaches to target our molecular genetic analyses to specific genes and transcriptional regulatory elements.

Monday, April 24, 2006 Completed
Dr. Gopala Kovvali more info President and Founder of Carcinogenesis Foundation, Edison, NJ
"Carcinogenesis in gastrointestinal tract: mechanisms and markers "
Ulcerative colitis and Barrett’s esophagus are the precancerous syndromes of colon and the esophagus respectively. I will discuss potential mechanisms and biomarkers that are associated with the carcinogenesis in these two diseases.

Thursday, April 20, 2006 Completed
Dr. Adam Eyre-Walker  Center for the Study of Evolution, University of Sussex, U.K.
"TBA"
TBA

Monday, April 10, 2006 Completed
Dr. Peter L. Hammer  RUTCOR - Rutgers Center for Operations Research
"Logical Analysis of Data and Its Medical Applications"
After briefly outlining the basic concepts and methods of the Logical Analysis of Data, we present applications of it for detection of ovarian cancer, risk stratification among cardiac patients, prediction of the quality of biomaterials, distinction of various types of diffuse large B-cell lymphomas, etc.

Thursday, March 02, 2006 Completed
Dr. Pin-Xian Xu  more info McLaughlin Research Institute, Great Falls, MT
"The Role of Eya and Six genes in mammalian sensory organ development"
Mutations in the human EYA1 and SIX1 cause Branchio-Oto-Renal (BOR) syndrome and we have generated mutant mice for Eya1 and Six1, providing two mouse models for studying the human syndrome. We have recently found that these two genes are also critical for sensory neurogenesis. The presentation will focus on their function in the neurogenesis and development of cranial sensory organs.

Monday, February 27, 2006 Completed
Dr. Dario Boffelli   Genomics, Lawrence Berkeley National Laboratory, Berkeley, CA
"Comparative genomics at the vertebrate extremes"
Comparisons with genomes at both the distal and proximal evolutionary edges of the vertebrate tree reveal different aspects of the functional components of the human genome. Sequence comparisons with distant, non-mammalian vertebrates identify only the most constrained functional elements and reveal several common regulatory sequences participating in the regulation of early vertebrate development. Conversely, the study of primate-specific biological functions is limited to comparisons using primate genomes. Multiple primate comparisons of the sequences of important genes participating in cholesterol homeostasis and atherosclerosis susceptibility have revealed regulatory sequences emerged in anthropoid primates after they split from prosimians, suggesting a role for the evolution of gene-regulatory sequences in contributing to phenotypic differences between species.

Wednesday, February 22, 2006 Completed
Dr. Douglas Ruden more info Environmental Health Sciences, Univ. of Alabama at Birmingham, Birmingham, AL
"Drosophila as a Model for Gene-Environment Interactions "

Monday, February 13, 2006 Completed
Dr. David Axelrod, Genetics Dept.; Dr. Howard Passmore, Genetics Dept.; Dr. Emmanuel Hey, Genetics Dept.; Dr. Philip Pauly, Dept. of History; Dr. Chi-hua Chiu-Groff, Genetics Dept.; Dr. Bill Sofer, Genetics Dept. 
"Darwin Day"
An informal symposium to celebrate the 197th anniversary of the birth of Charles Darwin

Thursday, February 09, 2006 Completed
Dr. Michael Olivier more info Med. College of WI, Human & Molecular Genetics Ctr, Physiology Dept., Milwaukee, WI
"How to find a needle in a haystack: The genetic analysis of complex disorders in humans."
The completion of the human genome project and the identification of large numbers of SNPs has opened the door to large-scale analyses of complex human disorders such as obesity or diabetes. I will describe novel integrated approaches combining genomics, proteomics, and systems biology for the dissection of these disorders.

Thursday, February 02, 2006 Completed
Dr. Sathees C. Raghavan  Univ. of Southern California, Keck School of Medi., Pathology Dept., Los Angeles, CA
"Mechanism of Lymphoid Chromosomal Translocation in Cancer"
It has been unclear why certain defined DNA regions are consistently sites of chromosomal translocations. Some of these are simply sequences of recognition by endogenous recombination enzymes, but most are not. Recent progress indicates that some of the most common fragile sites in human neoplasm assume a non-B DNA structures, namely deviations from the Watson-Crick helix. Because of the single-strandedness within these non-B structures, they are vulnerable to structure-specific nucleases. In my presentation I discuss these new findings.

Monday, January 30, 2006 Completed
Dr. George Gerton more info University of Pennsylvania Medical Center
"Progranulin Regulates Preimplantation Mouse Embryo Development"
Progranulin is an unusual cysteine-rich growth factor that regulates the growth of many epithelia. My laboratory has found that progranulin regulates the development of mouse preimplantation embryos by affecting the proliferation and, possibly, the formation of the first epithelium, the trophectoderm. Progranulin is an essential growth factor for the development of embryos to the blastocyst stage.

Monday, January 23, 2006 Completed
Dr. Joseph Bertino  CINJ, New Brunswick, NJ
"GENE THERAPY - Still Promising?"
Gene therapy studies began with the hope of correcting genetic diseases. Active areas of cancer research are to use gene therapy to kill cancer cells, e.g., “suicide gene therapy”, to boost the immune response against the tumor, or to transfer drug resistant genes into marrow progenitors to protect patients from marrow toxicity. Initial enthusiasm has been dampened by setbacks that are slowly being overcome. We now have found or generated by site directed mutagenesis, mutant forms of genes that express proteins (dihydrofolate reductase, thymidylate synthase) that are targets for drugs that are used to treat cancer. Based on preclinical studies, we have planned a clinical study that uses a retroviral construct, containing a fusion cDNA that will protect marrow cells from methotrexate and cytosine arabinoside, thus allowing higher and more effective doses of these drugs to be administered.

Monday, January 09, 2006 Completed
Dr. Goncalo Abecasis more info University of Michigan
"Large Scale Association Studies: Lessons from the HapMap Project and a Study of Macular Degeneration "
I will present a summary of linkage disequilibrium patterns in the genome, using data from the recently completed International HapMap Project. To illustrate the issues in using these data to conduct large scale association studies, I will present examples from a study of age-related macular degeneration.

Monday, December 19, 2005 Completed
Dr. Leonid Kruglyak  Princeton University
"Genetics of whole-genome gene expression patterns in yeast"

Monday, December 05, 2005 Completed
Dr. Gertrud Schupbach  Princeton University
"Regulation of EGF Receptor Signaling during oogenesis in Drosophila"
The spatial patterning of the egg and embryo of Drosophila depends on signaling events that occur during oogenesis. In particular the gene gurken (grk)which encodes a secreted molecule and acts as a ligand of the Drosophila EGF receptor, plays an important role in transmitting pattern information from the oocyte to the overlying follicle cells. The grk RNA is asymmetrically localized in oogenesis through the activity of several factors. Its translation is also highly regulated, in particular, there is an input from the meiotic cell cycle via two checkpoint kinases

Monday, November 28, 2005 Completed
Dr. Bruce G. Haffty  UMDNJ; Cancer Institute of NJ
"BRCA1/BRCA2 and the conservative management of breast cancer "
The conservative management of breast cancer by lumpectomy and radiation remains controversial in women who are carriers of BRCA1 and BRCA2 germline mutations. An overview of the controversy and current literature regarding breast conserving therapy as well as avenues for future investigation will be discussed.

Monday, November 21, 2005 Completed
Dr. Rene' Hen  Columbia University, New York City, NY
"Serotonin, the hippocampus and emotional behavior"
Serotonin is implicated in mood regulation, and drugs acting via the serotonergic system are effective in treating anxiety and depression. Specifically, agonists of the serotonin1A receptor have anxiolytic properties, and knockout mice lacking this receptor show increased anxiety-like behavior. We have used a tissue-specific, conditional rescue strategy to show that expression of the serotonin1A receptor primarily in the hippocampus and cortex, but not in the raphe nuclei, is sufficient to rescue the behavioral phenotype of the knockout mice. In addition, our results suggest that hippocampal neurogenesis is required to mediate the behavioral effects of antidepressants and point to a new role for the hippocampus in mood control.

Monday, November 14, 2005 Completed
Dr. Meng-Chao Yao  Fred Hutchinson Cancer Center, Seattle, WA.
"Genome reorganization through RNA-guided DNA deletion in Tetrahymena"

Monday, November 07, 2005 Completed
Dr. Josh Dubnau  Cold Spring Harbor Lab, New York
"Deconstructing memory in a fly"
The Dubnau lab studies memory formation in Drosophila using a variety of genetic techniques, behavioral assays and confocal imaging. We have used microarrays to identify genes involved with memory formation, and are using expression patterns of these genes to identify relevant anatomical circuitry. We then use a novel strategy transiently silence small groups of these neurons in vivo. This technique allows us to functionally manipulate the circuitry involved in learning, in memory storage, and even in memory recall.

Monday, October 10, 2005 Completed
Dr. Cooduvalli Shashikant  Pennsylvania State University
"Cis regulatory analysis of a mouse homeobox gene"
How cis-regulatory modifications drive morphological changes among closely related species is a subject of considerable recent interest. Employing comparative sequence and reporter gene analysis in transgenic mouse embryos, we have identified many changes among vertebrate Hoxc8 early enhancers. I will discuss how these enhancer modifications contribute to cis-regulatory evolution

Monday, September 19, 2005 Completed
Dr. Andrew Golden  NIH
"The C. elegans Myt1 ortholog is required for the proper timing of oocyte maturation"
Cdk1 drives cell cycle progression in all mitotic cells and is required for oocyte maturation. A negative regulator of Cdk1, Myt1, phosphorylates and inhibits Cdk1 activity in interphase cells and in developing oocytes. Myt1 depletion in C. elegans oocytes causes precocious maturation, inappropriate cell cycle progression and numerous developmental defects, which contribute to an infertile phenotype

Monday, September 12, 2005 Completed
Dr. Chris Rongo  Department of Genetics, Rutgers University, Piscataway, NJ
"The dynamic trafficking of glutamate receptors at neuronal synapses"
Neuronal communication occurs at chemical synapses, which are specialized junctions between presynaptic cells, which release neurotransmitters, and postsynaptic cells, which detect these neurotransmitters using receptor proteins. My research focuses on glutamate receptors (GluRs), which are ligand-gated ion channels that detect glutamate, the major excitatory neurotransmitter in the brain. The regulated localization of AMPA-type GluRs to synaptic membranes plays a critical role in synaptic plasticity, as well as in learning and memory. My lab has been identifying factors that regulate GluR localization and function using a genetic approach in the nematode C. elegans. We have developed fluorescent tools to monitor the dynamics of GluR localization in intact, behaving animals. So far we have identified and characterized over a dozen genes that facilitate channel assembly, activity-dependent trafficking, anchoring, endocytosis, ubiquitination, recycling, and degradation of GluRs. Our findings highlight the dynamic nature of synapses and synaptic components

Thursday, September 08, 2005 Completed
Dr. Andrew Singson  Department of Genetics, Rutgers University, Piscataway, NJ
"Sperm and egg genes required for fertilization in C. elegans: An overview from both the sides of the fertilization equation"
My lab has been pioneering the use of C. elegans as a model system for understanding the molecular mechanisms of fertilization. The most powerful advantage of this system is our ability to use both forward and reverse genetic approaches to identify genes that encode proteins required for sperm-egg interactions. We have recently identified a number of new genes required either by sperm or eggs for the events of fertilization. The spe-19 gene encodes a sperm surface receptor required for sperm activation and the acquisition of motility. The spe-38 gene encodes a novel sperm tetraspan integral membrane protein. Structurally similar tetraspan molecules have been implicated in many different cell-cell interaction events. The egg-1 and egg-2 genes encode LDL receptor repeat containing proteins that are localized to the oocyte plasma membrane. egg-1 and egg-2 are partially redundant. Loss of either egg-1 or egg-2 leads to a reduction in fertility. Loss of both genes leads to complete sterility and the production of oocytes that can never be fertilized by wild type sperm. The egg-3 gene encodes an anti-phosphatase required for egg activation or the egg to embryo transition after sperm entry. Our work is providing new insights into cell-cell interactions, conception and complements studies of fertilization in other species.

Monday, May 09, 2005 Completed
Dr. Andrew I. Brooks more info Department of Genetics/EOHSI, Rutgers University/UMDNJ
"Successes and Failures of Applied Genomics: A CNS Case Study"

Monday, May 02, 2005 Completed
Dr. Magnus Nordborg more info Biological Sciences, Molecular & Computational Biology Section, Univ. of Southern California, Los Angeles, CA
"Population Genetics and Genomics of Arabidopsis with Implications for Human Population Genetics and Evolution"
The results of a genome-wide survey of DNA sequence polymorphism in Arabidopsis thaliana will be presented, with particular emphasis on the practicability of carrying out genome-wide association mapping in this species.

Monday, April 25, 2005 Completed
Dr. Janis O’Donnell more info Biological Sciences, University of Alabama, Tuscaloosa, AL
"Stress tolerance in Drosophila: Roles of interacting genes in dopamine regulation"
Gene-environment interactions are thought to play roles in the etiology of the 90% of Parkinson’s disease cases with unknown causes. Variation in genes regulating dopamine homeostasis may be a key point of intersection with environmental agents. Data will be presented showing that mutations in dopamine regulating genes confer altered susceptibility to oxidative stress, which preferentially targets subsets of dopaminergic neurons. These effects are linked to physical interactions of the dopamine-regulating gene products.

Monday, April 18, 2005 Completed
Dr. Diana Myles  Molecular and Cellular Biology, University of California Davis, Davis, CA
"Genetic dissection of mammalian fertilization"
Sperm-egg interaction is a multistep process and determination of the molecular basis of these interactions has been difficult. Our recent studies have used mice with targeted deletions to study mammalian fertilization, extending from the first encounter of gametes at the zona pellucida through membrane fusion and the development of a block to polyspermy.

Monday, April 04, 2005 Completed
Dr. Vadim Bolshakov  MacLean Hospital, Harvard Medical School, Boston, MA
"Mechanisms of Synaptic Plasticity in Fear Learning"
My laboratory is using fear conditioning training paradigm as a model of associative learning. Our recent findings indicate that fear conditioning-induced neuronal plasticity and long-term potentiation in the amygdala synapses share common mechanisms of induction and expression. These findings provide the most direct evidence yet available that the mechanisms of LTP are recruited in the experimental animals and that such mechanisms might be utilized for memory storage.

Wednesday, March 30, 2005 Completed
Dr. Charles R. Cantor  Chief Scientific Director, SEQUENOM, Inc., San Diego, CA
"Applications of DNA Mass Spectrometry in Cancer and Other Human Diseases"

Monday, March 28, 2005 Completed
Dr. Shaying Zhao more info Mammalian Genomics, The Institute for Genomic Research (TIGR), Rockville, MD
"Genome Rearrangements in Mammalian Genome Evolution and Human Cancer Development"
Genome rearrangements cause genome reconfiguration, facilitating speciation during evolution but contributing to cancer development and progression in abnormal conditions. To understand significance and mechanisms of rearrangements in these two biological processes, we have been comparing genomes of different species as well as normal vs. diseased genomes within the same species.

Monday, March 28, 2005 Completed
Dr. John H. Wilson  Department of Biochemistry, Baylor College of Medicine, Houston, TX
"Triplet Repeat Instability "
Expansions of triplet repeats cause several human neurological diseases. Two critical questions are: Why are repeats unstable? How do expansions cause disease? We focus on the pathways for repeat instability in mammalian cells. Our work points to likely processes that destabilize repeats in the germline and somatic cells of patients.

Monday, March 21, 2005 Completed
Dr. Patrick Sung  Yale University, New Haven, CT
"Biochemistry of Recombination"

Friday, March 18, 2005 Completed
Dr. Ju-Seog Lee more info Lab of experimental carcinogenesis, National Cancer Institute/ NIH, Bethesda, MD
"Integrative functional genomics: classification of cancer and identification of potential therapeutic targets for patient treatment"
In order to gain better insights on human tumor development, gene expression profiles of mouse cancer models as well as other animal models for organ regeneration were integrated with those of human cancer. This approach, integrative functional genomics, allows reclassifying human cancers that are homogeneous in prognosis and underlying biology of tumor development.

Wednesday, March 16, 2005 Completed
Dr. Kyriacos Markianos  Computational Biol. Program, Public Health Sciences Div., Fred Hutchinson Cancer Research Ctr., Seattle, WA
"Efficient Calculation of Linkage Statistics and Sequence-based Linkage Analysis"
At present, multipoint algorithms used to reconstruct inheritance in linkage studies run into computational limits for pedigrees containing more than one to two dozen individuals. I will present new approaches that allow exact and approximate solutions for pedigrees that were previously intractable. In a separate project, I investigate the utility of DNA sequencing for simultaneous discovery and typing of polymorphisms in family linkage studies.

Monday, March 07, 2005 Completed
Dr. Youhai Chen more info Pathology, Univ. of Pennsylvania School of Medicine, Philadelphia, PA
"Genes and genomics of autoimmune inflammation"
Development of autoimmune diseases requires coordinated expression of myriad genes. Functional genomic studies of autoimmune inflammation in the central nervous system (CNS) revealed a number of unique clusters of genes which represent putative immune and nervous responses in autoimmune inflammation. Using animal models of multiple sclerosis and arthritis, Dr. Chen and colleagues are focusing on the following groups of genes: the Rel/nuclear factor-kB family, arginase, p53 and PDCD4.

Monday, February 07, 2005 Completed
Dr. Kendal Broadie more info Biological Sciences, Vanderbilt University, Nashville, TN
"A Drosophila Model of Fragile X Disease"
Fragile X is the most common form of inherited mental retardation. The disease is caused by loss of the selective RNA-binding protein FMRP, believed to result in defective synapse formation and/or plasticity. We generated a Drosophila model to test these hypotheses. This seminar will include genetics tests, mutant clonal analyses, ultrastructural imaging and proteomics.

Monday, January 31, 2005 Completed
Dr. James Millonig  Dept. Neurosci. & Cell Biol., UMDNJ and Dept. of Genetics Rutgers Univ., Piscataway, NJ
"Vacuolin and ENGRAILED2: Integrating mouse CNS development with the genetics of human cataracts and Autism Spectrum Disorder."
My lab uses mouse genetics to study the genetic basis of 3 human neurodevelopmental disorders: congenital cataracts, neural tube defects and Autism Spectrum Disorder (ASD). Our recent positional cloning of the vacuolated lens locus has identified a novel receptor necessary for both neural tube closure and lens development. Using our background in mouse genetics, developmentally relevant candidate genes were selected and tested for association. In collaboration with Linda Brzustowicz MD, Neda Gharani PhD, and Emanuel DiCicco-Bloom MD, genetic and functional data have been generated that is consistent with the homeobox transcription factor ENGRAILED 2 acting as an ASD susceptibility locus.

Monday, November 15, 2004 Completed
Dr. Susan Slaugenhaupt  Center for Human Genetic Research, Massachusetts General Hospital/Harvard Medical School, Boston, MA
"Tissue-specific mis-splicing of IKBKAP in Familial Dysautonomia "
Familial dysautonomia is a hereditary sensory and autonomic neuropathy, and all FD patients tested to date carry an IVS20+6T→C mutation in the IKBKAP gene. This mutation causes mis-splicing of the mRNA and results in incomplete skipping of exon 20. Previously, we reported that all FD tissues tested express both wild-type (WT) and mutant (MU) IKBKAP mRNA and protein. Accurate measurement of the ratio of the two mRNA species using both densitometry and real-time quantitative PCR has revealed that the levels of WT IKBKAP mRNA vary between tissues and are lowest in central and peripheral nervous systems. Our observations suggest that the relative inefficiency of WT IKBKAP mRNA production from the mutant alleles in the nervous system underlies the selective degeneration of sensory and autonomic neurons in FD. Therefore, a promising route toward an effective therapy for FD may come from enhancement of correct mRNA splicing in order to increase cellular levels of IKAP. I will discuss our efforts aimed at understanding and repairing the defective splicing process.

Monday, November 08, 2004 Completed
Dr. J