Stanford University » Ph.D. Programs » Biosciences Programs

The Department of Genetics at Stanford University School of Medicine provides opportunities for Ph.D. study in a broad array of areas overlying a consistent intellectual framework. All major areas of modern genetics are represented in the Department, including identification and analysis of human disease genes; molecular evolution; host-pathogen/symbiont interactions; gene therapy; statistical genetics; application of model organisms to problems in biology, medicine, and environmental conservation; and computational and experimental approaches to genome biology. The Department also includes the Stanford Human Genome Center, the Stanford Genome & Technology Center, the Saccharomyces Genome Database (SGD), the Pharmacogenetics and Pharmacogenomics Knowledge Base (PharmGKB), the Tetrahymena Genome Database (TGD), the Candida Genome Database (CGD), and the Stanford Microarray Database (SMD); together, these provide resources and opportunities for large-scale and/or high-throughput approaches to biomedical research.
       An underlying theme in our Department is that genetics is not merely a set of tools but a coherent and fruitful way of thinking about biology and medicine. To this end, we emphasize a spectrum of approaches based on molecules, organisms, populations, and genomes. We provide training through laboratory rotations, dissertation research, seminar series, didactic and interactive coursework, and an annual three-day retreat of nearly 200 students, faculty, postdoctoral fellows, and research staff. The mission of the Department includes education and teaching as well as research; graduates from our program pursue careers in many different venues including research in academic or industrial settings, health care, health policy, and education. The Department is committed to increasing diversity, and also plays a leading role in local community educational outreach programs.

For more information contact:
Graduate Program
Administrative Associate
Department of Genetics
300 Pasteur Drive
Lane Building Rm. 329
Stanford, CA 94305-5120
(650) 723-3335
(650) 725-7016 (fax)
genetics-info@genome.stanford.edu
http://genetics.stanford.edu

Faculty and their Research Interests

Russ Altman. The Helix Group (http://helix-web.stanford.edu/) applies techniques from bioinformatics and computational biology to problems in pharmacogenomics, protein structure/function annotation, RNA folding and dynamics, and physics-based simulation of biological structure. A major thrust is informatics resources to help understand the link between genotypes and phenotype, in order to accelerate personalized medicine. Methods include machine learning, data mining, natural language (text) processing, nonlinear optimization, and simulation methods.

Laura Attardi. Our laboratory uses the mouse as a model system to dissect the function of the p53 tumor suppressor gene. Our interests include studying target genes involved in p53-mediated apoptosis by cell biological and genetic methods. Our studies of one such p53 apoptosis-associated gene, Perp, have revealed important roles in both apoptosis and epithelial function. In addition, through the generation and analysis of p53 knock-in mutant mice, we are dissecting p53 function in tumor suppression in vivo.

Julie C. Baker. Molecular basis for cellular differentiation and patterning during mammalian gastrulation; mesoderm induction; neural induction; anterior/posterior patterning; TGFb signal transduction Xenopus embryology; expression cloning; functional genomics

Gregory S. Barsh. We study the genetic pathways that give rise to color variation, in model systems and in natural populations. We are interested both in both mechanisms relevant to human biology and disease, and in genetic architecture of natural variation as a way to learn about the history and diversity of our species.

Anne Brunet. Our lab studies the molecular basis of aging and age-related diseases. We use a combination of genetic, genomics, and proteomics approaches to investigate the genes involved in longevity in a range of model organisms. We are particularly interested in the role of FOXO transcription factors and SIRT deacetylases in aging and age-related disorders. We are also exploring the importance of the nervous system in controlling aging and longevity.

Michele P. Calos. Our laboratory is developing novel vectors and strategies for gene therapy and genome engineering. Our work centers on the development and application of site-specific integrases for genomic integration.

L. Luca Cavalli-Sforza. My research is dedicated to the study of the origin of modern humans and their evolutionary history by using genetic markers. In my laboratory, researchers generate a great variety of new markers using new techniques such as DHPLC. Presently, the laboratory is concentrating on the study of the Ychromosomes.

J. Michael Cherry. Bioinfomatics and computational biology applied to genomic information describe the efforts in the group. We specialize in exploring the volumes of information that have been elucidated for the budding yeast, Saccharomyces cerevisiae. Our focus is in two areas of research using computers and databases as tools: designing databases and software tools to effectively provide biological information to the biomolecular research community, and development of ontologies and controlled vocabularies used in biological annotation.

Stanley N. Cohen. Regulation of gene expression in prokaryotes and eukaryotes. This work includes investigation of the Tsg101 tumor susceptibility gene, replicative senescence, RNA decay, and aspects of plasmid biology. A small bioinformatics group has developed a computer-based expert system for analyzing genetic data.

Ronald W. Davis. Our laboratory is focused on the development and application of molecular biology, manipulative genetics to a variety of problems. As model organisms, we generally use Saccharomyces cerevisiae and Arabidopsis thaliana. We are studying the replication of artificial yeast chromosomes and are investigating the effect of spacing of the origins of replication on chromosomal stability.

Andrew Fire. We study a variety of natural mechanisms that are utilized by cells adapting to genetic change. These include mechanisms activated during normal development and systems for detecting and responding to foreign or unwanted genetic activity. At the root of these studies are questions of how a cell can distinguish “self” versus “nonself” and “wanted” versus “unwanted” gene expression.

James M. Ford. Mammalian DNA repair and DNA damage inducible responses; P53 tumor suppressor gene; transcription in nucleotide excision repair and mutagenesis; genetic determinants of cancer cell sensitivity to DNA damage; genetics of inherited cancer susceptibility syndromes and human GI malignancies; clinical cancer genetics of BRCA1 and BRCA2 breast cancer and mismatch repair deficient colon cancer.

Uta Francke. Human genetic disorders and mouse models: Functional consequences of MECP2 mutations causing Rett syndrome; imprinted genes in Prader-Willi syndrome; genes responsible for cognitive and behavioral profile in Williams syndrome

Margaret T. Fuller. Regulation of stem cell division and self-renewal; Cell type specific transcription machinery and the regulation of cell differentiation; Developmeantal regulation of cell cycle progression during male meiosis; Molecular dissection of the mechanism of cytokinesis.

Leonard A. Herzenberg. Gene Regulation; Molecular Immunology; Lymphocyte subsets; Fluorescence-Activated Cell Sorter (FACS) development; AIDS; Apoptosis; Redox Regulation; Gene Arrays; and the therapy of AIDS using the anti-oxidant N’ acetylcysteine (NAC)

Leonore A. Herzenberg. B-cell development; 1g rearrangement and repertoire analysis; T cell regulation of antibody responses; T cell subsets; glutathione regulation of HIV disease progression; Fluorescence-Activated Cell Sorting (FACS) related software development and gene arrays.

Mark A. Kay. The laboratory focus is to: (1) develop the scientific principles required for developing novel non-viral and viral-vector based gene transfer technologies,  (2) study the molecular process of vector transduction in vivo, (3) develop RNAi based therapeutics, (4) define the mechanisms of RNAi/microRNA induced gene silencing in mammals, and (5)   establish the molecular process of RNA-directed RNA transcription in mammals. Our major disease targets are viral hepatitis, hemophilia, and diabetes mellitus.

Joseph Lipsick. Our laboratory utilizes genetics, biochemistry, and cell biology to understand the function and evolution of chromosomes in animals. Our wedge into this problem is the Myb gene family, first identified because altered forms of c-Myb cause leukemias and lymphomas in vertebrate animals. Three closely related Myb genes are present in vertebrates, whereas invertebrate animals including the sea urchin and the fruit fly have a single Myb gene. The Myb proteins are nuclear and bind to specific DNA sequences. We have shown that in the absence of Myb, Drosophila display abnormalities of chromosome condensation, chromosome segregation, and mitotic spindle assembly. The Myb protein localizes to euchromatin, not pericentric heterochromatin. Myb is part of a larger complex that includes the protein products of the RB tumor suppressor gene, the E2F-DP DNA binding proteins, and various other proteins that modify and/or bind to histones.

Richard M. Myers. Our laboratory studies the human genome, with interests in understanding how allelic variation and gene expression changes contribute to understanding a wide range of human traits, including diseases, behaviors and other phenotypes. We use high-throughput genomic methods, including DNA sequencing, genotyping, ChIP, mRNA expression profiling, transcriptional promoter and methylation measurements, and computational and statistical tools to identify, characterize and understand the functional elements encoded in our genomes.

John Pringle. The work in my laboratory exploits the power of yeast as an experimentally tractable model eukaryote to investigate fundamental problems in cell and developmental biology such as the mechanisms of cell polarization and the role of membrane reorganization in cytokinesis. In addition, a new project involves developing the small sea anemone Aiptasia pallida as a model system for study of the cell biology of the dinoflagellate-cnidarian symbiosis, which is critical for the survival of the reef-building corals.

Julien Sage. The retinoblastoma tumor suppressor gene (RB) is mutated in a broad range of human tumors. Our goal is to take advantage of the central role of RB in cell cycle control and tumorigenesis in order to address basic issues in cancer. To this end, we develop mouse models of human cancers associated with loss of RB function. Using these models, we aim to identify the cell of origin of cancer, the order of mutations involved in cancer progression, and the molecular mechanisms of tumorigenesis.

Matthew P. Scott. We study the genetic regulation of development and disease. Our research is focused on evolutionarily conserved regulators of development and their links to birth defects, cancer, and degenerative disease. We employ genetics and genomics approaches, along with molecular cell biology, to study fly and mouse development. Specific areas include Hedgehog/ patched signaling and its links to brain cancer, genetic control of body size, development of the neural tube and cerebellum, intracellular organelle trafficking and Niemann-Pick neurodegenerative disease, and effects of neural activity on neural development.

Gavin Sherlock. We use experimental laboratory and computational approaches to solve biological problems. We are using microarray technology to define all transcripts in the yeast genome, and to understand the changes in genome architecture and the transcriptome that occur in yeast as they evolve in vitro. We are also developing novel yeast strains for use in biofuel production, with the aim of being able to ferment five carbon sugars such as xylose, as well as 6 carbon sugars into ethanol. In addition, we developed and run the Stanford Microarray Database, the Tuberculosis Database, the Candida Genome Database, and SOURCE. Finally, we also write software for the analysis and visualization of microarray data, including GO::TermFinder, Caryoscope, and GeneXplorer.

Arend Sidow. We are computationally oriented with a significant experimental component. All projects in the lab leverage genome-scale evolutionary sequence analyses to illuminate the function of regulatory elements and proteins. (1) We have established an oracle database and java analysis pipeline by the name of ProPhylER (Protein Phylogenies and Evolutionary Rates) for comprehensive evolutionary analyses and functional predictions of eukaryotic proteins. (2) We are developing methodology to predict the deleteriousness of SNPs on the basis of comparative sequence analyses. (3) We are using the urochordate Ciona as a model for comparative genomics, and for experimental tests of predicted regulatory elements during embryonic development.

Tim Stearns. The central question in our work is how cells accurately segregate their genome at each cell division. The work is focused on the centrosome, a unique organelle at the center of the cell that organizes the cytoskeleton and serves as a site for integration of cellular signals. We use the tools of cell biology, genetics, and biochemistry in systems ranging from yeast to human cells to understand how the centrosome duplicates once per cell cycle, and how centrosome defects are involved in the genome instability that is observed in many types of cancer.

Zijie Sun. We investigate the transcriptional processes that govern the transformation of normal mammalian cells to neoplastic state. Specifically we are interested in the molecular mechanism of the nuclear hormone receptors in the pathogenesis of human tumors.

Man-Wah Tan. Genome-wide analysis of host-pathogen interactions. We apply a variety of genetic and genomic tools on our model host C. elegans to dissect the components of the innate immune system as it interacts with the human pathogens P. aeruginosa, S. enterica and E. faecalis. We focus on defining the roles of the conserved TGF-beta and the Insulin pathways, and GATA transcription factors in modulating innate immune response. Our other focus is the elucidation P. aeruginosa virulence mechanisms.

Hua Tang. I am interested in various aspects of human genetics and genomics, including statistical and population genetics, mapping of disease-susceptibility loci, and the inference of evolutionary history of human populations. By integrating evolutionary theory into statistical modeling, my theoretical research aims at developing methods for identifying disease-susceptibility loci in stratified or admixed populations, and methods for genome-wide association studies. My applied research includes a large population-based study of the genetics of hypertension in humans. I have also collaborated on genetic studies of asthma in the Hispanic population, neurological disorders in the Romani population, and lysosomal storage diseases in the Jewish population.

Anne M. Villeneuve. Mechanisms underlying pairing and recombination between homologous chromosomes during meiosis, using the nematode Caenorhabditis elegans as an experimental system. High-resolution 3-D imaging of meiotic chromosomes. Transgene-mediated cosuppression of germline gene expression.

Douglas E. Vollrath. Work in our laboratory is focused on understanding basic processes in the eye that are relevant to human health and disease. We use a combination of human and rodent genetics, genomics, and cell biology to understand processes such as circadian regulation of photoreceptor renewal, phagocytic clearance of apoptotic cells and debris, the interdependence of photoreceptors and adjacent polarized retinal epithelial cells, age-related retinal changes, and the mechanisms by which misfolded proteins cause neurodegenerative blindness. Our studies connect with areas of investigation outside of the eye including tissue remodeling, autoimmunity, and neurodegeneration.

 

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