Faculty: A–F

Our lab studies the interaction between neurons and their enviroment. We use genetics and cell biolgy to examine how the extracellular matrix orchestrates the formation of neural networks by directing axon outgrowth and synapse formation. We examine mutants in the matrix that cause Muscular Dystrophy like defects in the C. elegans neuromuscular system. Our research is focused on understanding how these molecules function in establishing these essential structures.

Ewing sarcoma is the second most common bone tumor in children. The common molecular abnormality in Ewing sarcoma is the aberrant chimeric fusion protein, EWS/FLI1. My research goal is to elucidate the molecular mechanism whereby the Ewing sarcoma fusion protein EWS/FLI1 leads to malignant transformation. We will directly address the molecular basis for the EWS/FLI1 fusion in vivo in the zebrafish, an animal model that is amenable to genetic screening for second hit mutations or suppressor genes.

My lab is focusing to understand the role of posttranslational modification by SUMO in respect to cell cycle regulation. Both genetic and biochemical evidence indicate that the SUMO modification pathway have critical role in mitosis. My lab will study the biochemical and cell biological function of SUMO modification in mitosis by using frog egg extracts in vitro assay system. I have identified couple of SUMO-modified proteins in mitotic egg extracts and would pursue biochemical analysis of these proteins.

We study how multiple T cell signaling regulates T cell activation, adhesion, migration/homing, differentiation and function, and how the T cell surface molecule ICAM-1 plays a role in these processes. We use mouse models to study thymic differentiation and the role of ICAM-1 in resistance to infectious disease. We study post thymic differentiation of naïve T cells in young and aged humans. We study the participation of signaling through ICAM-1 in autoimmune diseases such as rheumatoid arthritis.

The specialized shapes of epithelial cells determine the structure of organs, which in turn helps determine organ function. How doges an initially round cell change its form to become a long hollow tubule, as in the kidney and blood vessels? We have taken two genetic approaches to studying this problem in the small roundworm C. elegans. We are cloning 12 genes that regulate the structure of tiny tubules in this worm, and characterizing their function by means of light and electron microscopy. The genes encode proteins that form and maintain the protein cytoskeleton at the inner surface of the tubule. In addition, we are studying gene that affect formation of the human kidney, and examining the function of this gene in worms. It is an ion channel that regulates worm behaviour, and we are studying the electrical properties of this protein.

In Drosophila, proteins that direct the formation of the embryo's head and tail are prelocalized to the egg's anterior and posterior ends, respectively, during oogenesis. My lab is interested in understanding how such asymmetries arise. More than a dozen localized mRNAs have been identified in the Drosophila oocyte. Related projects include a study of the mechanisms that prevent the translation of mRNAs during localization, and the identification of genes that control microtubule organization.

My lab is interested in the molecular switches that control cell fate decisions during development. Our focus is muscle formation during embryogenesis of the fruit fly, D. melanogaster. In a second project, we are studying the structure-function relationship of the neurogenic gene, big brain (bib).

Herpes simplex virus type 1 (HSV-1) is a human pathogen that has two distinct infections during its viral lifecycle: productive and latent. A key player in determining the outcome of whether an infection will be productive or latent is the viral gene product, infected cell protein 0 (ICP0). My laboratory is interested in examining how cellular factors regulate the function of ICP0 during viral infection, and how ICP0, in turn, modulates the activities of cellular factors.

Our research is focused on understanding the protein-protein interactions involved in bacterial and viral pathogenesis. Our goal is to determine how bacterial pathogens assemble a protein machinery used to deliver protein toxins into target cells and thereby cause human diseases. We are also interested in the protein-protein and protein-RNA interactions involved in the assembly of hantaviruses, a group of emerging infectious agents that can cause the hantaviral cardiopulmonary syndrome and the hemorrhagic fever with renal syndrome in humans. We use protein NMR spectroscopy, biophysical spectroscopy, mutagenesis, and cell-based assays to achieve our research goals.

The goal of my lab is to understand the mechanisms that regulate cell and organelle growth. Most of our work is focused on the growth and disassembly of microtubules in eukaryotic cilia and flagella because these organelles can be approached with a variety of morphological, biochemical, and molecular biological techniques.

My primary research interest is understanding the regulation of gene expression (especially positive regulation) at a molecular level. In our lab we examine the molecular biology of gene regulation in E. coli, with a focus on the L-rhamnose catabolic genes, and the fact that the L-rhamnose regulator genes are members of the AraC family of regulatory proteins. Many AraC family proteins are regulators of virulence factors in bacterial pathogens, therefore, we use the L-rhamnose regulators as models to understand the function of proteins in this family. Our ultimate goal is to identify small molecules that block the function of AraC family proteins and have potential as anti-bacterial agents.