Pearce Lab

Dave Pearce, PhD. (Principle Investigator)
I am fortunate to guide the following individuals in our pursuit of understanding the molecular basis of lysosomal storage disorders such as Batten disease. (top)

Brenda Cadiz-Rivera - Graduate student, Biochemistry, Molecular and Cell Biology  (top)

Chun-Hung Chan, PhD. - Post Doctoral Fellow
As a developmental neurobiologist, I am interested in the mouse Cln3-/- mutant model from a developmental standpoint. In particular, I am looking at changes observed in the structure of the cerebral cortex in animal models of Batten disease, with the aim to link these structural abnormalities to functional changes in the brain. Using classical histological methods combined with molecular biology, biochemistry, and cell biology techniques, we hope to elucidate further the neurodegenerative changes that occur, thus helping us to understand the underlying causes of this disease. (top)

Timothy Curran, M.S. - Technical Associate
I manage the everyday operation of the lab which includes ordering supplies, managing the animal colonies, purchasing equipment and supplies, maintaining equipment, maintaining the web sites, supervising undergraduates and technicians and helping lab members with their work. My scientific duties include: overseeing the animal colonies, genotyping mice and various molecular biology projects involving mutagenesis and dissection of yeast. (top)

Rozzy Finn - Graduate student, Biochemistry, Molecular and Cell Biology  (top)

Amanda Getty - Graduate student, Biochemistry, Molecular and Cell Biology As a biochemist, I focus on the proteins and the subsequent mutations that cause JNCL.   Specifically, I use a mouse model to elucidate the role of protein interactions in hopes of understanding how these proteins function and how alterations in these interactions and functions lead to Batten disease. (top)

Attila Kovacs, PhD. - Research Assistant Professor
Mutations in the CLN3 gene cause Batten disease but the function of the CLN3 protein is still unknown. To shed some light on CLN3 function in neurons, I have been performing comparative studies in cerebellar granule cell cultures prepared from wild type and CLN3 knockout mice. Using cell and molecular biological approaches, the involvement of CLN3 in cell fate determination, neurotransmitter receptor expression, trafficking and degradation will be determined. (top)

Neda Muzaffar - Graduate student Genetics, Genomics and Development
I am currently working on using Caenorhabditis elegans as a model system to study Battens disease. My work involves studying the three worm orthologs cln-3.1, cln-3.2 and cln-3.3 which through protein sequence analysis show about 40% similarity to the human cln3 gene implicated in Battens disease. I am currently in the process of screening deletion strains, comparing multiple sequence alignments for phylogenetic analysis as well as generating a triple mutant strain for further phenotypic characterization of the cln3 worm mutants. I expect these efforts to provide powerful and novel insights into the function of the human cln3 gene and possible relevance to Batten's disease. (top)

Seasson Phillips, PhD. - Post Doctoral Fellow
Mutations in CLN3 are found in patients with JNCL or Batten disease. I work on the yeast model of the disease. The gene product of BTN1, the yeast homolog of human CLN3, is implicated in vacuolar amino acid transport, but whether it is the actual transporter or has some other function is yet to be determined. My project takes advantage of the relative ease in using yeast biochemically and genetically to elucidate the function of Btn1p in the vacuole. (top)

Karyn Schmidt - Graduate student, Biochemistry, Molecular and Cell Biology  (top)

Sabrina Seehafer, M.S. - Graduate student Biochemistry, Molecular and Cell Biology
As a biochemistry graduate student the focus of my thesis research will be looking at the biochemical defects in the Battens disease patient lymphocyte cells line and the mouse model. I will use various biochemical and molecular techniques to help get an understanding for different defects caused by the disease and their implications, whether it be a upstream or downstream effect. (top)