2012 bioinformatics projects in Louisiana:
Molecular etiology of neural tube defects under conditions of maternal diabetes
Principal Investigator: J. Michael. Salbaum, PhD
Associate Professor, Regulation of Gene Expression
Pennington Biomedical Research Center, Baton Rouge, LA
The main research focus of the laboratory is the molecular etiology of neural tube defects under conditions of maternal diabetes. Diabetes is a well-known teratogen that can cause neurulation failure, leading to defects such as anencephaly or spina bifida. Using mouse models of either chemically induced or naturally occurring diabetes, we seek to understand how maternal diabetes affects transcriptome and epigenome of the developing embryo at the time of neural tube closure, and how those changes relate to birth defect phenotypes. We use next-generation sequencing technology to address these questions, with tag sequencing to measure gene expression, and chromatin immunoprecipitation sequencing to evaluate epigenomic changes. Bioinformatics approaches are used for determination of differential gene expression, identification of expression variability, pattern extraction and pathway analyses, comparative gene expression analyses between different diabetes modalities, evaluation of epigenomic landscapes under normal or diabetic conditions, and the correlation between respective epigenomic and transcriptomic differences elicited by maternal diabetes.
Mobile element related genetic variation
Principal Investigator: Mark A. Batzer, Ph.D.
LSU System Boyd Professor, Comparative Genomics
Department of Biological Sciences, LSU, Baton Rouge, LA
My laboratory is interested in the study of mobile element related genetic variation. The Alu family of mobile elements comprise approximately 10% of primate genomes and are responsible for a number of different genetic disorders. These elements are one type of L1 element dependent retrotransposon that is specific to the Primate order. A third composite retrotransposon termed SVA is restricted to hominids and also dependent on L1 elements for mobilization. Collectively these retrotransposons make up over half of primate genomes both in terms of copy number and overall mass. Mobile elements play a significant role in the generation of genomic diversity through a variety of processes such as insertional mutagenesis, transduction, recombination and double strand break repair. The projects within the laboratory focus on the computational analysis of mobile elements derived from different mammalian genome assemblies and the experimental analysis of the various types of genetic variation associated with the elements.