Common diseases, such as osteoporosis, impart significant societal health burdens. These diseases are, in part, regulated by genetic determinants and understanding their genetic basis is critical to the development of effective therapeutics. In recent years, technological advances, such as sequencing the genomes of multiple species and the ability to perform bioassays in a massively parallel fashion, have made it possible to begin to understand disease in a systems context. Systems-biology attempts to determine the direct and interactive roles of all cellular and physiological components (transcripts, proteins, metabolites, etc.) in diseased and normal states using data from high-throughput genomic studies.

Our lab is using systems approaches to investigate the molecular basis of bone strength. The goal of this work is to combine genetics and global gene expression profiling in the mouse to identify genes and pathways which influence bone strength related traits using techniques such as causality modeling between expression and physiological traits and generating disease focused gene co-expression networks. An additional component of this work is testing hypotheses generated by systems-analyses using in vitro cell based assays and transgenic mouse models.