To ensure that cells function normally, tens of thousands of genes must be turned on or off together. To do this, regulatory molecules – transcription factors and non-coding RNAs – simultaneously control hundreds of genes. The Hammell lab studies how the resulting gene networks function and how they can be compromised in human disease. This includes an emphasis on developing novel tools for the statistical analysis of high-throughput data, developing novel algorithms for modeling the flow of signals through genetic pathways, and importantly, testing these models using the tools of molecular genetics.
One particular focus of the M. Hammell lab is to apply these novel statistical analysis methods to better understand how transposable elements are controlled in animal cells. Transposons are viral-like parasites that lay dormant within our genomes, but have the capacity to hop into new genomic locations, causing mutations as they break the surrounding DNA sequence. Mounting evidence has implicated transposon activity in a host of human diseases, with particular evidence for activation in several neurodegenerative diseases, including Amyotrophic lateral sclerosis (ALS) and Fronto-Temporal Dementia (FTD). By combining the power of systems-level, high-throughput data analysis with patient-derived ALS and FTD diseased tissue samples, the lab aims to better understand how these viral-like parasites contribute to cell death and disease.
Gene regulatory networks; integrated genomic analysis; bioinformatics; RNA biology; small RNAs; Transposable Elements
External funding sources
We wish to acknowledge the following groups for providing us additional funding for our research.