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. My group studies how the resulting gene networks function and how they can be compromised in human disease.
Human development requires the regulated activity of thousands of genes in hundreds of distinct cell types throughout life. One requirement for this process is that each cell must contain an intact, functional genome free from mutations. One type of mutation can arise from the activation of transposable elements (TEs). These viral-like parasites 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 TE activation in neurodegenerative diseases: Amyotrophic lateral sclerosis (ALS) and fronto-temporal dimensia (FTD).