During normal development and ageing the cells in our body can acquire somatic mutations through diverse genome instability processes. These mutations are propagated and selected for over time. As consequence, we are actually a mosaic of unique somatic cell genomes, where any given cell in a tissue may be genetically distinct from another.
Understanding how somatic mosaicism develops and evolves are central questions in the Sanders laboratory. With a focus on the genome, we develop and apply innovative single cell methods that explore the mechanisms of genome instability to understand how mutations arise and change cellular phenotypes in normal human tissues and disease states.
By integrating multi-omic experimental and computational readouts, we ask how individual cells differ in terms of their unique genomic profiles, epigenetic programs and transcriptional outputs, and directly test the functional outcomes of somatic mutations to understand how they contribute to tissue homeostasis and human disease.
