The Watson lab is focused on the notorious human pathogen, Mycobacterium tuberculosis, which remains a major global health threat.  M. tuberculosis has evolved a variety of specific adaptations to not only survive but also replicate within the harsh environment inside a macrophage.  We want to understand how host macrophages sense and respond to M. tuberculosis and how specific host proteins regulate the outcome of M. tuberculosis infection, both inside macrophages ex vivo and in a mouse model of infection. We have recently started to focus on the interface between mitochondria and M. tuberculosis. Specifically, we are interested in uncovering the molecular mechanisms that explain why mutations in several genes related to mitochondrial function confer susceptibility to M. tuberculosis in humans.

The Patrick lab is passionate about post-transcriptional regulation of gene expression in eukaryotic cells. Using a multi-disciplinary toolset, we probe the molecular mechanisms that macrophages use to activate an innate immune response that is rapid, robust, and regulated. We mainly study how RNA binding proteins control the ability of macrophages to respond to infection, using a variety of bacterial and viral models. By working to uncover how RNA binding proteins work and how macrophages functionalize RNA binding proteins to orchestrate a fine-tuned innate immune response, our work furthers our understanding of a variety of human diseases. We have also started to study how myeloid cancer-associated splicing factor mutations alter inflammation and innate immune responses.