Lab focus: Functional epigenomics and gene regulation

In normal and healthy cells, the activity of genes encoded in our DNA must be precisely controlled to prevent disease. My lab studies exactly how errors in this gene regulation can change the behavior and function of B cells, an important cell type in our immune system that makes antibodies to fight and remember infections.

We use advanced genomics and bioinformatics to understand how specific proteins interact with and regulate DNA in B cells, as well as examining how changes in the DNA sequence disrupt normal gene activity to cause autoimmune diseases like lupus.

Research interest

The King lab aims to understand how defects in the epigenetic control of gene expression are involved in human disease. Building on our recent detailed single-cell transcriptomic and epigenomic profiling of the human immune system, with a particular focus on B cells, we are currently studying:

1. How immune-specific chromatin-based mechanisms regulate gene expression
2. Whether autoimmune-associated genetic risk loci disrupt regulatory function of enhancers
3. If disease-specific epigenomic networks exist in autoimmunity

To achieve this, the lab uses both experimental and computational approaches, combined with in vitro cell cultures and ex vivo immune organoids as model experimental systems for human B cell biology. We integrate results from our lab-based analyses with datasets from “real world” patient single-cell transcriptomic and epigenomic datasets, and vice versa, with the long-term aim to provide translational insights into how epigenetic dysregulation in the immune system is linked with disease.