Our lab studies how genome structure and chromatin regulation shape cell identity, stability, and dysfunction. While cell types are often defined by their gene expression profiles, we aim to understand the deeper regulatory architectures that enable cells to maintain or lose their identity across development, aging, and disease. In particular, we are interested in how epigenetic and higher-order chromatin states constrain transcriptional programs, and how breakdowns in these constraints contribute to cellular plasticity, senescence, and cancer.

To decode these systems, we develop sophisticated single-cell multi-modal genomics methods, such as scMAbID, which enable us to simultaneously measure (epi)genetic landscapes and matching transcriptomes within the very same cell. On the computational side, we use these rich, complex datasets to build predictive models that go beyond correlation, aiming to infer causal regulatory relationships and uncover the governing principles of gene regulation.

Biologically, we focus on mammalian model systems where chromatin organization undergoes dramatic transitions. We use retinal organoids to study developmental chromatin remodeling and lineage commitment, and tumor organoids to investigate cancer progression, chromatin instability, and cellular senescence. A central goal of the lab is to pinpoint where and how chromatin regulation fails in diseased states, and to map these failures back to specific genetic, epigenetic, or structural perturbations. Ultimately, we aim to translate single-cell chromatin complexity into generalizable rules that explain and eventually predict cellular behavior.