Our research

We develop spatial genomics methods that are powerful and practical. Our goal is to reveal genome organization at the scale at which nuclear processes occur.

One focus is expansion genomics, which combines expansion microscopy and genomics to study DNA, RNA and proteins in situ at nanoscale resolution. We aim to image the genome at higher resolution and begin working with it directly inside intact cells. We ask how chromatin structure, transcription and epigenetic regulation are organized in space, and how this organization changes in disease.

In the longer term, we seek to build multimodal workflows that jointly map DNA, RNA and proteins in intact samples, allowing us to connect molecular structure with function in development, aging and disease. We also aim to develop cost-effective spatial methods for tissue sections, making nanoscale multimodal profiling more accessible.

Aging is often accompanied by chronic, low-grade inflammation, known as inflammaging, which is linked to many age-associated diseases. Its effects on health are well recognized, but the underlying epigenetic mechanisms remain poorly understood.

We study how inflammatory experiences leave a lasting molecular memory in the genome. We want to identify the chromatin changes, epigenetic regulators and changes in nuclear structure that allow this memory to persist.

To investigate these questions, we will use cell culture systems and organoid models of different inflammatory states, together with expansion-based spatial genomics and single-cell genomics. By examining genome architecture, chromatin state and gene expression in individual cells, we aim to understand how inflammaging develops and why recovery becomes difficult. Our goal is to map the epigenetic factors and structural changes that contribute to cellular dysfunction with age.

Understanding the mechanisms of inflammaging is the first step. We also ask whether the aging genome can be made more resilient.

We will use CRISPR-based approaches, including gene perturbation and base editing, to test candidate epigenetic regulators identified in our studies. These experiments will help distinguish factors that protect the genome from those that contribute to its decline under chronic inflammatory stress.

We also want to test whether harmful age-associated epigenetic states can be reversed. By restoring or modulating key regulators, we will ask whether cells can recover a healthier epigenomic state while retaining their identity. We will assess these interventions using molecular, structural and functional assays. Our long-term goal is to understand how the genome can better resist inflammation and maintain cellular function with age.