A major goal of the lab is to develop spatial genomics methods that are both powerful and practical. We are especially interested in building tools that can reveal genome organization at the scale at which many nuclear processes actually occur.

One focus of the lab is the development of expansion genomics, an approach that brings together expansion microscopy and genomics to study DNA, RNA, and proteins in situ at nanoscale resolution. Our aim is not only to image the genome at higher resolution, but also to begin working with it directly inside intact cells. We want to understand how chromatin structure, transcription, and epigenetic regulation are organized in space, and how that organization changes in disease.

In the longer term, we seek to build multimodal workflows that jointly map DNA, RNA, and proteins in intact samples, enabling direct analysis of structure-function relationships in development, aging, and disease. A complementary thrust of the lab is to develop cost-effective spatial methods for tissue sections, making nanoscale multimodal profiling more accessible for biological and translational questions.

Aging is often accompanied by a chronic, low-grade inflammatory state known as "inflammaging", which is linked to many age-associated diseases. While its physiological consequences are widely recognized, the underlying epigenetic mechanisms remain poorly understood.

Our lab is interested in how inflammatory experiences become written into the genome as long-lasting molecular memory. We want to identify the chromatin changes, epigenetic regulators, and structural alterations in the nucleus that allow inflammation to leave a durable imprint on cells over time.

To study this, we will use cell culture systems and organoid models that capture different inflammatory states, and combine them with expansion-based spatial genomics and single-cell genomic approaches. By examining changes in genome architecture, chromatin state, and gene expression at single-cell resolution, we hope to build a clearer picture of how inflammaging emerges and why it becomes difficult for cells to recover from it. Our aim is to build a comprehensive atlas of the specific epigenetic factors and structural shifts that cause cells to malfunction as they age.

Understanding mechanism is only the first step. We also want to ask whether the aging genome can be made more resilient.

Recent advances in genome engineering now make it possible to perturb genes and regulatory elements with extraordinary precision. In our lab, we will use CRISPR-based approaches, including gene perturbation and base editing, to test the function of candidate epigenetic regulators identified in our studies of inflammaging. The goal is to determine which factors actively protect the genome, and which ones contribute to decline under chronic inflammatory stress.

We are also interested in whether harmful aging-associated epigenetic states can be reversed. By restoring or modulating key regulators, we hope to test whether cells can recover a healthier epigenomic state without losing their identity. Cells that undergo such interventions will be studied in depth using molecular, structural, and functional assays. Ultimately, we want to define a set of principles for building a genome that is more resistant to inflammation and more capable of maintaining cellular function with age.