DNA repair is essential for maintaining genetic and epigenetic stability, preserving cell identity, and preventing disease. Beyond the coordinated activity of DNA repair factors, the DNA damage response also involves the formation of dynamic chromatin structures that coordinate the different stages of repair and, ultimately, safeguard genome integrity in response to DNA lesions.

Our goal is to understand how these dynamic chromatin structures form, function, and orchestrate DNA repair. We hope to uncover therapeutic vulnerabilities rooted in these chromatin states, with the long-term goal of designing more efficient cancer treatments, with special focus on cancers with mutations in BRCA1/2 genes.

We investigate how chromatin organization and dynamics regulate two key processes: homologous recombination repair of DNA breaks and the response to stalled DNA replication forks. We do this by combining innovative CRISPR technologies, cell biology, genomics, molecular modeling, advanced microscopy and machine learning.