Research

The laboratory dissects how chromatin-associated factors control the architecture and metabolism of DNA double-strand breaks. Particular emphasis is placed on end protection, repair-factor recruitment and pathway choice.

Biochemical, genetic and cell-biological approaches reveal how repair decisions preserve chromosome integrity and how their disruption creates cancer-selective vulnerabilities.

Replication forks encounter secondary DNA structures, transcription complexes and damaged templates that can slow or collapse DNA synthesis. The group studies structure-specific helicases and fork-remodelling factors that protect these vulnerable intermediates.

Mechanistic work connects fork slowing, lesion bypass and repair to mutation avoidance, chromosome stability and potential synthetic-lethal treatment strategies.

Genetic studies in model organisms and human cells are used to define conserved repair pathways for interstrand cross-links and recombination intermediates. These pathways prevent deletions, repeat instability and telomere dysfunction.

The work links rare inherited repair defects to general principles of genome maintenance and identifies enzymes whose inhibition may selectively affect repair-defective cancers.

The laboratory connects basic repair mechanisms with drug discovery and biomarker development. Genetic interactions and repair phenotypes are used to nominate targets and define tumour contexts most likely to respond.

This translational direction helped underpin the development of DNA-damage-response therapeutics and continues through collaborations linking mechanistic biology to clinical precision oncology.