We are a computational biology lab studying gene regulation in development, disease, and for therapeutics.

DDIAS is identified as a factor that protects single-stranded DNA during mitosis to maintain chromosome stability, and inactivating mutations in DDIAS are identified in a human neurodevelopmental disorder.

Faithful DNA replication is essential for genome stability, yet replication forks face constant stress. The Bloom syndrome helicase (BLM) safeguards fork integrity, but excessive BLM activity can itse...

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The analysis of DNA sequence outcomes provides molecular insights into double-strand break (DSB) repair mechanisms. Using parallel in-pool profiling of Cas9-induced insertions and deletions (indels) w...

Investigating the interplay between DNA damage repair mechanisms, genomic instability and radiotherapy resistance Primary supervisor: Sarah McClelland, Queen Mary University of London Secondary superv...

Incomplete DNA replication and chromosome breakage during mitosis pose major threats to chromosome segregation. The CIP2A-TOPBP1 complex acts to mitigate this peril, but its exact role is not yet unde...

DNA double-strand breaks and unresolved DNA replication intermediates are particularly dangerous during mitosis. Paradoxically, cells inactivate canonical DNA repair mechanisms during chromosome segre...

Distinctively, pancreatic ductal adenocarcinoma (PDAC) consists of sparse tumour lesions intertwined with extensive desmoplastic stroma. The complexity of tumour–microenvironment interactions within t...

Assistant Professor, Teaching Stream (CLTA) - Molecular Biology, Genetics, and Microbiology

Using biochemical assays and a mutant disrupting RNF168-dependent ubiquitination of the histone variant macroH2A1.2, Galloy et al. identified an unexpected role for histone mH2A1.2 ubiquitination in p...

Chemical inducers of proximity (CIPs) can elicit durable, and often neomorphic, biological effects through the formation of a ternary complex, even at low equilibrium occupancy of their targets. This ...

Provide leadership and mentorship to members of the Developmental, Stem Cell & Cancer and influence the scientific direction of the Research Institute

The DNA-dependent protease SPRTN cleaves toxic DNA-protein crosslinks (DPCs). Here, the authors show that SPRTN is activated by DPC-ubiquitylation through an allosteric ubiquitin binding interface. Th...

imageimageFANCM employs a sophisticated dual recognition mechanism in genome maintenance, using distinct DNA-binding domains to identify and move around on branched DNA structures. This study reveals how FANCM evolved from an ancient repair motor ...

Antagonistic activities of the 53BP1 axis and the tumor suppressor BRCA1-BARD1 determine whether DNA double-strand breaks (DSBs) are repaired by end joining or homologous recombination. We show that t...

A multigenerational single-cell tracking approach provides a framework to dissect phenotypic plasticity at the single-cell level, offering insights into cellular processes that may resemble early even...

Nature - Ku limits RNA-induced innate immunity to allow Alu-expansion in primates