I completed my PhD in 2012 at the University of Queensland, Australia, in the laboratory of Associate Professor James Fraser, where I worked on the fungus Cryptococcus neoformans, an AIDS-associated opportunistic pathogen that causes meningoencephalitis. I investigated aspects of purine metabolism that could be targeted for antifungal therapy, as well as mechanisms of rapid microevolution that occurred in the fungus during long-term infection of a human host.
In 2013 I moved to the University of Oxford to the laboratory of Professor Matthew Whitby, where I studied mechanisms of replication fork restart via homologous recombination in the yeast Schizosaccharomyces pombe. In particular, I uncovered a new mechanism of genome instability encountered when a restarting replication fork encounters a normal terminating fork, which was mediated by the structure specific nuclease Mus81.
In 2016 I moved to the laboratory of Dr Andrew Blackford, where I work on genome stability and DNA damage repair, in particular the Bloom syndrome tumour suppressor complex. The complex performs myriad roles in protecting and repairing the genome during DNA replication and repair and is a particularly potent suppressor of cancer formation in all cell types. I am utilising cutting-edge proteomics approaches to uncover and investigate key protein-protein interactions of the complex that may potentially mediate its role in maintaining and repairing the integrity of the genome and in turn prevent the development of cancer.
Morrow CA, Nguyen MO, Fower A, Wong IN, Osman F, Bryer C & Whiyby MC 2017. Inter-fork strand annealing causes genomic deletions during the termination of DNA replication. Elife Jun 6; 6:e25490.
Nguyen MO, Jalan M, Morrow CA, Osman F, Whitby MC 2015. Recombination occurs within minutes of replication blockage by RTS1 producing forks that are prone to collapse. Elife Mar 25; 4:e04539.