Simon Boulton receives the EMBO Gold Medal 2011
Simon Boulton receives the award in recognition of his groundbreaking research on DNA repair mechanisms. The election committee was particularly impressed by his pioneering role in establishing the nematode worm, C. elegans, as a model system to study genome instability. The EMBO Gold Medal annually recognizes outstanding contributions of young researchers in the molecular life sciences.
Boultons outstanding scientific work was honored with numerous important scientific awards like the Colworth Medal in 2006, the EMBO young investigator award in 2007, EACR Young Cancer Reseracher of the Year 2008, Eppendorf Award for Young European Investigators in 2008 and the Royal Society Wolfson Merit Award in 2010.
Throughout his career, 38-year-old Boulton and his research team have exploited the experimental strengths of several complementary systems, including C. elegans and mouse genetics, proteomics in mammalian cells and in vitro biochemistry. Some of the most important discoveries have come from contrasting the results obtained in different systems and cellular contexts. Boulton's PhD supervisor at Cancer Research UK's London research institute, Clare Hall Laboratories, Stephen P. Jackson described him as an "absolutely outstanding scientist" and praised his unique combination of approaches that allowed him to make seminal contributions to the field encompassing DNA repair, genome instability and cancer.
Boulton made groundbreaking discoveries like:
Discovering the gene RTEL1 as an anti-recombinase that impacts on genome stability and cancer and counteracts toxic recombination, which is also required in meiosis to execute non-crossover repair.
Discovering the PBZ motif and establishing that ALC1 (Amplified in Liver Cancer 1) is a poly(ADP-ribose)-activated chromatin-remodelling enzyme required for DNA repair. Poly (ADP-ribosyl)ation (PAR) is a post-translational modification of proteins that play an important role in mediating protein interactions and the recruitment of specific protein targets. These results provided new insights into the mechanisms by which PAR regulates DNA repair.
Discovering that the Fanconi Anemia proteins FANCM and FAAP24 are required for checkpoint-kinase signalling (ATR) in response to DNA damage and establishing that DNA repair defects of Fanconi.