Frederic Langevin

TL;DR: The results show that the acetaldehyde-catabolising enzyme Aldh2 is essential for the development of Fancd2−/− embryos, and that these embryos are unusually sensitive to ethanol exposure in utero, and ethanol consumption by postnatal double-deficient mice rapidly precipitates bone marrow failure.

TL;DR: This work identifies a new link between endogenous reactive metabolites and DNA damage in HSCs, and defines the protective mechanisms that counteract this threat, and finds that only HSPCs, and not more mature blood precursors, require Aldh2 for protection against acetaldehyde toxicity.

TL;DR: The features and mutational landscape of DNA damage caused by acetaldehyde, an endogenous and alcohol-derived metabolite, are described and how the choice of DNA-repair pathway and a stringent p53 response limit the transmission of aldehyde-induced mutations in stem cells are identified.

TL;DR: The phenotype of the Btbd12 knockout mouse is described, the mouse ortholog of SLX4, which recapitulates many key features of the human genetic illness Fanconi anemia and genetically links a regulator of nuclease incision complexes to the FanconiAnemia DNA crosslink repair pathway.

TL;DR: The vertebrate Hef ortholog is isolated and a genetic interaction between the FANCC and Hef genes is found, which sheds light on the origins, regulation and molecular function of the FA tumor-suppressor pathway in the maintenance of genome stability.