OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
The Fanconi Anemia (FA) pathway repairs DNA damage caused by endogenous and chemotherapy-induced DNA crosslinks, and responds to replication stress. Genetic inactivation of this pathway impairs development, results in bone marrow failure and promotes cancer. The key molecular step in the FA pathway is the monoubiquitination of FANCD2-FANCI by the FA core complex-a megadalton multiprotein E3 ubiquitin ligase. Monoubiquitinated FANCD2 is thought to recruit enzymes to remove the DNA cross link or to stabilize the stalled replication fork. We recently reconstituted an active, recombinant FA core complex that efficiently monoubiquitinates FANCD2-FANCI in vitro and used electron cryo-microscopy (cryoEM) alongside mass spectrometry to determine the structures of several complexes. I will describe our efforts to understand how the proteins in the FA pathway signal and repair DNA crosslinks.
