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
De novo mutations (DNMs), i.e. genetic alterations not inherited from either parent, are an important contributor to disease, causing severe developmental disorders in ~1 in 300 births. Most DNMs (>80%) originate during spermatogenesis (sperm cell production) and their frequency increases with paternal age. We have previously described a mechanism taking place in the testis of all men that contributes to the paternal age-related increase in pathogenic DNMs called ‘selfish selection’ – whereby specific pathogenic DNMs arising in spermatogonial stem cells lead to their clonal expansion over time. This process explains the paternal age-effect and high birth prevalence observed for several inherited disorders that occur up to 1000-fold more frequently than background. Importantly, because the spermatogonial stem cells provide a source of heritable material, this phenomenon has long-term implications that extend far beyond the individual in whom it takes place, and is predicted to affect disease prevalence, apparent de novo mutation rate and the evolution of our species.
