Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
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.
