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.
The DNA of neurons is continually damaged due to lifelong, high-level metabolic and transcriptional activity. In addition, recent studies have demonstrated extensive “programmed” DNA damage in differentiating post-mitotic neurons. Here, we identify these endogenous lesions as single strand break intermediates of thymine DNA glycosylase (TDG)-mediated removal of oxidized methylcytosines at neuronal enhancers. Interrupting active DNA demethylation using anti-neoplastic cytosine analogs triggers TDG-dependent neuronal cell death associated with massive chromosomal rearrangements of neuronal enhancers. This suggests that the well-known neurotoxic side effects of certain chemotherapies, also called “chemobrain,” could be linked to DNA repair processes intrinsic to normal neuronal differentiation. We will discuss recent studies that describe the interplay between programmed DNA damage, cell fate specification and mutagenesis in post-mitotic neurons.
