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
Ataxia-telangiectasia (A-T) is a neurodegenerative disorder caused by ATM mutations, leading to progressive Purkinje neuron loss. While ATM regulates the DNA damage response, mechanisms of cell degeneration remain unclear. Using cerebella, hiPS cells, and cerebellar organoids from A-T patients, we show that Purkinje cells shift from a soft, low-viscosity state to hyperstiffness with nuclear deformation and chromatin hypermethylation. Proteomics reveal dysregulated mechanotransduction, chromatin remodelling, and loss of calcium channels. Epigenetic inhibition restores nuclear structure and ITPR1 levels. These findings identify A-T as a “mechano-disease” and suggest that targeting nuclear mechanics could offer new therapeutic avenues
