Oxford Events, the new replacement for OxTalks, will launch on 16th March. The two-week OxTalks freeze period starts on Monday 2nd March. During this time, there will be no facility to publish or edit events. The existing OxTalks site will remain available to view during this period. Once Oxford Events launches, you will need a Halo login to submit events. Full details are available on the Staff Gateway.
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
