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
Germinal center (GC)-B cell proliferation relies on oxidative phosphorylation. Positively selected GC-B cells initiate cell division in the hypoxic light zone (LZ) microenvironment and continue vigorous proliferation upon migration to the dark zone. However, the mechanisms underlying how these GC-B cells reprogram mitochondrial bioenergetic functions to sustain cell division while overcoming hypoxia-driven energy stress are not understood. We found that microRNA (miR)-155 directly repressed the expression of hypoxia-induced histone lysine demethylase 2a, resulting in fine-tuning of histone H3 di-methylated lysine 36 levels. This optimized the expression of vital nuclear mitochondrial genes in LZ GC-B cells, thereby preventing excessive mitochondrial reactive oxygen species production and apoptosis. Thus, miR-155-regulated epigenetic mechanisms functions as a metabolic switch facilitating dynamic mitochondrial remodelling of LZ GC-B cells, ensuring positive selection and affinity maturation.
