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.
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.
