On 28th November OxTalks will move to the new Halo platform and will become 'Oxford Events' (full details are available on the Staff Gateway).
There will be an OxTalks freeze beginning on Friday 14th November. This means you will need to publish any of your known events to OxTalks by then as there will be no facility to publish or edit events in that fortnight. During the freeze, all events will be migrated to the new Oxford Events site. It will still be possible to view events on OxTalks during this time.
If you have any questions, please contact halo@digital.ox.ac.uk
Contact sites between organelles are vital to the function of eukaryotic cells. Lipid droplets are dynamic organelles specialized in lipid storage, and interact physically with mitochondria in several cell types. The mechanisms generating this contact site are, however, poorly understood. Here, we discover in adipocytes, professional fat storing cells, that the mitochondrial outer-membrane protein MIGA2 tethers mitochondria to lipid droplets. We identify a lipid droplet targeting motif, and reveal that MIGA2 additionally interacts with the endoplasmic reticulum by binding to the membrane-proteins VAP-A/B. Depleting MIGA2 by CRISPR-Cas9 causes severe perturbation of triacylglycerol production during adipocyte differentiation. Specifically, our data indicate that MIGA2 is required for the de novo synthesis of lipids from non-lipid precursors. Based on its nearly ubiquitous expression pattern, we anticipate that MIGA2 is critical for lipid and energy homeostasis in a wide spectrum of cell-types.
