MOSPD3 mediates the ER recruitment of ATG2A to promote autophagy.

MOSPD3 acts as the ER adaptor that recruits ATG2A to promote autophagy by mediating its anchoring to ER subdomains in mammalian cells.

• Why it matters: Understanding how ATG2A is anchored to the ER is crucial for elucidating the mechanisms of autophagosome formation, a key process in cellular homeostasis and disease.
• What they did: The study identified MOSPD3 as the ER adaptor for ATG2A, demonstrating that its MSP domain directly interacts with an FFNT motif near ATG2A’s N terminus, and disrupting this interaction impairs autophagy.
• The result: Disruption of the MOSPD3-ATG2A interaction abolishes ER recruitment and autophagic flux, highlighting the importance of MSP-FFNT recognition in autophagosome biogenesis.