MOSPD3 mediates the ER recruitment of ATG2A to promote autophagy.

MOSPD3 acts as the ER anchor for ATG2A, facilitating autophagy by enabling lipid transfer during autophagosome formation in mammalian cells.

• Why it matters: Understanding how ATG2A is anchored to the ER is crucial because it underpins the process of autophagosome biogenesis, a vital cellular function, yet this mechanism was previously unclear.
• What they did: The study identified MOSPD3 as the ER adaptor for ATG2A through direct MSP-FFNT domain interactions, showing that disrupting this interface impairs ER recruitment and autophagy.
• The result: This discovery reveals that MSP-FFNT recognition is essential for positioning ATG2A at the ER, enabling lipid transfer and autophagic flux, with implications for understanding autophagy regulation.