Dynamin-2 promotes Atg9A retrieval from phagophores during autophagy.

Apr 10, 2026bioRxiv : the preprint server for biology

Dynamin-2 helps recycle Atg9A from early cell recycling structures during autophagy

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Longevity & Aging on OpenScience ↗PubMed ↗DOI ↗

Abstract

Dynamin-2 is identified as the membrane scission protein that retrieves Atg9A from phagophores during autophagy.

Autophagy is linked to the growth of phagophores facilitated by vesicles containing Atg9A protein.
Atg9A does not become part of mature autophagosomes.
Dynamin-2 colocalizes with Endophilin-B1 and other autophagy proteins during autophagy induction.
Blocking the recycling of Atg9A leads to its degradation within autophagosomes.
These findings highlight the importance of membrane-scission proteins in the autophagy process.

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Autophagy involves the rapid growth of phagophores through membrane addition. This growth is triggered by vesicles containing the Atg9A protein. However, Atg9A is not incorporated into mature autophagosomes. We now demonstrate that Dynamin-2 (Dnm2) colocalizes with the BAR domain protein Endophilin-B1 (EndoB1/Bif-1/SH3GLB1) and other autophagy proteins when autophagy is induced. Our data suggest that Atg9A is retrieved from phagophores via fission, with Dnm2 acting as the membrane scission protein. Blocking Atg9A recycling, either by mutating Dnm2, using RNA interference, or applying chemical inhibitors, results in Atg9A remaining in autophagosomes and being degraded during autophagy. Overall, these findings provide new insights into the roles of membrane-scission proteins in autophagy.

Dynamin-2 promotes Atg9A retrieval from phagophores during autophagy.

Abstract

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