SNX18 regulates ATG9A trafficking from recycling endosomes by recruiting Dynamin-2

EMBO Rep. 2018 Apr;19(4):e44837. doi: 10.15252/embr.201744837.

Kristiane Søreng ¹, Michael J Munson ¹, Christopher A Lamb ², Gunnveig T Bjørndal ¹, Serhiy Pankiv ¹, Sven R Carlsson ³, Sharon A Tooze ², Anne Simonsen ⁴

Affiliations

1 Deparment of Molecular Medicine, Institute of Basic Medical Sciences and Centre for Cancer Cell Reprogramming, Institute of Clinical Medicine Faculty of Medicine University of Oslo, Oslo, Norway.
2 Molecular Cell Biology of Autophagy Group, Francis Crick Institute, London, UK.
3 Department of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.
4 Deparment of Molecular Medicine, Institute of Basic Medical Sciences and Centre for Cancer Cell Reprogramming, Institute of Clinical Medicine Faculty of Medicine University of Oslo, Oslo, Norway anne.simonsen@medisin.uio.no.

PMID: 29437695 DOI: 10.15252/embr.201744837

Abstract

Trafficking of mammalian ATG9A between the Golgi apparatus, endosomes and peripheral ATG9A compartments is important for autophagosome biogenesis. Here, we show that the membrane remodelling protein SNX18, previously identified as a positive regulator of Autophagy, regulates ATG9A trafficking from recycling endosomes. ATG9A is recruited to SNX18-induced tubules generated from recycling endosomes and accumulates in juxtanuclear recycling endosomes in cells lacking SNX18. Binding of SNX18 to Dynamin-2 is important for ATG9A trafficking from recycling endosomes and for formation of ATG16L1- and WIPI2-positive autophagosome precursor membranes. We propose a model where upon Autophagy induction, SNX18 recruits Dynamin-2 to induce budding of ATG9A and ATG16L1 containing membranes from recycling endosomes that traffic to sites of autophagosome formation.

Keywords

ATG9; SNX18; autophagy; dynamin; recycling endosome.

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