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EMBO Rep. 2014 Apr;15(4):392-401. doi: 10.1002/embr.201337995. Epub 2014 Mar 6.

TBC1D5 and the AP2 complex regulate ATG9 trafficking and initiation of autophagy.

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  • 1Buchmann Institute for Molecular Life Sciences (BMLS) and Institute of Biochemistry II Goethe University School of Medicine, Frankfurt, Germany.

Abstract

The RabGAP protein TBC1D5 controls cellular endomembrane trafficking processes and binds the retromer subunit VPS29 and the ubiquitin-like protein ATG8 (LC3). Here, we describe that TBC1D5 also associates with ATG9 and the active ULK1 complex during autophagy. Moreover, ATG9 and TBC1D5 interact with clathrin and the AP2 complex. Depletion of TBC1D5 leads to missorting of ATG9 to late endosomes upon activation of autophagy, whereas inhibition of clathrin-mediated endocytosis or AP2 depletion alters ATG9 trafficking and its association with TBC1D5. Taken together, our data show that TBC1D5 and the AP2 complex are important novel regulators of the rerouting of ATG9-containing vesicular carriers toward sites of autophagosome formation.

PMID:
24603492
[PubMed - indexed for MEDLINE]
PMCID:
PMC3989670
[Available on 2015/4/1]
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