eIF5A is required for autophagy by mediating ATG3 translation

Michal Lubas, Lea M Harder, Caroline Kumsta, Imke Tiessen, Malene Hansen, Jens S Andersen, Anders H Lund, Lisa B Frankel

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Autophagy is an essential catabolic process responsible for recycling of intracellular material and preserving cellular fidelity. Key to the autophagy pathway is the ubiquitin-like conjugation system mediating lipidation of Atg8 proteins and their anchoring to autophagosomal membranes. While regulation of autophagy has been characterized at the level of transcription, protein interactions and post-translational modifications, its translational regulation remains elusive. Here we describe a role for the conserved eukaryotic translation initiation factor 5A (eIF5A) in autophagy. Identified from a high-throughput screen, we find that eIF5A is required for lipidation of LC3B and its paralogs and promotes autophagosome formation. This feature is evolutionarily conserved and results from the translation of the E2-like ATG3 protein. Mechanistically, we identify an amino acid motif in ATG3 causing eIF5A dependency for its efficient translation. Our study identifies eIF5A as a key requirement for autophagosome formation and demonstrates the importance of translation in mediating efficient autophagy.

Original languageEnglish
Article numbere46072
JournalE M B O Reports
Volume19
Issue number6
Number of pages17
ISSN1469-221X
DOIs
Publication statusPublished - 2018

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