Article open access publication

eIF5A is required for autophagy by mediating ATG3 translation

EMBO Reports, EMBO, ISSN 1469-221X

Volume 19, 6, 2018

DOI:10.15252/embr.201846072, Dimensions: pub.1103677922, PMC: PMC5989740, PMID: 29712776,



  1. (1) University of Copenhagen, grid.5254.6, KU
  2. (2) University of Southern Denmark, grid.10825.3e, SDU
  3. (3) Sanford Burnham Prebys Medical Discovery Institute, grid.479509.6


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.


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University of Copenhagen

University of Southern Denmark

Danish Open Access Indicator

2018: Realized

Research area: Medicine

Danish Bibliometrics Indicator

2018: Level 2

Research area: Medicine

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Times Cited: 33

Field Citation Ratio (FCR): 8.29

Relative Citation ratio (RCR): 2.14

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Green, Published