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eIF 5A is required for autophagy by mediating ATG 3 translation
Author(s) -
Lubas Michal,
Harder Lea M,
Kumsta Caroline,
Tiessen Imke,
Hansen Malene,
Andersen Jens S,
Lund Anders H,
Frankel Lisa B
Publication year - 2018
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201846072
Subject(s) - autophagy , atg8 , lipid anchored protein , microbiology and biotechnology , translation (biology) , ubiquitin , autophagosome , biology , eukaryotic translation , atg12 , messenger rna , biochemistry , gene , atg5 , apoptosis
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 ( eIF 5A) in autophagy. Identified from a high‐throughput screen, we find that eIF 5A is required for lipidation of LC 3B and its paralogs and promotes autophagosome formation. This feature is evolutionarily conserved and results from the translation of the E2‐like ATG 3 protein. Mechanistically, we identify an amino acid motif in ATG 3 causing eIF 5A dependency for its efficient translation. Our study identifies eIF 5A as a key requirement for autophagosome formation and demonstrates the importance of translation in mediating efficient autophagy.