A Mammalian Mitophagy Receptor, Bcl2-L-13, Recruits the ULK1 Complex to Induce Mitophagy.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
08 01 2019
Historique:
received: 05 07 2018
revised: 02 11 2018
accepted: 11 12 2018
entrez: 10 1 2019
pubmed: 10 1 2019
medline: 15 2 2020
Statut: ppublish

Résumé

Degradation of mitochondria by selective autophagy, termed mitophagy, contributes to the control of mitochondrial quality. Bcl2-L-13 is a mammalian homolog of Atg32, which is an essential mitophagy receptor in yeast. However, the molecular machinery involved in Bcl2-L-13-mediated mitophagy remains to be elucidated. Here, we show that the ULK1 (unc-51-like kinase) complex is required for Bcl2-L-13 to process mitophagy. Screening of a series of yeast Atg mutants revealed that a different set of ATG genes is used for Bcl2-L-13- and Atg32-mediated mitophagy in yeast. The components of the Atg1 complex essential for starvation-induced autophagy were indispensable in Bcl2-L-13-, but not Atg32-mediated, mitophagy. The ULK1 complex, a counterpart of the Atg1 complex, is necessary for Bcl2-L-13-mediated mitophagy in mammalian cells. We propose a model where, upon mitophagy induction, Bcl2-L-13 recruits the ULK1 complex to process mitophagy and the interaction of LC3B with ULK1, as well as Bcl2-L-13, is important for the mitophagy.

Identifiants

pubmed: 30625316
pii: S2211-1247(18)31980-6
doi: 10.1016/j.celrep.2018.12.050
pmc: PMC6326162
pii:
doi:

Substances chimiques

Atg32 protein, S cerevisiae 0
Autophagy-Related Proteins 0
BCL2L13 protein, human 0
Intracellular Signaling Peptides and Proteins 0
Proto-Oncogene Proteins c-bcl-2 0
Receptors, Cytoplasmic and Nuclear 0
Saccharomyces cerevisiae Proteins 0
Protein Kinases EC 2.7.-
ATG1 protein, S cerevisiae EC 2.7.1.-
Autophagy-Related Protein-1 Homolog EC 2.7.11.1
ULK1 protein, human EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

338-345.e6

Subventions

Organisme : British Heart Foundation
ID : CH/11/3/29051
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE/13/2/30182
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/16/15/32294
Pays : United Kingdom

Informations de copyright

Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

Références

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Auteurs

Tomokazu Murakawa (T)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, UK.

Koji Okamoto (K)

Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan.

Shigemiki Omiya (S)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, UK.

Manabu Taneike (M)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, UK.

Osamu Yamaguchi (O)

Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

Kinya Otsu (K)

The School of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, UK. Electronic address: kinya.otsu@kcl.ac.uk.

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Classifications MeSH