ATG7 and ATG14 restrict cytosolic and phagosomal Mycobacterium tuberculosis replication in human macrophages.


Journal

Nature microbiology
ISSN: 2058-5276
Titre abrégé: Nat Microbiol
Pays: England
ID NLM: 101674869

Informations de publication

Date de publication:
05 2023
Historique:
received: 24 01 2022
accepted: 24 01 2023
medline: 8 5 2023
pubmed: 25 3 2023
entrez: 24 3 2023
Statut: ppublish

Résumé

Autophagy is a cellular innate-immune defence mechanism against intracellular microorganisms, including Mycobacterium tuberculosis (Mtb). How canonical and non-canonical autophagy function to control Mtb infection in phagosomes and the cytosol remains unresolved. Macrophages are the main host cell in humans for Mtb. Here we studied the contributions of canonical and non-canonical autophagy in the genetically tractable human induced pluripotent stem cell-derived macrophages (iPSDM), using a set of Mtb mutants generated in the same genetic background of the common lab strain H37Rv. We monitored replication of Mtb mutants that are either unable to trigger canonical autophagy (Mtb ΔesxBA) or reportedly unable to block non-canonical autophagy (Mtb ΔcpsA) in iPSDM lacking either ATG7 or ATG14 using single-cell high-content imaging. We report that deletion of ATG7 by CRISPR-Cas9 in iPSDM resulted in increased replication of wild-type Mtb but not of Mtb ΔesxBA or Mtb ΔcpsA. We show that deletion of ATG14 resulted in increased replication of both Mtb wild type and the mutant Mtb ΔesxBA. Using Mtb reporters and quantitative imaging, we identified a role for ATG14 in regulating fusion of phagosomes containing Mtb with lysosomes, thereby enabling intracellular bacteria restriction. We conclude that ATG7 and ATG14 are both required for restricting Mtb replication in human macrophages.

Identifiants

pubmed: 36959508
doi: 10.1038/s41564-023-01335-9
pii: 10.1038/s41564-023-01335-9
pmc: PMC10159855
doi:

Substances chimiques

ATG7 protein, human EC 6.2.1.45
Autophagy-Related Protein 7 EC 6.2.1.45
ATG14 protein, human 0
Autophagy-Related Proteins 0
Adaptor Proteins, Vesicular Transport 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

803-818

Subventions

Organisme : Cancer Research UK
ID : FC001092
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001092
Pays : United Kingdom
Organisme : Medical Research Council
ID : FC001092
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2023. The Author(s).

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Auteurs

Beren Aylan (B)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Elliott M Bernard (EM)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.
Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.

Enrica Pellegrino (E)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Laure Botella (L)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Antony Fearns (A)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Natalia Athanasiadi (N)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Claudio Bussi (C)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

Pierre Santucci (P)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.
Aix-Marseille University, CNRS, LISM, Marseille, France.

Maximiliano G Gutierrez (MG)

Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK. MAX.G@CRICK.AC.UK.

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