Host cell egress of Brucella abortus requires BNIP3L-mediated mitophagy.
EMBO J
; 42(14): e112817, 2023 07 17.
Article
en En
| MEDLINE
| ID: mdl-37232029
ABSTRACT
The facultative intracellular pathogen Brucella abortus interacts with several organelles of the host cell to reach its replicative niche inside the endoplasmic reticulum. However, little is known about the interplay between the intracellular bacteria and the host cell mitochondria. Here, we showed that B. abortus triggers substantive mitochondrial network fragmentation, accompanied by mitophagy and the formation of mitochondrial Brucella-containing vacuoles during the late steps of cellular infection. Brucella-induced expression of the mitophagy receptor BNIP3L is essential for these events and relies on the iron-dependent stabilisation of the hypoxia-inducible factor 1α. Functionally, BNIP3L-mediated mitophagy appears to be advantageous for bacterial exit from the host cell as BNIP3L depletion drastically reduces the number of reinfection events. Altogether, these findings highlight the intricate link between Brucella trafficking and the mitochondria during host cell infection.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Brucella abortus
/
Mitofagia
Idioma:
En
Revista:
EMBO J
Año:
2023
Tipo del documento:
Article
País de afiliación:
Bélgica