Format:
Online-Ressource
ISSN:
1460-2075
Content:
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.
In:
volume:42
In:
number:14
In:
year:2023
In:
extent:26
In:
European Molecular Biology Organization, The EMBO journal, Heidelberg : EMBO Press, 1982-, 42, Heft 14 (2023) (gesamt 26), 1460-2075
Language:
English
DOI:
10.15252/embj.2022112817
URN:
urn:nbn:de:101:1-2023071715113216172716
URL:
https://doi.org/10.15252/embj.2022112817
URL:
https://nbn-resolving.org/urn:nbn:de:101:1-2023071715113216172716
URL:
https://d-nb.info/1296384381/34
URL:
https://doi.org/10.15252/embj.2022112817
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