Stress granules plug and stabilize damaged endolysosomal membranes

Claudio Bussi (), Agustín Mangiarotti, Christian Vanhille-Campos, Beren Aylan, Enrica Pellegrino, Natalia Athanasiadi, Antony Fearns, Angela Rodgers, Titus M. Franzmann, Anđela Šarić, Rumiana Dimova and Maximiliano G. Gutierrez ()
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Claudio Bussi: The Francis Crick Institute
Agustín Mangiarotti: Max Planck Institute of Colloids and Interfaces
Christian Vanhille-Campos: Institute of Science and Technology Austria
Beren Aylan: The Francis Crick Institute
Enrica Pellegrino: The Francis Crick Institute
Natalia Athanasiadi: The Francis Crick Institute
Antony Fearns: The Francis Crick Institute
Angela Rodgers: The Francis Crick Institute
Titus M. Franzmann: Technische Universität Dresden
Anđela Šarić: Institute of Science and Technology Austria
Rumiana Dimova: Max Planck Institute of Colloids and Interfaces
Maximiliano G. Gutierrez: The Francis Crick Institute

Nature, 2023, vol. 623, issue 7989, 1062-1069

Abstract: Abstract Endomembrane damage represents a form of stress that is detrimental for eukaryotic cells1,2. To cope with this threat, cells possess mechanisms that repair the damage and restore cellular homeostasis3–7. Endomembrane damage also results in organelle instability and the mechanisms by which cells stabilize damaged endomembranes to enable membrane repair remains unknown. Here, by combining in vitro and in cellulo studies with computational modelling we uncover a biological function for stress granules whereby these biomolecular condensates form rapidly at endomembrane damage sites and act as a plug that stabilizes the ruptured membrane. Functionally, we demonstrate that stress granule formation and membrane stabilization enable efficient repair of damaged endolysosomes, through both ESCRT (endosomal sorting complex required for transport)-dependent and independent mechanisms. We also show that blocking stress granule formation in human macrophages creates a permissive environment for Mycobacterium tuberculosis, a human pathogen that exploits endomembrane damage to survive within the host.

Date: 2023
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DOI: 10.1038/s41586-023-06726-w

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