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Autophagosome-lysosome fusion triggers a lysosomal response mediated by TLR9 and controlled by OCRL.

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De Leo, Maria Giovanna Staiano, Leopoldo Vicinanza, Mariella Luciani, Alessandro Carissimo, Annamaria Devuyst, Olivier [UCL] De Matteis, Maria Antonietta

Phosphoinositides (PtdIns) control fundamental cell processes, and inherited defects of PtdIns kinases or phosphatases cause severe human diseases, including Lowe syndrome due to mutations in OCRL, which encodes a PtdIns(4,5)P2 5-phosphatase. Here we unveil a lysosomal response to the arrival of autophagosomal cargo in which OCRL plays a key part. We identify mitochondrial DNA and TLR9 as the cargo and the receptor that triggers and mediates, respectively, this response. This lysosome-cargo response is required to sustain the autophagic flux and involves a local increase in PtdIns(4,5)P2 that is confined in space and time by OCRL. Depleting or inhibiting OCRL leads to an accumulation of lysosomal PtdIns(4,5)P2, an inhibitor of the calcium channel mucolipin-1 that controls autophagosome-lysosome fusion. Hence, autophagosomes accumulate in OCRL-depleted cells and in the kidneys of Lowe syndrome patients. Importantly, boosting the activity of mucolipin-1 with selective agonists restores the autophagic flux in cells from Lowe syndrome patients.

Document type Article de périodique (Journal article) – Article de recherche
Access type Accès restreint
Publication date 2016
Language Anglais
Journal information "Nature Cell Biology" - Vol. 18, no. 8, p. 839-850 (2016)
Peer reviewed yes
Publisher Nature Publishing Group ((United Kingdom) London)
issn 1465-7392
e-issn 1476-4679
Publication status Publié
Affiliations UCL - SSS/IREC/NEFR - Pôle de Néphrologie
UCL - (SLuc) Service de néphrologie
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Permanent URL http://hdl.handle.net/2078.1/175996