Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 225, Issue 6, Pages 1005-1010Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiaa367
Keywords
Listeria monocytogenes; Taok2; STE1-like kinase; vacuolar escape; siRNA screen
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Funding
- Institut Pasteur, Universite Paris Diderot, Agence Nationale de la Recherche [ANR-15-CE15-0017, ANR-10-INSB-04-01]
- Spanish Ministry of Science, Innovation and Universities [RYC-2018-024985-I]
- European Research Council
- Region Ile de France (DIM1Health)
- Groupement d'Interet Scientifique Infrastructures en Biologie Sante et Agronomie
- Agence Nationale de la Recherche (ANR) [ANR-15-CE15-0017] Funding Source: Agence Nationale de la Recherche (ANR)
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This study identified for the first time the host factors that regulate L. monocytogenes vacuolar rupture and cytoplasmic access in epithelial cells.
The bacterial pathogen Listeria monocytogenes invades host cells, ruptures the internalization vacuole, and reaches the cytosol for replication. A high-content small interfering RNA (siRNA) microscopy screen allowed us to identify epithelial cell factors involved in L. monocytogenes vacuolar rupture, including the serine/threonine kinase Taok2. Kinase activity inhibition using a specific drug validated a role for Taok2 in favoring L. monocytogenes cytoplasmic access. Furthermore, we showed that Taok2 recruitment to L. monocytogenes vacuoles requires the presence of pore-forming toxin listeriolysin O. Overall, our study identified the first set of host factors modulating L. monocytogenes vacuolar rupture and cytoplasmic access in epithelial cells.
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