| Literature DB >> 29902442 |
Chen Chen1, Brittney N Nguyen2, Gabriel Mitchell1, Shally R Margolis1, Darren Ma1, Daniel A Portnoy3.
Abstract
Listeriolysin O (LLO) is a cholesterol-dependent cytolysin that mediates escape of Listeria monocytogenes from a phagosome, enabling growth of the bacteria in the host cell cytosol. LLO contains a PEST-like sequence that prevents it from killing infected cells, but the mechanism involved is unknown. We found that the LLO PEST-like sequence was necessary to mediate removal of LLO from the interior face of the plasma membrane, where it coalesces into discrete puncta. LLO interacts with Ap2a2, an adaptor protein involved in endocytosis, via its PEST-like sequence, and Ap2a2-dependent endocytosis is required to prevent LLO-induced cytotoxicity. An unrelated PEST-like sequence from a human G protein-coupled receptor (GPCR), which also interacts with Ap2a2, could functionally complement the PEST-like sequence in L. monocytogenes LLO. These data revealed that LLO co-opts the host endocytosis machinery to protect the integrity of the host plasma membrane during L. monocytogenes infection.Entities:
Keywords: LLO; adaptor protein complex 2; ap2a2; bacteria; human calcium receptor; macrophage; membrane repair; pathogen
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Year: 2018 PMID: 29902442 PMCID: PMC6007032 DOI: 10.1016/j.chom.2018.05.006
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023