Listeria monocytogenes Co-Opts the Host Exocyst Complex To Promote Internalin A-Mediated Entry.
In: Infection and immunity, Jg. 90 (2022-12-15), Heft 12, S. e0032622
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Zugriff:
The bacterial pathogen Listeria monocytogenes induces its internalization (entry) into intestinal epithelial cells through interaction of its surface protein, internalin A (InlA), with the human cell-cell adhesion molecule, E-cadherin. While InlA-mediated entry requires bacterial stimulation of actin polymerization, it remains unknown whether additional host processes are manipulated to promote internalization. Here, we show that interaction of InlA with E-cadherin induces the host membrane-trafficking process of polarized exocytosis, which augments uptake of Listeria . Imaging studies revealed that exocytosis is stimulated at sites of InlA-dependent internalization. Experiments inhibiting human N -ethylmaleimide-sensitive factor (NSF) demonstrated that exocytosis is needed for efficient InlA-mediated entry. Polarized exocytosis is mediated by the exocyst complex, which comprises eight proteins, including Sec6, Exo70, and Exo84. We found that Exo70 was recruited to sites of InlA-mediated entry. In addition, depletion of Exo70, Exo84, or Sec6 by RNA interference impaired entry without affecting surface levels of E-cadherin. Similar to binding of InlA to E-cadherin, homophilic interaction of E-cadherin molecules mobilized the exocyst and stimulated exocytosis. Collectively, these results demonstrate that ligation of E-cadherin induces exocytosis that promotes Listeria entry, and they raise the possibility that the exocyst might also control the normal function of E-cadherin in cell-cell adhesion.
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Listeria monocytogenes Co-Opts the Host Exocyst Complex To Promote Internalin A-Mediated Entry.
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Autor/in / Beteiligte Person: | Gyanwali, GC ; Herath, TUB ; Gianfelice, A ; Ireton, K |
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Zeitschrift: | Infection and immunity, Jg. 90 (2022-12-15), Heft 12, S. e0032622 |
Veröffentlichung: | Washington, DC : American Society For Microbiology ; <i>Original Publication</i>: [Bethesda, Md.] American Society for Microbiology., 2022 |
Medientyp: | academicJournal |
ISSN: | 1098-5522 (electronic) |
DOI: | 10.1128/iai.00326-22 |
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