MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1111/cmi.12768

Медицинская библиотека · Cellular microbiology · 2017

A role for host cell exocytosis in InlB-mediated internalisation of Listeria monocytogenes.

Van Ngo Hoan, Bhalla Manmeet, Chen Da-Yuan, Ireton Keith

СтатьяПеревод в очереди

Аннотация

The bacterial surface protein InlB mediates internalisation of Listeria monocytogenes into human cells through interaction with the host receptor tyrosine kinase, Met. InlB-mediated entry requires localised polymerisation of the host actin cytoskeleton. Apart from actin polymerisation, roles for other host processes in Listeria entry are unknown. Here, we demonstrate that exocytosis in the human cell promotes InlB-dependent internalisation. Using a probe consisting of VAMP3 with an exofacial green fluorescent protein tag, focal exocytosis was detected during InlB-mediated entry. Exocytosis was dependent on Met tyrosine kinase activity and the GTPase RalA. Depletion of SNARE proteins by small interfering RNA demonstrated an important role for exocytosis in Listeria internalisation. Depletion of SNARE proteins failed to affect actin filaments during internalisation, suggesting that actin polymerisation and exocytosis are separable host responses. SNARE proteins were required for delivery of the human GTPase Dynamin 2, which promotes InlB-mediated entry. Our results identify exocytosis as a novel host process exploited by Listeria for infection.

Для цитирования: Van Ngo Hoan, Bhalla Manmeet, Chen Da-Yuan, Ireton Keith. A role for host cell exocytosis in InlB-mediated internalisation of Listeria monocytogenes.. Cellular microbiology. 2017. DOI: 10.1111/cmi.12768.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.