English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance Intracellular pathogens hijack many host processes, including the vesicle trafficking pathway, to help their survival and replication.Legionella pneumophila is the causative agent of Legionnaires’ disease, which utilizes numerous effector proteins, including RidL during infection. RidL suppresses retromer transport activity, but the exact mechanism for this has remained unclear. Using a combination of structural, biochemical, and cellular approaches, we show how retromer specifically targets to retromer subunit VPS29. The RidL–VPS29 interaction is necessary for the proper localization and function of RidL. Mechanistically, RidL inhibits retromer activity by direct competition with TBC1d5, an essential retromer regulator. Our study highlights the beauty of studying host–pathogen interaction in the discovery of novel aspects of host cell biology.

Mechanism of inhibition of retromer transport by the bacterial effector RidL