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The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication

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The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication. / Finsel, Ivo; Ragaz, Curdin; Hoffmann, Christine; Harrison, Christopher F; Weber, Stephen; van Rahden, Vanessa A; Johannes, Ludger; Hilbi, Hubert.

In: CELL HOST MICROBE, Vol. 14, No. 1, 17.07.2013, p. 38-50.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Finsel, I, Ragaz, C, Hoffmann, C, Harrison, CF, Weber, S, van Rahden, VA, Johannes, L & Hilbi, H 2013, 'The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication', CELL HOST MICROBE, vol. 14, no. 1, pp. 38-50. https://doi.org/10.1016/j.chom.2013.06.001

APA

Finsel, I., Ragaz, C., Hoffmann, C., Harrison, C. F., Weber, S., van Rahden, V. A., Johannes, L., & Hilbi, H. (2013). The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication. CELL HOST MICROBE, 14(1), 38-50. https://doi.org/10.1016/j.chom.2013.06.001

Vancouver

Finsel I, Ragaz C, Hoffmann C, Harrison CF, Weber S, van Rahden VA et al. The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication. CELL HOST MICROBE. 2013 Jul 17;14(1):38-50. https://doi.org/10.1016/j.chom.2013.06.001

Bibtex

@article{1ca2a39341b64fa0a9e674a2d845e0a2,
title = "The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication",
abstract = "The bacteria causing Legionnaires' disease, Legionella pneumophila, replicate intracellularly within unique Legionella-containing vacuoles (LCVs). LCV formation involves a type IV secretion system (T4SS) that translocates effector proteins into host cells. We show that the T4SS effector RidL localizes to LCVs, supports intracellular bacterial growth, and alters retrograde trafficking, in which selected proteins are transported from endosomes to the Golgi. The retromer complex that mediates retrograde trafficking localizes to LCVs independently of RidL and restricts intracellular bacterial growth. RidL binds the Vps29 retromer subunit and the lipid PtdIns(3)P, which localizes retromer components to membranes. Additionally, specific retromer cargo receptors and sorting nexins that mediate protein capture and membrane remodeling preferentially localize to LCVs in the absence of ridL. Ectopic RidL production inhibits retrograde trafficking, and L. pneumophila blocks retrograde transport at endosome exit sites in a ridL-dependent manner. Collectively, these findings suggest that RidL inhibits retromer function to promote intracellular bacterial replication.",
keywords = "Animals, Bacterial Proteins, Cell Line, Endosomes, Humans, Legionella pneumophila, Legionnaires' Disease, Mice, Protein Transport, Vacuoles",
author = "Ivo Finsel and Curdin Ragaz and Christine Hoffmann and Harrison, {Christopher F} and Stephen Weber and {van Rahden}, {Vanessa A} and Ludger Johannes and Hubert Hilbi",
note = "Copyright {\textcopyright} 2013 Elsevier Inc. All rights reserved.",
year = "2013",
month = jul,
day = "17",
doi = "10.1016/j.chom.2013.06.001",
language = "English",
volume = "14",
pages = "38--50",
journal = "CELL HOST MICROBE",
issn = "1931-3128",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - The Legionella effector RidL inhibits retrograde trafficking to promote intracellular replication

AU - Finsel, Ivo

AU - Ragaz, Curdin

AU - Hoffmann, Christine

AU - Harrison, Christopher F

AU - Weber, Stephen

AU - van Rahden, Vanessa A

AU - Johannes, Ludger

AU - Hilbi, Hubert

N1 - Copyright © 2013 Elsevier Inc. All rights reserved.

PY - 2013/7/17

Y1 - 2013/7/17

N2 - The bacteria causing Legionnaires' disease, Legionella pneumophila, replicate intracellularly within unique Legionella-containing vacuoles (LCVs). LCV formation involves a type IV secretion system (T4SS) that translocates effector proteins into host cells. We show that the T4SS effector RidL localizes to LCVs, supports intracellular bacterial growth, and alters retrograde trafficking, in which selected proteins are transported from endosomes to the Golgi. The retromer complex that mediates retrograde trafficking localizes to LCVs independently of RidL and restricts intracellular bacterial growth. RidL binds the Vps29 retromer subunit and the lipid PtdIns(3)P, which localizes retromer components to membranes. Additionally, specific retromer cargo receptors and sorting nexins that mediate protein capture and membrane remodeling preferentially localize to LCVs in the absence of ridL. Ectopic RidL production inhibits retrograde trafficking, and L. pneumophila blocks retrograde transport at endosome exit sites in a ridL-dependent manner. Collectively, these findings suggest that RidL inhibits retromer function to promote intracellular bacterial replication.

AB - The bacteria causing Legionnaires' disease, Legionella pneumophila, replicate intracellularly within unique Legionella-containing vacuoles (LCVs). LCV formation involves a type IV secretion system (T4SS) that translocates effector proteins into host cells. We show that the T4SS effector RidL localizes to LCVs, supports intracellular bacterial growth, and alters retrograde trafficking, in which selected proteins are transported from endosomes to the Golgi. The retromer complex that mediates retrograde trafficking localizes to LCVs independently of RidL and restricts intracellular bacterial growth. RidL binds the Vps29 retromer subunit and the lipid PtdIns(3)P, which localizes retromer components to membranes. Additionally, specific retromer cargo receptors and sorting nexins that mediate protein capture and membrane remodeling preferentially localize to LCVs in the absence of ridL. Ectopic RidL production inhibits retrograde trafficking, and L. pneumophila blocks retrograde transport at endosome exit sites in a ridL-dependent manner. Collectively, these findings suggest that RidL inhibits retromer function to promote intracellular bacterial replication.

KW - Animals

KW - Bacterial Proteins

KW - Cell Line

KW - Endosomes

KW - Humans

KW - Legionella pneumophila

KW - Legionnaires' Disease

KW - Mice

KW - Protein Transport

KW - Vacuoles

U2 - 10.1016/j.chom.2013.06.001

DO - 10.1016/j.chom.2013.06.001

M3 - SCORING: Journal article

C2 - 23870312

VL - 14

SP - 38

EP - 50

JO - CELL HOST MICROBE

JF - CELL HOST MICROBE

SN - 1931-3128

IS - 1

ER -