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Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells

Standard

Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells. / Berneking, Laura; Schnapp, Marie; Rumm, Andreas; Trasak, Claudia; Ruckdeschel, Klaus; Alawi, Malik; Grundhoff, Adam; Kikhney, Alexey G; Nolte, Friedrich; Buck, Friedrich; Perbandt, Markus; Betzel, Christian; Svergun, Dmitri I; Hentschke, Moritz; Aepfelbacher, Martin.

in: PLOS PATHOG, Jahrgang 12, Nr. 6, 13.06.2016, S. e1005660.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Berneking, L, Schnapp, M, Rumm, A, Trasak, C, Ruckdeschel, K, Alawi, M, Grundhoff, A, Kikhney, AG, Nolte, F, Buck, F, Perbandt, M, Betzel, C, Svergun, DI, Hentschke, M & Aepfelbacher, M 2016, 'Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells', PLOS PATHOG, Jg. 12, Nr. 6, S. e1005660. https://doi.org/10.1371/journal.ppat.1005660

APA

Berneking, L., Schnapp, M., Rumm, A., Trasak, C., Ruckdeschel, K., Alawi, M., Grundhoff, A., Kikhney, A. G., Nolte, F., Buck, F., Perbandt, M., Betzel, C., Svergun, D. I., Hentschke, M., & Aepfelbacher, M. (2016). Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells. PLOS PATHOG, 12(6), e1005660. https://doi.org/10.1371/journal.ppat.1005660

Vancouver

Berneking L, Schnapp M, Rumm A, Trasak C, Ruckdeschel K, Alawi M et al. Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells. PLOS PATHOG. 2016 Jun 13;12(6):e1005660. https://doi.org/10.1371/journal.ppat.1005660

Bibtex

@article{ffc4fe38a5b5462f8ea4fff3d2ce95b4,
title = "Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells",
abstract = "Yersinia outer protein M (YopM) is a crucial immunosuppressive effector of the plaque agent Yersinia pestis and other pathogenic Yersinia species. YopM enters the nucleus of host cells but neither the mechanisms governing its nucleocytoplasmic shuttling nor its intranuclear activities are known. Here we identify the DEAD-box helicase 3 (DDX3) as a novel interaction partner of Y. enterocolitica YopM and present the three-dimensional structure of a YopM:DDX3 complex. Knockdown of DDX3 or inhibition of the exportin chromosomal maintenance 1 (CRM1) increased the nuclear level of YopM suggesting that YopM exploits DDX3 to exit the nucleus via the CRM1 export pathway. Increased nuclear YopM levels caused enhanced phosphorylation of Ribosomal S6 Kinase 1 (RSK1) in the nucleus. In Y. enterocolitica infected primary human macrophages YopM increased the level of Interleukin-10 (IL-10) mRNA and this effect required interaction of YopM with RSK and was enhanced by blocking YopM's nuclear export. We propose that the DDX3/CRM1 mediated nucleocytoplasmic shuttling of YopM determines the extent of phosphorylation of RSK in the nucleus to control transcription of immunosuppressive cytokines.",
keywords = "Journal Article",
author = "Laura Berneking and Marie Schnapp and Andreas Rumm and Claudia Trasak and Klaus Ruckdeschel and Malik Alawi and Adam Grundhoff and Kikhney, {Alexey G} and Friedrich Nolte and Friedrich Buck and Markus Perbandt and Christian Betzel and Svergun, {Dmitri I} and Moritz Hentschke and Martin Aepfelbacher",
year = "2016",
month = jun,
day = "13",
doi = "10.1371/journal.ppat.1005660",
language = "English",
volume = "12",
pages = "e1005660",
journal = "PLOS PATHOG",
issn = "1553-7366",
publisher = "Public Library of Science",
number = "6",

}

RIS

TY - JOUR

T1 - Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells

AU - Berneking, Laura

AU - Schnapp, Marie

AU - Rumm, Andreas

AU - Trasak, Claudia

AU - Ruckdeschel, Klaus

AU - Alawi, Malik

AU - Grundhoff, Adam

AU - Kikhney, Alexey G

AU - Nolte, Friedrich

AU - Buck, Friedrich

AU - Perbandt, Markus

AU - Betzel, Christian

AU - Svergun, Dmitri I

AU - Hentschke, Moritz

AU - Aepfelbacher, Martin

PY - 2016/6/13

Y1 - 2016/6/13

N2 - Yersinia outer protein M (YopM) is a crucial immunosuppressive effector of the plaque agent Yersinia pestis and other pathogenic Yersinia species. YopM enters the nucleus of host cells but neither the mechanisms governing its nucleocytoplasmic shuttling nor its intranuclear activities are known. Here we identify the DEAD-box helicase 3 (DDX3) as a novel interaction partner of Y. enterocolitica YopM and present the three-dimensional structure of a YopM:DDX3 complex. Knockdown of DDX3 or inhibition of the exportin chromosomal maintenance 1 (CRM1) increased the nuclear level of YopM suggesting that YopM exploits DDX3 to exit the nucleus via the CRM1 export pathway. Increased nuclear YopM levels caused enhanced phosphorylation of Ribosomal S6 Kinase 1 (RSK1) in the nucleus. In Y. enterocolitica infected primary human macrophages YopM increased the level of Interleukin-10 (IL-10) mRNA and this effect required interaction of YopM with RSK and was enhanced by blocking YopM's nuclear export. We propose that the DDX3/CRM1 mediated nucleocytoplasmic shuttling of YopM determines the extent of phosphorylation of RSK in the nucleus to control transcription of immunosuppressive cytokines.

AB - Yersinia outer protein M (YopM) is a crucial immunosuppressive effector of the plaque agent Yersinia pestis and other pathogenic Yersinia species. YopM enters the nucleus of host cells but neither the mechanisms governing its nucleocytoplasmic shuttling nor its intranuclear activities are known. Here we identify the DEAD-box helicase 3 (DDX3) as a novel interaction partner of Y. enterocolitica YopM and present the three-dimensional structure of a YopM:DDX3 complex. Knockdown of DDX3 or inhibition of the exportin chromosomal maintenance 1 (CRM1) increased the nuclear level of YopM suggesting that YopM exploits DDX3 to exit the nucleus via the CRM1 export pathway. Increased nuclear YopM levels caused enhanced phosphorylation of Ribosomal S6 Kinase 1 (RSK1) in the nucleus. In Y. enterocolitica infected primary human macrophages YopM increased the level of Interleukin-10 (IL-10) mRNA and this effect required interaction of YopM with RSK and was enhanced by blocking YopM's nuclear export. We propose that the DDX3/CRM1 mediated nucleocytoplasmic shuttling of YopM determines the extent of phosphorylation of RSK in the nucleus to control transcription of immunosuppressive cytokines.

KW - Journal Article

U2 - 10.1371/journal.ppat.1005660

DO - 10.1371/journal.ppat.1005660

M3 - SCORING: Journal article

C2 - 27300509

VL - 12

SP - e1005660

JO - PLOS PATHOG

JF - PLOS PATHOG

SN - 1553-7366

IS - 6

ER -