Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB

Dorothy Truong; Kirsten C. Boddy; Veronica Canadien; Danielle Brabant; Gregory D. Fairn; Vanessa M. D'Costa; Etienne Coyaud; Brian Raught; Dolores Pérez-Sala; Wei Sun Park; Won Do Heo; Sergio Grinstein; John H. Brumell

doi:10.1111/cmi.12938

Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB

Dorothy Truong, Kirsten C. Boddy, Veronica Canadien, Danielle Brabant, Gregory D. Fairn, Vanessa M. D'Costa, Etienne Coyaud, Brian Raught, Dolores Pérez-Sala, Wei Sun Park, Won Do Heo, Sergio Grinstein, John H. Brumell

Research output: Contribution to journal › Article › peer-review

27 Citations (Scopus)

Abstract

Salmonella uses Type 3 secretion systems (T3SSs) to deliver virulence factors, called effectors, into host cells during infection. The T3SS effectors promote invasion into host cells and the generation of a replicative niche. SopB is a T3SS effector that plays an important role in Salmonella pathogenesis through its lipid phosphatase activity. Here, we show that SopB mediates the recruitment of Rho GTPases (RhoB, RhoD, RhoH, and RhoJ) to bacterial invasion sites. RhoJ contributes to Salmonella invasion, and RhoB and RhoH play an important role in Akt activation. R-Ras1 also contributes to SopB-dependent Akt activation by promoting the localised production of PI(3,4)P ₂ /PI(3,4,5)P ₃ . Our studies reveal new signalling factors involved in SopB-dependent Salmonella infection.

Original language	English
Article number	e12938
Journal	Cellular Microbiology
Volume	20
Issue number	10
DOIs	https://doi.org/10.1111/cmi.12938
Publication status	Published - Oct 2018
Externally published	Yes

Bibliographical note

Funding Information:
We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J. H. B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D. P.‐S.'s lab was supported by the Spanish Ministerio de Economía y Competitividad/FEDER grants SAF2012‐36519 and SAF2015‐68590R. D. T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K. C. B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329).

Funding Information:
Natural Sciences and Engineering Research Council of Canada; Ontario Graduate Scholarship; Canadian Institutes of Health Research, Grant/Award Number: 154329; Spanish Ministerio de Economía y Competitividad/ FEDER, Grant/Award Numbers: SAF2015‐ 68590R and SAF2012‐36519

Funding Information:
We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J.?H.?B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D.?P.-S.'s lab was supported by the Spanish Ministerio de Econom?a y Competitividad/FEDER grants SAF2012-36519 and SAF2015-68590R. D.?T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K.?C.?B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329).

Publisher Copyright:
© 2018 John Wiley & Sons Ltd

ASJC Scopus Subject Areas

Microbiology
Immunology
Virology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

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10.1111/cmi.12938

Cite this

@article{5e44b2a378924dc498d4430384cb39eb,

title = "Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB",

abstract = " Salmonella uses Type 3 secretion systems (T3SSs) to deliver virulence factors, called effectors, into host cells during infection. The T3SS effectors promote invasion into host cells and the generation of a replicative niche. SopB is a T3SS effector that plays an important role in Salmonella pathogenesis through its lipid phosphatase activity. Here, we show that SopB mediates the recruitment of Rho GTPases (RhoB, RhoD, RhoH, and RhoJ) to bacterial invasion sites. RhoJ contributes to Salmonella invasion, and RhoB and RhoH play an important role in Akt activation. R-Ras1 also contributes to SopB-dependent Akt activation by promoting the localised production of PI(3,4)P 2 /PI(3,4,5)P 3 . Our studies reveal new signalling factors involved in SopB-dependent Salmonella infection. ",

author = "Dorothy Truong and Boddy, {Kirsten C.} and Veronica Canadien and Danielle Brabant and Fairn, {Gregory D.} and D'Costa, {Vanessa M.} and Etienne Coyaud and Brian Raught and Dolores P{\'e}rez-Sala and Park, {Wei Sun} and Heo, {Won Do} and Sergio Grinstein and Brumell, {John H.}",

note = "Funding Information: We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J. H. B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D. P.‐S.'s lab was supported by the Spanish Ministerio de Econom{\'i}a y Competitividad/FEDER grants SAF2012‐36519 and SAF2015‐68590R. D. T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K. C. B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329). Funding Information: Natural Sciences and Engineering Research Council of Canada; Ontario Graduate Scholarship; Canadian Institutes of Health Research, Grant/Award Number: 154329; Spanish Ministerio de Econom{\'i}a y Competitividad/ FEDER, Grant/Award Numbers: SAF2015‐ 68590R and SAF2012‐36519 Funding Information: We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J.?H.?B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D.?P.-S.'s lab was supported by the Spanish Ministerio de Econom?a y Competitividad/FEDER grants SAF2012-36519 and SAF2015-68590R. D.?T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K.?C.?B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329). Publisher Copyright: {\textcopyright} 2018 John Wiley & Sons Ltd",

year = "2018",

month = oct,

doi = "10.1111/cmi.12938",

language = "English",

volume = "20",

journal = "Cellular Microbiology",

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AU - Truong, Dorothy

AU - Boddy, Kirsten C.

AU - Canadien, Veronica

AU - Brabant, Danielle

AU - Fairn, Gregory D.

AU - D'Costa, Vanessa M.

AU - Coyaud, Etienne

AU - Raught, Brian

AU - Pérez-Sala, Dolores

AU - Park, Wei Sun

AU - Heo, Won Do

AU - Grinstein, Sergio

AU - Brumell, John H.

N1 - Funding Information: We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J. H. B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D. P.‐S.'s lab was supported by the Spanish Ministerio de Economía y Competitividad/FEDER grants SAF2012‐36519 and SAF2015‐68590R. D. T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K. C. B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329). Funding Information: Natural Sciences and Engineering Research Council of Canada; Ontario Graduate Scholarship; Canadian Institutes of Health Research, Grant/Award Number: 154329; Spanish Ministerio de Economía y Competitividad/ FEDER, Grant/Award Numbers: SAF2015‐ 68590R and SAF2012‐36519 Funding Information: We are grateful to members of the Brumell Laboratory for the critical reading of this manuscript and to Clara L. Oeste (C.S.I.C.) for helpful comments. We thank Michael Woodside and Paul Paroutis for help with confocal microscopy. J.?H.?B. holds the Pitblado Chair in Cell Biology at the Hospital for Sick Children. Infrastructure for the Brumell Laboratory was provided by a Leader's Opportunity Fund grant from the Canadian Foundation for Innovation and the Ontario Innovation Trust. D.?P.-S.'s lab was supported by the Spanish Ministerio de Econom?a y Competitividad/FEDER grants SAF2012-36519 and SAF2015-68590R. D.?T. was supported by a studentship from The Canadian Institutes of Health Research and an Ontario Graduate Scholarship. K.?C.?B. was supported by a studentship from the Natural Sciences and Engineering Research Council of Canada and an Ontario Graduate Scholarship. This work was supported by an operating grant from the Canadian Institutes of Health Research (FDN 154329). Publisher Copyright: © 2018 John Wiley & Sons Ltd

PY - 2018/10

Y1 - 2018/10

N2 - Salmonella uses Type 3 secretion systems (T3SSs) to deliver virulence factors, called effectors, into host cells during infection. The T3SS effectors promote invasion into host cells and the generation of a replicative niche. SopB is a T3SS effector that plays an important role in Salmonella pathogenesis through its lipid phosphatase activity. Here, we show that SopB mediates the recruitment of Rho GTPases (RhoB, RhoD, RhoH, and RhoJ) to bacterial invasion sites. RhoJ contributes to Salmonella invasion, and RhoB and RhoH play an important role in Akt activation. R-Ras1 also contributes to SopB-dependent Akt activation by promoting the localised production of PI(3,4)P 2 /PI(3,4,5)P 3 . Our studies reveal new signalling factors involved in SopB-dependent Salmonella infection.

AB - Salmonella uses Type 3 secretion systems (T3SSs) to deliver virulence factors, called effectors, into host cells during infection. The T3SS effectors promote invasion into host cells and the generation of a replicative niche. SopB is a T3SS effector that plays an important role in Salmonella pathogenesis through its lipid phosphatase activity. Here, we show that SopB mediates the recruitment of Rho GTPases (RhoB, RhoD, RhoH, and RhoJ) to bacterial invasion sites. RhoJ contributes to Salmonella invasion, and RhoB and RhoH play an important role in Akt activation. R-Ras1 also contributes to SopB-dependent Akt activation by promoting the localised production of PI(3,4)P 2 /PI(3,4,5)P 3 . Our studies reveal new signalling factors involved in SopB-dependent Salmonella infection.

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DO - 10.1111/cmi.12938

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Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB

Abstract

Bibliographical note

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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