Salmonella effector SopD2 interferes with Rab34 function

Teo, Wei Xuan, Yang, Zhe, Kerr, Markus Charles, Luo, Lin, Guo, Zhong, Alexandrov, Kirill, Stow, Jenny Lea and Teasdale, Rohan David (2017) Salmonella effector SopD2 interferes with Rab34 function. Cell Biology International, 41 4: 433-446. doi:10.1002/cbin.10739


Author Teo, Wei Xuan
Yang, Zhe
Kerr, Markus Charles
Luo, Lin
Guo, Zhong
Alexandrov, Kirill
Stow, Jenny Lea
Teasdale, Rohan David
Title Salmonella effector SopD2 interferes with Rab34 function
Formatted title
Salmonella effector SopD2 interferes with Rab34 function
Journal name Cell Biology International   Check publisher's open access policy
ISSN 1095-8355
1065-6995
Publication date 2017-04-01
Year available 2017
Sub-type Article (original research)
DOI 10.1002/cbin.10739
Open Access Status Not yet assessed
Volume 41
Issue 4
Start page 433
End page 446
Total pages 14
Place of publication Chichester, West Sussex, United Kingdom
Publisher John Wiley & Sons
Language eng
Subject 1307 Cell Biology
Abstract Many intracellular pathogens have evolved highly specialized mechanisms to isolate themselves from the host cell's innate immune response while still obtaining the necessary nutrients to survive. Salmonella utilizes type 3 secretion systems (T3SSs) to deliver bacterial proteins called effectors, across the encompassing Salmonella Containing vacuole (SCV) membrane, to subvert the host's membrane trafficking pathways and alter other cellular processes. The Salmonella Pathogenicity Island (SPI)-2 effector SopD2 has recently been demonstrated to modulate multiple members of the Rab GTPase family such as Rab7, Rab8, Rab10, and Rab32 (D'Costa et al., Cell Reports, 12:1508–18; Spano et al., Cell Host & Microbe, 19:216–26). Here, we demonstrate the additional capacity of SopD2 to bind Rab34 and modulate its function. Our data indicate that depletion of Rab34 delays maturation of the SCV, and consequently, inhibits intracellular Salmonella enterica serotype typhimurium (S. typhimurium) growth. Interestingly, intracellular growth of the S. typhimurium lacking SopD2 was severely impaired in Rab34-depleted cells, suggesting a compounding virulence effect. Overall this study reveals an additional member of the Rab GTPase family, Rab34, that is modulated by SopD2 and provides insight into its role in Salmonella biology.
Formatted abstract
Many intracellular pathogens have evolved highly specialized mechanisms to isolate themselves from the host cell's innate immune response while still obtaining the necessary nutrients to survive. Salmonella utilizes type 3 secretion systems (T3SSs) to deliver bacterial proteins called effectors, across the encompassing Salmonella Containing vacuole (SCV) membrane, to subvert the host's membrane trafficking pathways and alter other cellular processes. The Salmonella Pathogenicity Island (SPI)-2 effector SopD2 has recently been demonstrated to modulate multiple members of the Rab GTPase family such as Rab7, Rab8, Rab10, and Rab32 (D'Costa et al., Cell Reports, 12:1508–18; Spano et al., Cell Host & Microbe, 19:216–26). Here, we demonstrate the additional capacity of SopD2 to bind Rab34 and modulate its function. Our data indicate that depletion of Rab34 delays maturation of the SCV, and consequently, inhibits intracellular Salmonella enterica serotype typhimurium (S. typhimurium) growth. Interestingly, intracellular growth of the S. typhimurium lacking SopD2 was severely impaired in Rab34-depleted cells, suggesting a compounding virulence effect. Overall this study reveals an additional member of the Rab GTPase family, Rab34, that is modulated by SopD2 and provides insight into its role in Salmonella biology.
Keyword Host–pathogen interaction
Rab34
Salmonella
SopD2
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 606788
DP150100364
DE120102321
APP1041929
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
Institute for Molecular Bioscience - Publications
 
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