The Salmonella Effector SseK3 Targets Small Rab GTPases
dc.contributor.author
Gan, Jiyao
dc.contributor.author
Scott, Nichollas E.
dc.contributor.author
Newson, Joshua
dc.contributor.author
Wibawa, Rachelia R.
dc.contributor.author
Lung, Tania W.F.
dc.contributor.author
Pollock, Georgina L.
dc.contributor.author
Ng, Garrett Z.
dc.contributor.author
van Driel, Ian
dc.contributor.author
Pearson, Jaclyn S.
dc.contributor.author
Hartland, Elizabeth L.
dc.contributor.author
Giogha, Cristina
dc.date.accessioned
2020-09-11T07:49:27Z
dc.date.available
2020-09-11T02:56:00Z
dc.date.available
2020-09-11T07:49:27Z
dc.date.issued
2020-08
dc.identifier.issn
2235-2988
dc.identifier.other
10.3389/fcimb.2020.00419
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/439885
dc.identifier.doi
10.3929/ethz-b-000439885
dc.description.abstract
During infection, Salmonella species inject multiple type III secretion system (T3SS) effector proteins into host cells that mediate invasion and subsequent intracellular replication. At early stages of infection, Salmonella exploits key regulators of host intracellular vesicle transport, including the small GTPases Rab5 and Rab7, to subvert host endocytic vesicle trafficking and establish the Salmonella-containing vacuole (SCV). At later stages of intracellular replication, interactions of the SCV with Rab GTPases are less well defined. Here we report that Rab1, Rab5, and Rab11 are modified at later stages of Salmonella infection by SseK3, an arginine N-acetylglucosamine (GlcNAc) transferase effector translocated via the Salmonella pathogenicity island 2 (SPI-2) type III secretion system. SseK3 modified arginines at positions 74, 82, and 111 within Rab1 and this modification occurred independently of Rab1 nucleotide binding. SseK3 exhibited Golgi localization that was independent of its glycosyltransferase activity but Arg-GlcNAc transferase activity was required for inhibition of alkaline phosphatase secretion in transfected cells. While SseK3 had a modest effect on SEAP secretion during infection of HeLa229 cells, inhibition of IL-1 and GM-CSF cytokine secretion was only observed upon over-expression of SseK3 during infection of RAW264.7 cells. Our results suggest that, in addition to targeting death receptor signaling, SseK3 may contribute to Salmonella infection by interfering with the activity of key Rab GTPases.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Frontiers Media
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
Salmonella enterica
en_US
dc.subject
Rab
en_US
dc.subject
glycosyltransferase
en_US
dc.subject
protein secretion
en_US
dc.subject
host-pathogen interaction
en_US
dc.title
The Salmonella Effector SseK3 Targets Small Rab GTPases
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2020-08-19
ethz.journal.title
Frontiers in Cellular and Infection Microbiology
ethz.journal.volume
10
en_US
ethz.pages.start
419
en_US
ethz.size
17 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Lausanne
ethz.publication.status
published
en_US
ethz.date.deposited
2020-09-11T02:56:05Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-09-11T07:49:41Z
ethz.rosetta.lastUpdated
2024-02-02T12:01:44Z
ethz.rosetta.versionExported
true
ethz.COinS
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