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The Salmonella SPI1 type three secretion system responds to periplasmic disulfide bond status via the flagellar apparatus and the RcsCDB system.
J Bacteriol. 2008 Jan; 190(1):87-97.JB

Abstract

Upon contact with intestinal epithelial cells, Salmonella enterica serovar Typhimurium injects a set of effector proteins into the host cell cytoplasm via the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS) to induce inflammatory diarrhea and bacterial uptake. The master SPI1 regulatory gene hilA is controlled directly by three AraC-like regulators: HilD, HilC, and RtsA. Previous work suggested a role for DsbA, a periplasmic disulfide bond oxidase, in SPI1 T3SS function. RtsA directly activates dsbA, and deletion of dsbA leads to loss of SPI1-dependent secretion. We have studied the dsbA phenotypes by monitoring expression of SPI1 regulatory, structural, and effector genes. Here we present evidence that loss of DsbA independently affects SPI1 regulation and SPI1 function. The dsbA-mediated feedback inhibition of SPI1 transcription is not due to defects in the SPI1 T3SS apparatus. Rather, the transcriptional response is dependent on both the flagellar protein FliZ and the RcsCDB system, which also affects fliZ transcription. Thus, the status of disulfide bonds in the periplasm affects expression of the SPI1 system indirectly via the flagellar apparatus. RcsCDB can also affect SPI1 independently of FliZ. All regulation is through HilD, consistent with our current model for SPI1 regulation.

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Authors+Show Affiliations

Lin D
Department of Microbiology, College of Medicine, University of Illinois, Urbana, IL 61801, USA.
Rao CV
No affiliation info available
Slauch JM
No affiliation info available

MeSH

Bacterial ProteinsDisulfidesDrug Resistance, MicrobialEscherichia coliFlagellaGene AmplificationGene DeletionGenes, ReporterHumansIntestinal MucosaMutagenesis, InsertionalPlasmidsProtein KinasesSalmonella typhimuriumTranscription FactorsTranscription, Genetic

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17951383

Citation

Lin, Dongxia, et al. "The Salmonella SPI1 Type Three Secretion System Responds to Periplasmic Disulfide Bond Status Via the Flagellar Apparatus and the RcsCDB System." Journal of Bacteriology, vol. 190, no. 1, 2008, pp. 87-97.
Lin D, Rao CV, Slauch JM. The Salmonella SPI1 type three secretion system responds to periplasmic disulfide bond status via the flagellar apparatus and the RcsCDB system. J Bacteriol. 2008;190(1):87-97.
Lin, D., Rao, C. V., & Slauch, J. M. (2008). The Salmonella SPI1 type three secretion system responds to periplasmic disulfide bond status via the flagellar apparatus and the RcsCDB system. Journal of Bacteriology, 190(1), 87-97.
Lin D, Rao CV, Slauch JM. The Salmonella SPI1 Type Three Secretion System Responds to Periplasmic Disulfide Bond Status Via the Flagellar Apparatus and the RcsCDB System. J Bacteriol. 2008;190(1):87-97. PubMed PMID: 17951383.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Salmonella SPI1 type three secretion system responds to periplasmic disulfide bond status via the flagellar apparatus and the RcsCDB system. AU - Lin,Dongxia, AU - Rao,Christopher V, AU - Slauch,James M, Y1 - 2007/10/19/ PY - 2007/10/24/pubmed PY - 2008/1/16/medline PY - 2007/10/24/entrez SP - 87 EP - 97 JF - Journal of bacteriology JO - J Bacteriol VL - 190 IS - 1 N2 - Upon contact with intestinal epithelial cells, Salmonella enterica serovar Typhimurium injects a set of effector proteins into the host cell cytoplasm via the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS) to induce inflammatory diarrhea and bacterial uptake. The master SPI1 regulatory gene hilA is controlled directly by three AraC-like regulators: HilD, HilC, and RtsA. Previous work suggested a role for DsbA, a periplasmic disulfide bond oxidase, in SPI1 T3SS function. RtsA directly activates dsbA, and deletion of dsbA leads to loss of SPI1-dependent secretion. We have studied the dsbA phenotypes by monitoring expression of SPI1 regulatory, structural, and effector genes. Here we present evidence that loss of DsbA independently affects SPI1 regulation and SPI1 function. The dsbA-mediated feedback inhibition of SPI1 transcription is not due to defects in the SPI1 T3SS apparatus. Rather, the transcriptional response is dependent on both the flagellar protein FliZ and the RcsCDB system, which also affects fliZ transcription. Thus, the status of disulfide bonds in the periplasm affects expression of the SPI1 system indirectly via the flagellar apparatus. RcsCDB can also affect SPI1 independently of FliZ. All regulation is through HilD, consistent with our current model for SPI1 regulation. SN - 1098-5530 UR - https://www.unboundmedicine.com/medline/citation/17951383/The_Salmonella_SPI1_type_three_secretion_system_responds_to_periplasmic_disulfide_bond_status_via_the_flagellar_apparatus_and_the_RcsCDB_system_ L2 - https://journals.asm.org/doi/10.1128/JB.01323-07?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -