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SseL is a salmonella-specific translocated effector integrated into the SsrB-controlled salmonella pathogenicity island 2 type III secretion system.
Infect Immun. 2007 Feb; 75(2):574-80.II

Abstract

Bacterial pathogens use horizontal gene transfer to acquire virulence factors that influence host colonization, alter virulence traits, and ultimately shape the outcome of disease following infection. One hallmark of the host-pathogen interaction is the prokaryotic type III secretion system that translocates virulence factors into host cells during infection. Salmonella enterica possesses two type III secretion systems that are utilized during host colonization and intracellular replication. Salmonella pathogenicity island 2 (SPI2) is a genomic island containing approximately 30 contiguous genes required to assemble a functional secretion system including the two-component regulatory system called SsrA-SsrB that positively regulates transcription of the secretion apparatus. We used transcriptional profiling with DNA microarrays to search for genes that coregulate with the SPI2 type III secretion machinery in an SsrB-dependent manner. Here we report the identification of a Salmonella-specific translocated effector called SseL that is required for full virulence during murine typhoid-like disease. Analysis of infected macrophages using fluorescence-activated cell sorting revealed that sseL is induced inside cells and requires SsrB for expression. SseL is retained predominantly in the cytoplasm of infected cells following translocation by the type III system encoded in SPI2. Animal infection experiments with sseL mutant bacteria indicate that integration of SseL into the SsrB response regulatory system contributes to systemic virulence of this pathogen.

Authors+Show Affiliations

Department of Biochemistry and Biomedical Sciences, McMaster University, Health Sciences Centre, Room 4H17, 1200 Main St. West, Hamilton, Ontario L8N 3Z5, Canada. coombes@mcmaster.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

17158898

Citation

Coombes, Brian K., et al. "SseL Is a Salmonella-specific Translocated Effector Integrated Into the SsrB-controlled Salmonella Pathogenicity Island 2 Type III Secretion System." Infection and Immunity, vol. 75, no. 2, 2007, pp. 574-80.
Coombes BK, Lowden MJ, Bishop JL, et al. SseL is a salmonella-specific translocated effector integrated into the SsrB-controlled salmonella pathogenicity island 2 type III secretion system. Infect Immun. 2007;75(2):574-80.
Coombes, B. K., Lowden, M. J., Bishop, J. L., Wickham, M. E., Brown, N. F., Duong, N., Osborne, S., Gal-Mor, O., & Finlay, B. B. (2007). SseL is a salmonella-specific translocated effector integrated into the SsrB-controlled salmonella pathogenicity island 2 type III secretion system. Infection and Immunity, 75(2), 574-80.
Coombes BK, et al. SseL Is a Salmonella-specific Translocated Effector Integrated Into the SsrB-controlled Salmonella Pathogenicity Island 2 Type III Secretion System. Infect Immun. 2007;75(2):574-80. PubMed PMID: 17158898.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - SseL is a salmonella-specific translocated effector integrated into the SsrB-controlled salmonella pathogenicity island 2 type III secretion system. AU - Coombes,Brian K, AU - Lowden,Michael J, AU - Bishop,Jennifer L, AU - Wickham,Mark E, AU - Brown,Nat F, AU - Duong,Nancy, AU - Osborne,Suzanne, AU - Gal-Mor,Ohad, AU - Finlay,B Brett, Y1 - 2006/12/11/ PY - 2006/12/13/pubmed PY - 2007/3/9/medline PY - 2006/12/13/entrez SP - 574 EP - 80 JF - Infection and immunity JO - Infect Immun VL - 75 IS - 2 N2 - Bacterial pathogens use horizontal gene transfer to acquire virulence factors that influence host colonization, alter virulence traits, and ultimately shape the outcome of disease following infection. One hallmark of the host-pathogen interaction is the prokaryotic type III secretion system that translocates virulence factors into host cells during infection. Salmonella enterica possesses two type III secretion systems that are utilized during host colonization and intracellular replication. Salmonella pathogenicity island 2 (SPI2) is a genomic island containing approximately 30 contiguous genes required to assemble a functional secretion system including the two-component regulatory system called SsrA-SsrB that positively regulates transcription of the secretion apparatus. We used transcriptional profiling with DNA microarrays to search for genes that coregulate with the SPI2 type III secretion machinery in an SsrB-dependent manner. Here we report the identification of a Salmonella-specific translocated effector called SseL that is required for full virulence during murine typhoid-like disease. Analysis of infected macrophages using fluorescence-activated cell sorting revealed that sseL is induced inside cells and requires SsrB for expression. SseL is retained predominantly in the cytoplasm of infected cells following translocation by the type III system encoded in SPI2. Animal infection experiments with sseL mutant bacteria indicate that integration of SseL into the SsrB response regulatory system contributes to systemic virulence of this pathogen. SN - 0019-9567 UR - https://www.unboundmedicine.com/medline/citation/17158898/SseL_is_a_salmonella_specific_translocated_effector_integrated_into_the_SsrB_controlled_salmonella_pathogenicity_island_2_type_III_secretion_system_ L2 - http://iai.asm.org/cgi/pmidlookup?view=long&pmid=17158898 DB - PRIME DP - Unbound Medicine ER -