Background: The central role of Type III secretion systems (T3SS) in bacteria-plant interactions is well established, yet unexpected findings are being uncovered through bacterial genome sequencing. Some Pseudomonas syringae strains possess an uncharacterized cluster of genes encoding putative components of a second T3SS (T3SS-2) in addition to the well characterized Hrc1 T3SS which is associated with disease lesions in host plants and with the triggering of hypersensitive response in non-host plants. The aim of this study is to perform an in silico analysis of T3SS-2, and to compare it with other known T3SSs.
Results: Based on phylogenetic analysis and gene organization comparisons, the T3SS-2 cluster of the P. syringae pv. phaseolicola strain is grouped with a second T3SS found in the pNGR234b plasmid of Rhizobium sp. These additional T3SS gene clusters define a subgroup within the Rhizobium T3SS family. Although, T3SS-2 is not distributed as widely as the Hrc1 T3SS in P. syringae strains, it was found to be constitutively expressed in P. syringae pv phaseolicola through RT-PCR experiments.
Conclusions: The relatedness of the P. syringae T3SS-2 to a second T3SS from the pNGR234b plasmid of Rhizobium sp., member of subgroup II of the rhizobial T3SS family, indicates common ancestry and/or possible horizontal transfer events between these species. Functional analysis and genome sequencing of more rhizobia and P. syringae pathovars may shed light into why these bacteria maintain a second T3SS gene cluster in their genome.
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http://dx.doi.org/10.1186/1471-2180-12-188 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of General Practice, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou, 510515, China.
Large-scale studies indicate a strong relationship between the gut microbiome, type 2 diabetes mellitus (T2DM), and atherosclerotic cardiovascular disease (ASCVD). Here, a higher abundance of the type III secretion system (T3SS) virulence factors of Enterobacteriaceae/Escherichia-Shigella in patients with T2DM-related-ASCVD, which correlates with their atherosclerotic stenosis is reported. Overexpression of T3SS via Citrobacter rodentium (CR) infection in Apoe-/- T2DM mice exacerbated atherosclerotic lesion formation and increased gut permeability.
View Article and Find Full Text PDFmSphere
November 2024
Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Melioidosis is a serious infectious disease caused by the Gram-negative bacterium . Recently, Rab32-dependent immune vesicles emerge as a critical defense pathway to restrict the intracellular . However, can evade host immune vesicles and survive in the cytoplasm, although this mechanism is not well understood.
View Article and Find Full Text PDFPLoS Pathog
October 2024
Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky, United States of America.
Leukotriene B4 (LTB4) is an inflammatory lipid produced in response to pathogens that is critical for initiating the inflammatory cascade needed to control infection. However, during plague, Yersinia pestis inhibits the timely synthesis of LTB4 and subsequent inflammation. Using bacterial mutants, we previously determined that Y.
View Article and Find Full Text PDFInfect Immun
October 2024
Paul G. Allen School for Global Health, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA.
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View Article and Find Full Text PDFJ Cell Biochem
January 2025
College of Information Technology, Shanghai Ocean University, Shanghai, China.
The Type III secretion effectors (T3SEs) are bacterial proteins synthesized by Gram-negative pathogens and delivered into host cells via the Type III secretion system (T3SS). These effectors usually play a pivotal role in the interactions between bacteria and hosts. Hence, the precise identification of T3SEs aids researchers in exploring the pathogenic mechanisms of bacterial infections.
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