Tags

Type your tag names separated by a space and hit enter

PagR mediates the precise regulation of Salmonella pathogenicity island 2 gene expression in response to magnesium and phosphate signals in Salmonella Typhimurium.
Cell Microbiol. 2020 02; 22(2):e13125.CM

Abstract

To establish systemic infections, Salmonella enterica serovar Typhimurium (S. Typhimurium) requires Salmonella pathogenicity island 2 (SPI-2) to survive and replicate within macrophages. High expression of many SPI-2 genes during the entire intracellular growth period within macrophages is essential, as it contributes to the formation of Salmonella-containing vacuole and bacterial replication. However, the regulatory mechanisms underlying the sustained induction of SPI-2 within macrophages are not fully understood. Here, we revealed a time-dependent regulation of SPI-2 expression mediated by a novel regulator PagR (STM2345) in response to the low Mg2+ and low phosphate (Pi) signals, which ensured the high induction of SPI-2 during the entire intramacrophage growth period. Deletion of pagR results in reduced bacterial replication in macrophages and attenuation of systemic virulence in mice. The effects of pagR on virulence are dependent on upregulating the expression of slyA, a regulator of SPI-2. At the early (0-4 hr) and later (after 4 hr) stage post-infection of macrophages, pagR is induced by the low Pi via PhoB/R two-component systems and low Mg2+ via PhoP/Q systems, respectively. Collectively, our findings revealed that the PagR-mediated regulatory mechanism contributes to the precise and sustained activation of SPI-2 genes within macrophages, which is essential for S. Typhimurium systemic virulence.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Jiang L
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China. Tianjin Key Laboratory of Microbial Functional Genomics, Nankai University, Tianjin, China.
Wang P
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China.
Li X
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China.
Lv R
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China.
Wang L
Inspection and Quarantine Technical Center, Beijing Entry-Exit Inspection and Quarantine Bureau, Beijing, China.
Yang B
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China. Tianjin Key Laboratory of Microbial Functional Genomics, Nankai University, Tianjin, China.
Huang D
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China. Tianjin Key Laboratory of Microbial Functional Genomics, Nankai University, Tianjin, China.
Feng L
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China. Tianjin Key Laboratory of Microbial Functional Genomics, Nankai University, Tianjin, China.
Liu B
TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China. Tianjin Key Laboratory of Microbial Functional Genomics, Nankai University, Tianjin, China.

MeSH

AnimalsBacterial ProteinsCaco-2 CellsDNA-Binding ProteinsGene DeletionGene Expression Regulation, BacterialGenomic IslandsHumansMacrophagesMagnesiumMembrane ProteinsMicePhosphatesRAW 264.7 CellsRepressor ProteinsSalmonella typhimuriumTranscription FactorsVirulenceVirulence Factors

Pub Type(s)

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

Language

eng

PubMed ID

31610610

Citation

Jiang, Lingyan, et al. "PagR Mediates the Precise Regulation of Salmonella Pathogenicity Island 2 Gene Expression in Response to Magnesium and Phosphate Signals in Salmonella Typhimurium." Cellular Microbiology, vol. 22, no. 2, 2020, pp. e13125.
Jiang L, Wang P, Li X, et al. PagR mediates the precise regulation of Salmonella pathogenicity island 2 gene expression in response to magnesium and phosphate signals in Salmonella Typhimurium. Cell Microbiol. 2020;22(2):e13125.
Jiang, L., Wang, P., Li, X., Lv, R., Wang, L., Yang, B., Huang, D., Feng, L., & Liu, B. (2020). PagR mediates the precise regulation of Salmonella pathogenicity island 2 gene expression in response to magnesium and phosphate signals in Salmonella Typhimurium. Cellular Microbiology, 22(2), e13125. https://doi.org/10.1111/cmi.13125
Jiang L, et al. PagR Mediates the Precise Regulation of Salmonella Pathogenicity Island 2 Gene Expression in Response to Magnesium and Phosphate Signals in Salmonella Typhimurium. Cell Microbiol. 2020;22(2):e13125. PubMed PMID: 31610610.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - PagR mediates the precise regulation of Salmonella pathogenicity island 2 gene expression in response to magnesium and phosphate signals in Salmonella Typhimurium. AU - Jiang,Lingyan, AU - Wang,Peisheng, AU - Li,Xiaomin, AU - Lv,Runxia, AU - Wang,Lin, AU - Yang,Bin, AU - Huang,Di, AU - Feng,Lu, AU - Liu,Bin, Y1 - 2019/11/24/ PY - 2019/04/15/received PY - 2019/09/25/revised PY - 2019/09/26/accepted PY - 2019/10/15/pubmed PY - 2021/3/23/medline PY - 2019/10/15/entrez KW - Salmonella Typhimurium KW - Salmonella pathogenicity island 2 KW - signal transduction KW - systemic virulence SP - e13125 EP - e13125 JF - Cellular microbiology JO - Cell Microbiol VL - 22 IS - 2 N2 - To establish systemic infections, Salmonella enterica serovar Typhimurium (S. Typhimurium) requires Salmonella pathogenicity island 2 (SPI-2) to survive and replicate within macrophages. High expression of many SPI-2 genes during the entire intracellular growth period within macrophages is essential, as it contributes to the formation of Salmonella-containing vacuole and bacterial replication. However, the regulatory mechanisms underlying the sustained induction of SPI-2 within macrophages are not fully understood. Here, we revealed a time-dependent regulation of SPI-2 expression mediated by a novel regulator PagR (STM2345) in response to the low Mg2+ and low phosphate (Pi) signals, which ensured the high induction of SPI-2 during the entire intramacrophage growth period. Deletion of pagR results in reduced bacterial replication in macrophages and attenuation of systemic virulence in mice. The effects of pagR on virulence are dependent on upregulating the expression of slyA, a regulator of SPI-2. At the early (0-4 hr) and later (after 4 hr) stage post-infection of macrophages, pagR is induced by the low Pi via PhoB/R two-component systems and low Mg2+ via PhoP/Q systems, respectively. Collectively, our findings revealed that the PagR-mediated regulatory mechanism contributes to the precise and sustained activation of SPI-2 genes within macrophages, which is essential for S. Typhimurium systemic virulence. SN - 1462-5822 UR - https://www.unboundmedicine.com/medline/citation/31610610/PagR_mediates_the_precise_regulation_of_Salmonella_pathogenicity_island_2_gene_expression_in_response_to_magnesium_and_phosphate_signals_in_Salmonella_Typhimurium_ DB - PRIME DP - Unbound Medicine ER -