ArticleJournal of bacteriology2008
Sigma32-mediated negative regulation of Salmonella pathogenicity island 1 expression.
Article in Journal of bacteriology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Article
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- Lysophosphatidylcholine Potentiates Antibacterial Activity of Polymyxin B.Antimicrobial agents and chemotherapy · 2020Article
- Protective efficacy of the recombinant lysozyme-PMAP36 fusion protein-inactivatedCanadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2020Article
- Sequence Determinants Spanning -10 Motif and Spacer Region Implicated in UniqueFrontiers in microbiology · 2019Article
- A type 6 secretion system (T6SS) encoded gene within Salmonella enterica serovar Enteritidis contributes to virulence.Virulence · 2018Article
- Identification and Characterization of aFrontiers in microbiology · 2018Article
- Protective efficacy of aCanadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2017Article
- The Two-Component System CpxRA Negatively Regulates the Locus of Enterocyte Effacement of Enterohemorrhagic Escherichia coli Involving σ(32) and Lon protease.Frontiers in cellular and infection microbiology · 2016Article
- Poultry body temperature contributes to invasion control through reduced expression of Salmonella pathogenicity island 1 genes in Salmonella enterica serovars Typhimurium and Enteritidis.Applied and environmental microbiology · 2015Article
- The two-component system CpxR/A represses the expression of Salmonella virulence genes by affecting the stability of the transcriptional regulator HilD.Frontiers in microbiology · 2015Article
- Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and regulation.Clinical microbiology reviews · 2013Review
- Immediate reduction of Salmonella enterica serotype typhimurium viability via membrane destabilization following exposure to multiple-hurdle treatments with heated, acidified organic acid salt solutions.Applied and environmental microbiology · 2011Article
- Enhancement of immune responses by an attenuated Salmonella enterica serovar Typhimurium strain secreting an Escherichia coli heat-labile enterotoxin B subunit protein as an adjuvant for a live Salmonella vaccine candidate.Clinical and vaccine immunology : CVI · 2011Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salmonella pathogenicity island 1 (SPI1) enables infecting salmonellae to invade the intestinal epithelium and induce a proinflammatory response and macrophage cell death. SPI1 expression is controlled by a complex cascade with several transcriptional regulators within the island and global regulators outside it. Previously, we reported that DnaK-depleted salmonellae could neither invade epithelial cells nor secrete SPI1-encoded proteins, suggesting that DnaK is involved in the expression of SPI1. Here, we found that DnaK is involved in SPI1 expression through inhibition of sigma(32) protein, which directs the transcription of a group of genes in response to various global stresses. Overproduction of sigma(32) resulted in decreased levels of the SPI1-specific transcriptional regulators HilD and HilA. Further analysis demonstrated that the sigma(32)-mediated system negatively regulates HilD and HilA at the posttranslational and transcriptional levels, respectively. The executioner of this negative regulation was shown to be a sigma(32)-induced protein ATP-dependent Lon protease, which specifically degrades HilD. Since HilD can activate hilA transcription, is at the top of the hierarchical SPI1 regulatory loop, and has a dominant role, the posttranslational control of HilD by Lon is critically important for precise expression of SPI1. Consequently, we suggest that SPI1 expression is controlled by the feedback regulatory loop in which sigma(32) induces Lon to control turnover of HilD, and DnaK, which inhibits sigma(32) function, leading to the modulation of lon expression. This regulation in response to a specific combination of environmental signals would ensure that SPI1 expression is restricted to a few specific locations in the host.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.