ArticleGenetics2012
Integrating global regulatory input into the Salmonella pathogenicity island 1 type III secretion system.
Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 144 citations in OpenAlex.
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- Construction of a constitutively active type III secretion system for heterologous protein secretion.Applied microbiology and biotechnology · 2023Article
- Small RNAs Activate Salmonella Pathogenicity Island 1 by Modulating mRNA Stability through theJournal of bacteriology · 2023Article
- Measurement of Salmonella enterica Internalization and Vacuole Lysis in Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Salmonella enterica serovar Typhimurium uses the Salmonella pathogenicity island 1 (SPI1) type III secretion system to induce inflammatory diarrhea and bacterial uptake into intestinal epithelial cells. The expression of hilA, encoding the transcriptional activator of the SPI1 structural genes, is directly controlled by three AraC-like regulators, HilD, HilC, and RtsA, each of which can activate the hilD, hilC, rtsA, and hilA genes, forming a complex feed-forward regulatory loop. A large number of factors and environmental signals have been implicated in SPI1 regulation. We have developed a series of genetic tests that allows us to determine where these factors feed into the SPI1 regulatory circuit. Using this approach, we have grouped 21 of the known SPI1 regulators and environmental signals into distinct classes on the basis of observed regulatory patterns, anchored by those few systems where the mechanism of regulation is best understood. Many of these factors are shown to work post-transcriptionally at the level of HilD, while others act at the hilA promoter or affect all SPI1 promoters. Analysis of the published transcriptomic data reveals apparent coregulation of the SPI1 and flagellar genes in various conditions. However, we show that in most cases, the factors that affect both systems control SPI1 independently of the flagellar protein FliZ, despite its role as an important SPI1 regulator and coordinator of the two systems. These results provide a comprehensive model for SPI1 regulation that serves as a framework for future molecular analyses of this complex regulatory network.
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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.