ArticleJournal of bacteriology2013
DsbA and MgrB regulate steA expression through the two-component system PhoQ/PhoP in Salmonella enterica.
Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Impeding pathways of intrinsic resistance in Escherichia coli confers antibiotic sensitization and resistance proofing.PLoS biology · 2025Article
- An updated overview on the bacterial PhoP/PhoQ two-component signal transduction system.Frontiers in cellular and infection microbiology · 2025Review
- Article
- How the PhoP/PhoQ System Controls Virulence and MgMicrobiology and molecular biology reviews : MMBR · 2021Review
- MgrB Inactivation Confers Trimethoprim Resistance inFrontiers in microbiology · 2021Article
- CaJournal of bacteriology · 2018Article
- Increasing intracellular magnesium levels with the 31-amino acid MgtS protein.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Two-component regulators control hilA expression by controlling fimZ and hilE expression within Salmonella enterica serovar Typhimurium.Infection and immunity · 2015Article
- Host cell type-dependent translocation and PhoP-mediated positive regulation of the effector SseK1 of Salmonella enterica.Frontiers in microbiology · 2015Article
- Patterns of expression and translocation of the ubiquitin ligase SlrP in Salmonella enterica serovar Typhimurium.Journal of bacteriology · 2014Article
- Small proteins can no longer be ignored.Annual review of biochemistry · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SteA is a protein that can be translocated into host cells through the two virulence-related type III secretion systems that are present in Salmonella enterica. We used the T-POP system to carry out general screens for loci that exhibited activation or repression of a steA::lacZ fusion. These screens identified the histidine kinase PhoQ and the response regulator PhoP as positive regulators of steA. Transcription of this gene is σ70 dependent, and the promoter of steA contains a PhoP-binding site that mediates direct regulation by PhoP. Our screens also detected MgrB (also known as YobG) as a negative regulator of the expression of steA. Disruption of the gene encoding the periplasmic disulfide oxidoreductase DsbA or addition of the reducing agent dithiothreitol increases transcription of steA. The effects of MgrB and DsbA on steA are mediated by PhoP. These results suggest that the cellular redox status is a factor contributing to regulation of steA and, probably, other virulence genes regulated by the PhoQ/PhoP two-component system.
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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.