ArticleJournal of bacteriology2005
Bordetella AlcS transporter functions in alcaligin siderophore export and is central to inducer sensing in positive regulation of alcaligin system gene expression.
Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Analysis of twelve genomes of the bacteriumPeerJ · 2024Article
- Overview ofBiology · 2023Review
- Roles of SmeYZ, SbiAB, and SmeDEF Efflux Systems in Iron Homeostasis of Stenotrophomonas maltophilia.Microbiology spectrum · 2022Article
- Recent Advances in the Siderophore Biology ofFrontiers in microbiology · 2022Review
- Intracellular Accumulation of Staphylopine Can Sensitize Staphylococcus aureus to Host-Imposed Zinc Starvation by Chelation-Independent Toxicity.Journal of bacteriology · 2020Article
- Intracellular accumulation of staphylopine impairs the fitness of Staphylococcus aureus cntE mutant.FEBS letters · 2019Article
- Interspecies variations in Bordetella catecholamine receptor gene regulation and function.Infection and immunity · 2015Article
- Self-poisoning of Mycobacterium tuberculosis by interrupting siderophore recycling.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Genome mining for methanobactins.BMC biology · 2013Article
- Discovery of a siderophore export system essential for virulence of Mycobacterium tuberculosis.PLoS pathogens · 2013Article
- Iron and pH-responsive FtrABCD ferrous iron utilization system of Bordetella species.Molecular microbiology · 2012Article
- Involvement of multiple distinct Bordetella receptor proteins in the utilization of iron liberated from transferrin by host catecholamine stress hormones.Molecular microbiology · 2012Article
- Expression of multidrug resistance efflux pump gene norA is iron responsive in Staphylococcus aureus.Journal of bacteriology · 2012Article
- The major facilitator superfamily-type protein LbtC promotes the utilization of the legiobactin siderophore by Legionella pneumophila.Microbiology (Reading, England) · 2012Article
- Hunger for iron: the alternative siderophore iron scavenging systems in highly virulent Yersinia.Frontiers in cellular and infection microbiology · 2012Review
- Yersiniabactin iron uptake: mechanisms and role in Yersinia pestis pathogenesis.Microbes and infection · 2011Review
- Role of the FeoB protein and siderophore in promoting virulence of Xanthomonas oryzae pv. oryzae on rice.Journal of bacteriology · 2010Article
- The yersiniabactin transport system is critical for the pathogenesis of bubonic and pneumonic plague.Infection and immunity · 2010Article
- Purification of Legiobactin and importance of this siderophore in lung infection by Legionella pneumophila.Infection and immunity · 2009Article
- Temporal signaling and differential expression of Bordetella iron transport systems: the role of ferrimones and positive regulators.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2009Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bordetella pertussis and Bordetella bronchiseptica, which are respiratory mucosal pathogens of mammals, produce and utilize the siderophore alcaligin to acquire iron in response to iron starvation. A predicted permease of the major facilitator superfamily class of membrane efflux pumps, AlcS (synonyms, OrfX and Bcr), was reported to be encoded within the alcaligin gene cluster. In this study, alcS null mutants were found to be defective in growth under iron starvation conditions, in iron source utilization, and in alcaligin export. trans complementation using cloned alcS genes of B. pertussis or B. bronchiseptica restored the wild-type phenotype to the alcS mutants. Although the levels of extracellular alcaligin measured in alcS strain culture fluids were severely reduced compared with the wild-type levels, alcS mutants had elevated levels of cell-associated alcaligin, implicating AlcS in alcaligin export. Interestingly, a deltaalcA mutation that eliminated alcaligin production suppressed the growth defects of alcS mutants. This suppression and the alcaligin production defect were reversed by trans complementation of the deltaalcA mutation in the double-mutant strain, confirming that the growth-defective phenotype of alcS mutants is associated with alcaligin production. In an alcA::mini-Tn5 lacZ1 operon fusion strain background, an alcS null mutation resulted in enhanced AlcR-dependent transcriptional responsiveness to alcaligin inducer; conversely, AlcS overproduction blunted the transcriptional response to alcaligin. These transcription studies indicate that the alcaligin exporter activity of AlcS is required to maintain appropriate intracellular alcaligin levels for normal inducer sensing and responsiveness necessary for positive regulation of alcaligin system gene expression.
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