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Transcription of the Salmonella invasion gene activator, hilA, requires HilD activation in the absence of negative regulators.
J Bacteriol. 2003 Jan; 185(2):525-33.JB

Abstract

Salmonella enterica serovar Typhimurium causes human gastroenteritis and a systemic typhoid-like infection in mice. Infection is initiated by entry of the bacteria into intestinal epithelial cells and is mediated by a type III secretion system that is encoded by genes in Salmonella pathogenicity island 1. The expression of invasion genes is tightly regulated by environmental conditions such as oxygen and osmolarity, as well as by many bacterial factors. The hilA gene encodes an OmpR/ToxR family transcriptional regulator that activates the expression of invasion genes in response to both environmental and genetic regulatory factors. HilD is an AraC/XylS regulator that has been postulated to act as a derepressor of hilA expression that promotes transcription by interfering with repressor binding at the hilA promoter. Our research group has identified four genes (hilE, hha, pag, and ams) that negatively affect hilA transcription. Since the postulated function of HilD at the hilA promoter is to counteract the effects of repressors, we examined this model by measuring hilA::Tn5lacZY expression in strains containing negative regulator mutations in the presence or absence of functional HilD. Single negative regulator mutations caused significant derepression of hilA expression, and two or more negative regulator mutations led to very high level expression of hilA. However, in all strains tested, the absence of hilD resulted in low-level expression of hilA, suggesting that HilD is required for activation of hilA expression, whether or not negative regulators are present. We also observed that deletion of the HilD binding sites in the chromosomal hilA promoter severely decreased hilA expression. In addition, we found that a single point mutation at leucine 289 in the C-terminal domain of the alpha subunit of RNA polymerase leads to very low levels of hilA::Tn5lacZY expression, suggesting that HilD activates transcription of hilA by contacting and recruiting RNA polymerase to the hilA promoter.

Authors+Show Affiliations

Department of Microbiology, University of Iowa School of Medicine, University of Iowa, Iowa City 52242, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12511499

Citation

Boddicker, Jennifer D., et al. "Transcription of the Salmonella Invasion Gene Activator, hilA, Requires HilD Activation in the Absence of Negative Regulators." Journal of Bacteriology, vol. 185, no. 2, 2003, pp. 525-33.
Boddicker JD, Knosp BM, Jones BD. Transcription of the Salmonella invasion gene activator, hilA, requires HilD activation in the absence of negative regulators. J Bacteriol. 2003;185(2):525-33.
Boddicker, J. D., Knosp, B. M., & Jones, B. D. (2003). Transcription of the Salmonella invasion gene activator, hilA, requires HilD activation in the absence of negative regulators. Journal of Bacteriology, 185(2), 525-33.
Boddicker JD, Knosp BM, Jones BD. Transcription of the Salmonella Invasion Gene Activator, hilA, Requires HilD Activation in the Absence of Negative Regulators. J Bacteriol. 2003;185(2):525-33. PubMed PMID: 12511499.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transcription of the Salmonella invasion gene activator, hilA, requires HilD activation in the absence of negative regulators. AU - Boddicker,Jennifer D, AU - Knosp,Boyd M, AU - Jones,Bradley D, PY - 2003/1/4/pubmed PY - 2003/2/1/medline PY - 2003/1/4/entrez SP - 525 EP - 33 JF - Journal of bacteriology JO - J Bacteriol VL - 185 IS - 2 N2 - Salmonella enterica serovar Typhimurium causes human gastroenteritis and a systemic typhoid-like infection in mice. Infection is initiated by entry of the bacteria into intestinal epithelial cells and is mediated by a type III secretion system that is encoded by genes in Salmonella pathogenicity island 1. The expression of invasion genes is tightly regulated by environmental conditions such as oxygen and osmolarity, as well as by many bacterial factors. The hilA gene encodes an OmpR/ToxR family transcriptional regulator that activates the expression of invasion genes in response to both environmental and genetic regulatory factors. HilD is an AraC/XylS regulator that has been postulated to act as a derepressor of hilA expression that promotes transcription by interfering with repressor binding at the hilA promoter. Our research group has identified four genes (hilE, hha, pag, and ams) that negatively affect hilA transcription. Since the postulated function of HilD at the hilA promoter is to counteract the effects of repressors, we examined this model by measuring hilA::Tn5lacZY expression in strains containing negative regulator mutations in the presence or absence of functional HilD. Single negative regulator mutations caused significant derepression of hilA expression, and two or more negative regulator mutations led to very high level expression of hilA. However, in all strains tested, the absence of hilD resulted in low-level expression of hilA, suggesting that HilD is required for activation of hilA expression, whether or not negative regulators are present. We also observed that deletion of the HilD binding sites in the chromosomal hilA promoter severely decreased hilA expression. In addition, we found that a single point mutation at leucine 289 in the C-terminal domain of the alpha subunit of RNA polymerase leads to very low levels of hilA::Tn5lacZY expression, suggesting that HilD activates transcription of hilA by contacting and recruiting RNA polymerase to the hilA promoter. SN - 0021-9193 UR - https://www.unboundmedicine.com/medline/citation/12511499/Transcription_of_the_Salmonella_invasion_gene_activator_hilA_requires_HilD_activation_in_the_absence_of_negative_regulators_ L2 - https://journals.asm.org/doi/10.1128/JB.185.2.525-533.2003?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -