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AraC/XylS family members, HilD and HilC, directly activate virulence gene expression independently of HilA in Salmonella typhimurium.
Mol Microbiol. 2003 Feb; 47(3):715-28.MM

Abstract

Salmonella typhimurium is a Gram-negative enteric pathogen that can infect intestinal epithelial cells and induce inflammation of the intestinal mucosa. These processes are mediated by a type III secretion system (TTSS), which is encoded on Salmonella pathogenicity island 1 (SPI1). Previous studies showed that four SPI1-encoded transcriptional regulators, HilD, HilC, HilA and InvF, act in an ordered fashion to co-ordinately activate expression of the SPI1 TTSS. HilD and HilC derepress hilA transcription. HilA activates invF as well as SPI1 genes that encode components of the TTS apparatus. InvF then activates genes that encode proteins secreted by the SPI1 TTS apparatus. In this scheme, HilD and HilC indirectly activate expression of the SPI1 TTS apparatus and its secreted substrates by affecting hilA expression. Here, we report that HilD and HilC can also activate expression of a subset of SPI1 genes independently of HilA. Our studies show that HilD and HilC activate transcription of invF from a promoter that is far upstream of its HilA-dependent promoter. This activation is most probably through direct binding of HilD and HilC to sequences upstream and downstream of this alternative HilA-independent promoter. We conclude that HilD and HilC have a second role in SPI1 gene regulation that is separate from their role in co-ordinating expression of the SPI1 TTSS through hilA.

Authors+Show Affiliations

Akbar S
Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
Schechter LM
No affiliation info available
Lostroh CP
No affiliation info available
Lee CA
No affiliation info available

MeSH

AraC Transcription FactorBacterial ProteinsDNA-Binding ProteinsGene Expression Regulation, BacterialPromoter Regions, GeneticRepressor ProteinsSalmonella typhimuriumTrans-ActivatorsTranscription FactorsTranscription, GeneticVirulence

Pub Type(s)

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

Language

eng

PubMed ID

12535071

Citation

Akbar, Samina, et al. "AraC/XylS Family Members, HilD and HilC, Directly Activate Virulence Gene Expression Independently of HilA in Salmonella Typhimurium." Molecular Microbiology, vol. 47, no. 3, 2003, pp. 715-28.
Akbar S, Schechter LM, Lostroh CP, et al. AraC/XylS family members, HilD and HilC, directly activate virulence gene expression independently of HilA in Salmonella typhimurium. Mol Microbiol. 2003;47(3):715-28.
Akbar, S., Schechter, L. M., Lostroh, C. P., & Lee, C. A. (2003). AraC/XylS family members, HilD and HilC, directly activate virulence gene expression independently of HilA in Salmonella typhimurium. Molecular Microbiology, 47(3), 715-28.
Akbar S, et al. AraC/XylS Family Members, HilD and HilC, Directly Activate Virulence Gene Expression Independently of HilA in Salmonella Typhimurium. Mol Microbiol. 2003;47(3):715-28. PubMed PMID: 12535071.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - AraC/XylS family members, HilD and HilC, directly activate virulence gene expression independently of HilA in Salmonella typhimurium. AU - Akbar,Samina, AU - Schechter,Lisa M, AU - Lostroh,C Phoebe, AU - Lee,Catherine A, PY - 2003/1/22/pubmed PY - 2003/4/12/medline PY - 2003/1/22/entrez SP - 715 EP - 28 JF - Molecular microbiology JO - Mol Microbiol VL - 47 IS - 3 N2 - Salmonella typhimurium is a Gram-negative enteric pathogen that can infect intestinal epithelial cells and induce inflammation of the intestinal mucosa. These processes are mediated by a type III secretion system (TTSS), which is encoded on Salmonella pathogenicity island 1 (SPI1). Previous studies showed that four SPI1-encoded transcriptional regulators, HilD, HilC, HilA and InvF, act in an ordered fashion to co-ordinately activate expression of the SPI1 TTSS. HilD and HilC derepress hilA transcription. HilA activates invF as well as SPI1 genes that encode components of the TTS apparatus. InvF then activates genes that encode proteins secreted by the SPI1 TTS apparatus. In this scheme, HilD and HilC indirectly activate expression of the SPI1 TTS apparatus and its secreted substrates by affecting hilA expression. Here, we report that HilD and HilC can also activate expression of a subset of SPI1 genes independently of HilA. Our studies show that HilD and HilC activate transcription of invF from a promoter that is far upstream of its HilA-dependent promoter. This activation is most probably through direct binding of HilD and HilC to sequences upstream and downstream of this alternative HilA-independent promoter. We conclude that HilD and HilC have a second role in SPI1 gene regulation that is separate from their role in co-ordinating expression of the SPI1 TTSS through hilA. SN - 0950-382X UR - https://www.unboundmedicine.com/medline/citation/12535071/AraC/XylS_family_members_HilD_and_HilC_directly_activate_virulence_gene_expression_independently_of_HilA_in_Salmonella_typhimurium_ DB - PRIME DP - Unbound Medicine ER -