Fur activates the expression of salmonella enterica pathogenicity island 1 by directly interacting with the hilD operator in Vivo and in Vitro

Laura Teixidó, Begoña Carrasco, Juan C. Alonso, Jordi Barbé, Susana Campoy

Research output: Contribution to journalArticleResearchpeer-review

49 Citations (Scopus)

Abstract

Previous studies have established that the expression of Salmonella enterica pathogenicity island 1 (SPI1), which is essential for epithelial invasion, is mainly regulated by the HilD protein. The ferric uptake regulator, Fur, in turn modulates the expression of the S. enterica hilD gene, albeit through an unknown mechanism. Here we report that S. enterica Fur, in its metal-bound form, specifically binds to an AT-rich region (BoxA), located upstream of the hilD promoter (PhilD), at position -191 to -163 relative to the hilD transcription start site. Furthermore, in a PhilD variant with mutations in BoxA, PhilD*, Fur·Mn2+ binding is impaired. In vivo experiments using S. enterica strains carrying wild-type PhilD or the mutant variant PhilD* showed that Fur activates hilD expression, while in vitro experiments revealed that the Fur·Mn2+ protein is sufficient to increase hilD transcription. Together, these results present the first evidence that Fur·Mn2+, by binding to the upstream BoxA sequence, directly stimulates the expression of hilD in S. enterica. © 2011 Teixidó et al.
Original languageEnglish
Article numbere19711
JournalPLoS ONE
Volume6
DOIs
Publication statusPublished - 16 May 2011

Fingerprint Dive into the research topics of 'Fur activates the expression of salmonella enterica pathogenicity island 1 by directly interacting with the hilD operator in Vivo and in Vitro'. Together they form a unique fingerprint.

Cite this