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The Iron-Responsive Regulator Fur Is Transcriptionally Autoregulated and Not Essential in Neisseria meningitidis

Isabel Delany,¹ Raffaele Ieva,¹ Cristina Alaimo,^1, Rino Rappuoli,¹ and Vincenzo Scarlato^1,2*

Biochemistry and Molecular Biology Unit, IRIS, Chiron S.r.l., 53100 Siena,¹ Department of Biology, University of Bologna, 40126 Bologna, Italy²

Received 21 April 2003/ Accepted 28 July 2003

Fur is a well-known iron-responsive repressor of gene transcription, which is used by many bacteria to respond to the low-iron environment that pathogens encounter during infection. The fur gene in Neisseria meningitidis has been described as an essential gene that may regulate a broad array of genes. We succeeded in obtaining an N. meningitidis mutant with the fur gene knocked out and used it to undertake studies of fur-mediated iron regulation. We show that expression of both Fur and the transferrin binding protein Tbp2 is iron regulated and demonstrate that this regulation is Fur mediated for the Tbp2 protein. Footprinting analysis revealed that Fur binds to two distinct sites upstream of its coding region with different affinities and that these binding sites overlap two promoters that differentially control transcription of the fur gene in response to iron. The presence of two independently regulated fur promoters may allow meningococcus to fine-tune expression of this regulator controlling iron homeostasis, possibly during infection.

Present address: Institut für Mikrobiologie ETH, CH-8092 Zürich, Switzerland.

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