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“Background Bacillus cereus is a facultative anaerobic bacterium that can cause two types of food-borne illness O-methylated flavonoid in humans. Among these, the diarrheal syndrome may result from the production in the human host’s small intestine of various extracellular

factors including hemolysin BL (Hbl) and nonhemolytic enterotoxin Nhe [1, 2]. The genes encoding Hbl and Nhe belong to the PlcR regulon [3]. The ability of B. cereus to produce enterotoxins and grow well in an O2-limited environment such as that prevailing in the human small intestine is controlled by both the two-component system ResDE and the redox regulator Fnr. Unlike ResDE, Fnr is essential for B. cereus growth under anaerobic fermentative conditions and for hbl and nhe expression, irrespective of the oxygenation conditions [4, 5]. B. cereus Fnr is a member of the large Fnr/Crp superfamily of transcription factors that bind as homodimers to palindromic sequences of DNA, each subunit binding to one half-site [6]. Like its homologue from Bacillus subtilis B. cereus Fnr contains a C-terminal extension with four cysteine residues, C(x4)C(x 2)C(x3)C. The last three cysteine residues were identified as [4Fe-4S]2+ cluster ligands in B. subtilis Fnr, the fourth ligand being an aspartate residue [7].