Molecular Cloning for the fur Gene from A.actinomyceterncornitans. A. actinomycetemcomitans causes localized juvenile periodontitis and other forms of periodontal disease by means of several putative virulence factors. In other bacterial species low levels of available free iron in host tissues can trigger the coordinate expression of virulence determinants trough the fur gene product. We hypothesized that an iron-responsive regulatory circuit similar to the fur system in E. coli might be present in A. actinomycetemcomitans. The presence of a fur homologue in A. actinomycetemconitans was supported by reactivity in Southern hybridization under low and high stringency conditions using a cloned E. coli fur gene probe. Subsequently, we cloned and characterized actinomycetemcomitans fur gene through complementation of an E. coli fur mutation and nucleotide sequence analysis. When expressed in E. , A. actinomycetemcomitans Fur expressed both fiu expression and siderophore production. The expressed protein was also determined to bind to the E. coli fur box by gel shift assay. DNA sequence analysis revealed the presence of a 146 amino acid open reading frame that exhibited 62% homology to E. coli Fur. Examination of a Sau 3Al A. actinomycetemcorritans library by Furta revealed 6 clones possibly regulated by the fur gene product. Key words: Fur, iron, periodontal pathogen, virulence, regulation
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