Disease relevance of fruA

• The fruA gene of Streptococcus mutans encodes for a secreted fructan hydrolase (fructanase), an established virulence determinant required for releasing d-fructose from levan- and inulin-type fructans [1].
• Genes with homology to fruA were detected in S. mutans serotype c, e, and f strains, Streptococcus rattus, Streptococcus salivarius, and Streptococcus sanguis [2].
• Toward this end, we have now constructed and evaluated three Escherichia coli-S. mutans shuttle expression vectors with the fruA and scrB promoters from S. mutans, as well as the tetR-controlled tetO promoter from Staphylococcus aureus [3].
• Accumulating data suggest that expression of fruA is regulated by a mechanism that has several unique features that distinguish it from archetypical polysaccharide catabolic operons of other gram-positive bacteria [4].

High impact information on fruA

• Using transcriptional fusions, it was found that fructose could signal induction of the fruA and levD operons through the two-component system/sugar-binding protein complex [1].
• All four genes were found to be required for optimal growth of S. mutans on inulin-containing medium and for transcriptional activation of fruA [1].
• A recombinant LevR protein was shown to bind to the promoter regions of fruA and levD in gel mobility shift assays [1].
• The complete nucleotide sequence (5,010 bp) of the fructanase gene (fruA) and flanking regions of the chromosome of Streptococcus mutans GS-5 was determined [2].
• Deletion or mutation of a consensus catabolite response element alleviated glucose repression of fruA, but interestingly, inactivation of the ccpA gene had no discernible effect on catabolite repression of fruA [4].

Chemical compound and disease context of fruA

• There are two primary levels of control of the expression of the fructanase gene (fruA) of Streptococcus mutans: induction by levan, inulin, or sucrose and repression in the presence of glucose and other readily metabolized sugars [4].

Biological context of fruA

• In this report, we identified an operon in S. mutans UA159 encoding a two-component system flanked by two predicted carbohydrate-binding proteins that is absolutely required for the expression of fruA [1].
• A dyadic sequence, ATGACA(TC)TGTCAT, located at -72 to -59 relative to the transcription initiation site was shown to be essential for expression of fruA [4].
• Located 3' to fruA was an open reading frame (ORF) with similarity to beta-fructosidases which was cotranscribed with fruA [5].
• Mutagenesis of a terminator-like structure located in the 165-base 5' untranslated region of the fruA mRNA or insertional inactivation of antiterminator genes revealed that antitermination was not a mechanism controlling induction or repression of fruA, although the untranslated leader mRNA may play a role in optimal expression of fructanase [4].

Associations of fruA with chemical compounds

• The levels of production of fruA mRNA and FruA were elevated in cells growing on levan, inulin, or sucrose as the sole carbohydrate source, and repression was observed when cells were grown on readily metabolizable hexoses [5].

Analytical, diagnostic and therapeutic context of fruA

• The fruA promoter and its derivatives generated by deletions and/or site-directed mutagenesis were fused to a promoterless chloramphenicol acetyltransferase (CAT) gene as a reporter, and strains carrying the transcriptional fusions were then analyzed for CAT activities in response to growth on various carbon sources [4].

References