Disease relevance of dexA

• Insertional inactivation of the Streptococcus mutans dexA (dextranase) gene results in altered adherence and dextran catabolism [1].
• Comparison with known sequences using the BLASTX program showed 56% homology at the amino acid level between the sequenced gene fragment and dextranase from Streptococcus sobrinus, strongly suggesting that the S. mutans dextranase gene (dexA) had been inactivated [1].
• Using DNA isolated from dental plaque, a 192 bp sequence was identified and amplified from the spaP gene and a 722 bp sequence from the dexA gene [2].

High impact information on dexA

• Oligonucleotide primers for polymerase chain reaction (PCR) were designed on the basis of the dexA DNA sequence [3].
• The open reading frame for dexA was 2,550 bp, ending with a stop codon TGA [4].
• The nucleotide sequence and the deduced amino acid sequences of S. mutans dexA exhibited homologies of 57.8% and 47.0%, respectively, to those of Streptococcus sobrinus dex [4].
• The complete nucleotide sequence (3,747 bp) of the dextranase gene (dexA) and flanking regions of the chromosome of Streptococcus mutans Ingbritt (serotype c) were determined [4].

Analytical, diagnostic and therapeutic context of dexA

• Primers for the dex and dexA PCR methods detected two species exclusively from the mutans streptococci [5].
• Sequence analysis of the Streptococcus mutans Ingbritt dexA gene encoding extracellular dextranase [4].

References