Disease relevance of dexB

• 0. By subcloning various combinations of DNA fragments from pSUCRI, it was demonstrated that the dextranase gene (designated dexB) can be separated from the gtfA gene and still be efficiently expressed in both E. coli and B. subtilis [1].
• Nucleotide sequence of the dextran glucosidase (dexB) gene of Streptococcus mutans [2].

High impact information on dexB

• These induced the msm operon, including dexB, and the DexB enzyme was able to act on the alpha-limit dextrins to give further fermentable substrates [3].
• However, purified intracellular polysaccharide from the wild-type S. mutans strain LT11 and a mutant deficient in dexB revealed no substantial differences in the extent of branching as demonstrated by iodine staining spectra and the degree of polymerization [3].
• The Streptococcus mutans dexB gene, a member of the multiple sugar metabolism (msm) operon, encodes an intracellular glucan 1,6-alpha-glucosidase which releases glucose from the non-reducing terminus of alpha-1,6-linked isomaltosaccharides and dextran [3].
• Inactivation of the aga gene in S. mutans resulted in loss of all alpha-galactosidase activity and abolished the ability to ferment melibiose; alpha-glucosidase activity was also lost, due to an indirect effect on the dexB gene [4].
• Comparison with other published sequences showed that the dexB gene product shares regions of similarity with enzymes, from a variety of sources, which attack other glucose polymers [2].

Biological context of dexB

• The genetic linkage of the gtfA and dexB genes in the S. mutans GS-5 chromosome was confirmed by Southern hybridization and by the independent isolation of four distinct clones containing the gtfA gene and common flanking sequences [1].

References