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Molecular characterization of group A Streptococcus maltodextrin catabolism and its role in pharyngitis
Author(s) -
Shelburne Samuel A.,
Keith David B.,
Davenport Michael T.,
Horstmann Nicola,
Brennan Richard G.,
Musser James M.
Publication year - 2008
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2008.06290.x
Subject(s) - biology , pharyngitis , catabolism , maltodextrin , streptococcus , genetics , microbiology and biotechnology , computational biology , bacteria , biochemistry , metabolism , medicine , spray drying , chemistry , organic chemistry
Summary We previously demonstrated that the cell‐surface lipoprotein MalE contributes to GAS maltose/maltodextrin utilization, but MalE inactivation does not completely abrogate GAS catabolism of maltose or maltotriose. Using a genome‐wide approach, we identified the GAS phosphotransferase system (PTS) responsible for non‐MalE maltose/maltotriose transport. This PTS is encoded by an open reading frame (M5005_spy1692) previously annotated as ptsG based on homology with the glucose PTS in Bacillus subtilis . Genetic inactivation of M5005_spy1692 significantly reduced transport rates of radiolabelled maltose and maltotriose, but not glucose, leading us to propose its reannotation as malT for mal tose t ransporter. The Δ malT , Δ malE and Δ malE:malT strains were significantly attenuated in their growth in human saliva and in their ability to catabolize α‐glucans digested by purified human salivary α‐amylase. Compared with wild‐type, the three isogenic mutant strains were significantly impaired in their ability to colonize the mouse oropharynx. Finally, we discovered that the transcript levels of maltodextrin utilization genes are regulated by competitive binding of the maltose repressor MalR and catabolite control protein A. These data provide novel insights into regulation of the GAS maltodextrin genes and their role in GAS host–pathogen interaction, thereby increasing the understanding of links between nutrient acquisition and virulence in common human pathogens.