ArticleMolecular microbiology2009
Contribution of AmyA, an extracellular alpha-glucan degrading enzyme, to group A streptococcal host-pathogen interaction.
Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
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- Elucidation of independently modulated genes inmSystems · 2023Article
- The exploitation of human glycans by Group A Streptococcus.FEMS microbiology reviews · 2022Article
- The involvement of MsmK in pathogenesis of the Streptococcus suis serotype 2.MicrobiologyOpen · 2017Article
- Maltose-Dependent Transcriptional Regulation of the mal Regulon by MalR in Streptococcus pneumoniae.PloS one · 2015Article
- MsmK, an ATPase, Contributes to Utilization of Multiple Carbohydrates and Host Colonization of Streptococcus suis.PloS one · 2015Article
- Comparative analysis of Klebsiella pneumoniae genomes identifies a phospholipase D family protein as a novel virulence factor.BMC biology · 2014Article
- PTS phosphorylation of Mga modulates regulon expression and virulence in the group A streptococcus.Molecular microbiology · 2013Article
- Serine/threonine protein kinase Stk is required for virulence, stress response, and penicillin tolerance in Streptococcus pyogenes.Infection and immunity · 2011Article
- Glycogen with short average chain length enhances bacterial durability.Die Naturwissenschaften · 2011Review
- Virulence gene pool detected in bovine group C Streptococcus dysgalactiae subsp. dysgalactiae isolates by use of a group A S. pyogenes virulence microarray.Journal of clinical microbiology · 2011Article
- The molecular basis of glycogen breakdown and transport in Streptococcus pneumoniae.Molecular microbiology · 2010Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
alpha-Glucans such as starch and glycogen are abundant in the human oropharynx, the main site of group A Streptococcus (GAS) infection. However, the role in pathogenesis of GAS extracellular alpha-glucan binding and degrading enzymes is unknown. The serotype M1 GAS genome encodes two extracellular proteins putatively involved in alpha-glucan binding and degradation; pulA encodes a cell wall anchored pullulanase and amyA encodes a freely secreted putative cyclomaltodextrin alpha-glucanotransferase. Genetic inactivation of amyA, but not pulA, abolished GAS alpha-glucan degradation. The DeltaamyA strain had a slower rate of translocation across human pharyngeal epithelial cells. Consistent with this finding, the DeltaamyA strain was less virulent following mouse mucosal challenge. Recombinant AmyA degraded alpha-glucans into beta-cyclomaltodextrins that reduced pharyngeal cell transepithelial resistance, providing a physiologic explanation for the observed transepithelial migration phenotype. Higher amyA transcript levels were present in serotype M1 GAS strains causing invasive infection compared with strains causing pharyngitis. GAS proliferation in a defined alpha-glucan-containing medium was dependent on the presence of human salivary alpha-amylase. These data delineate the molecular mechanisms by which alpha-glucan degradation contributes to GAS host-pathogen interaction, including how GAS uses human salivary alpha-amylase for its own metabolic benefit.
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