Abstract
We experimentally identified the activities of six predicted heptosyltransferases in Actinobacillus pleuropneumoniae genome serotype 5b strain L20 and serotype 3 strain JL03. The initial identification was based on a bioinformatic analysis of the amino acid similarity between these putative heptosyltrasferases with others of known function from enteric bacteria and Aeromonas. The putative functions of all the Actinobacillus pleuropneumoniae heptosyltrasferases were determined by using surrogate LPS acceptor molecules from well-defined A. hydrophyla AH-3 and A. salmonicida A450 mutants. Our results show that heptosyltransferases APL_0981 and APJL_1001 are responsible for the transfer of the terminal outer core D-glycero-D-manno-heptose (D,D-Hep) residue although they are not currently included in the CAZY glycosyltransferase 9 family. The WahF heptosyltransferase group signature sequence [S(T/S)(GA)XXH] differs from the heptosyltransferases consensus signature sequence [D(TS)(GA)XXH], because of the substitution of D261 for S261, being unique.
Highlights
Actinobacillus pleuropneumoniae is a non-motile Gram-negative bacterium causing porcine pleuropneumonia, a highly contagious respiratory disease transmitted through aerosols or close contact with infected animals including asymptomatic carriers [1]
Studies aimed at the identification of A. pleuropneumoniae virulence factors showed that, as in other pathogenic bacteria, there is an array of these factors
In order to attribute putative functions we performed a bioinformatic analysis based on the alignment (Clustal W) of heptosyltransferases whose function is experimentally proved with those of A. pleuropneumoniae strains L20 [26], JL03 [27], and AP76 [28]
Summary
Actinobacillus pleuropneumoniae is a non-motile Gram-negative bacterium causing porcine pleuropneumonia, a highly contagious respiratory disease transmitted through aerosols or close contact with infected animals including asymptomatic carriers [1]. This disease is often fatal and characterized by hemorrhagic, fibrinous and necrotic lung lesions; the clinical features ranging from acute to chronic [2], and it is an important cause economic losses worldwide in the porcine industry [2]. Studies aimed at the identification of A. pleuropneumoniae virulence factors showed that, as in other pathogenic bacteria, there is an array of these factors. Biofilm formation [14], autotransporter adhesion[15], and autotransporter protease synthesis [16] have been described to contribute to the pathogenicity of this bacterium
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