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Generation of Null Mutants to Elucidate the Role of Bacterial Glycosyltransferases in Bacterial Motility
12:29

Generation of Null Mutants to Elucidate the Role of Bacterial Glycosyltransferases in Bacterial Motility

Published on: March 11, 2022

[Pathogenicity factors of bacteria with glycosylating activity]

D I Tartakovskaia, V A Araslanova, Iu F Belyĭ

    Vestnik Rossiiskoi Akademii Meditsinskikh Nauk
    |December 16, 2011
    PubMed

    Insights

    Bacterial glycosylating factors, like large Clostridium toxins and Legionella glycosyltransferases, inactivate host cell pathways by modifying Rho/Ras proteins. These bacterial enzymes play a crucial role in pathogen virulence and infectious disease mechanisms.

    Area of Science:

    • Microbiology and Molecular Biology
    • Bacterial Pathogenesis
    • Eukaryotic Cell Signaling

    Context:

    • Large Clostridium toxins (e.g., from C. difficile, C. novyi, C. sordellii, C. perfringens) are known virulence factors.
    • These toxins target Rho/Ras family GTPases, crucial for eukaryotic cell signaling, via glycosylation.
    • Recent identification of Lgt glycosyltransferases in Legionella reveals a new class of bacterial glycosylating enzymes.

    Purpose:

    • To highlight the conserved mechanism of bacterial glycosylating factors in pathogen virulence.
    • To underscore the role of glycosylation in inactivating essential host cell functions.
    • To emphasize the significance of bacterial glycosyltransferases as novel pathogenicity factors.

    Summary:

    • Large Clostridium toxins and Legionella Lgt glycosyltransferases function as bacterial pathogenicity factors.
    • Both toxin types inactivate eukaryotic Rho/Ras GTPases and protein synthesis via glycosylation.
    • Legionella Lgt enzymes are translocated into host cells via type IV secretion systems, inhibiting protein synthesis by modifying elongation factor 1A.

    Impact:

    • Bacterial glycosylating factors are critical for pathogen survival and disease progression.
    • Understanding these mechanisms offers potential targets for therapeutic interventions against bacterial infections.
    • This highlights a conserved strategy employed by diverse bacterial pathogens to subvert host cell machinery.

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