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Genome-wide Gene Deletions in Streptococcus sanguinis by High Throughput PCR
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Genome-wide Gene Deletions in Streptococcus sanguinis by High Throughput PCR

Published on: November 23, 2012

Local anesthetics block transient expression of inducible functions for transformation in Streptococcus sanguis

J L Raina

    Journal of Bacteriology
    |October 1, 1983
    PubMed

    Insights

    Local anesthetics like procaine and tetracaine block bacterial transformation by inhibiting key cellular functions. These drugs bind to cell surface molecules, preventing the transfer of genetic information during this process.

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Pharmacology

    Background:

    • Bacterial transformation is a process of genetic material transfer.
    • Competence, a state of being able to take up foreign DNA, involves specific inducible functions.
    • Cellular stimulation with competence protein typically triggers these functions.

    Purpose of the Study:

    • To investigate the inhibitory effects of procaine and tetracaine on bacterial transformation.
    • To elucidate the mechanism by which these anesthetics interfere with competence-specific events.

    Main Methods:

    • Procaine and tetracaine were used to inhibit bacterial transformation.
    • Affinity studies using 14C-labeled procaine were conducted.
    • The binding of procaine to cell surface macromolecules was analyzed.

    Main Results:

    • Procaine and tetracaine reversibly inhibited bacterial transformation.
    • The anesthetics prevented the transient expression of competence-specific, inducible functions.
    • 14C-labeled procaine specifically bound to cell surface macromolecules during the initiation of competence-specific events.
    • This binding blocked the transfer of information from competence protein interaction with cellular receptors.

    Conclusions:

    • Procaine and tetracaine act as inhibitors of bacterial transformation.
    • These anesthetics function by blocking the early molecular events required for competence.
    • The mechanism involves the disruption of signal transduction initiated by competence protein binding to cell surface receptors.

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