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Cytolethal distending toxins.

M Thelestam1, T Frisan

  • 1Microbiology and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden. Monica.Thelestam@mtc.ki.se

Reviews of Physiology, Biochemistry and Pharmacology
|September 1, 2004
PubMed
Summary
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Cytolethal distending toxins (CDTs) are bacterial toxins that cause DNA double strand breaks (DSBs), leading to cell cycle arrest or death. Their full mechanism and role in disease pathogenesis require further investigation.

Area of Science:

  • Microbiology
  • Toxicology
  • Molecular Biology

Background:

  • Cytolethal distending toxins (CDTs) are a recently identified family of bacterial protein toxins.
  • CDTs induce DNA double-strand breaks (DSBs) in target cells, causing cell cycle arrest or death.
  • These toxins are encoded by three genes (cdtA, cdtB, cdtC) found in various Gram-negative pathogenic bacteria.

Purpose of the Study:

  • To summarize the known characteristics of cytolethal distending toxins (CDTs).
  • To highlight the unique DNA-damaging mechanism of CDTs.
  • To identify remaining questions regarding CDT biology and pathogenesis.

Main Methods:

  • Review of existing literature on CDTs.
  • Analysis of the genetic basis and protein structure of CDTs.

Related Experiment Videos

  • Discussion of cellular uptake and cytotoxic mechanisms.

    • Main Results:

    • CDTs require three gene products (CdtA, CdtB, CdtC) for full holotoxin activity.
    • The CdtB subunit exhibits deoxyribonuclease I (DNase I)-like activity, crucial for DSB induction.
    • CDT internalization occurs via clathrin-coated pits and requires the Golgi complex.

    Conclusions:

    • CDT-induced DNA damage is a key cytotoxic mechanism.
    • Further research is needed to understand the roles of CdtA and CdtC subunits, receptor interactions, internalization pathways, and DNA interaction.
    • The precise role of CDTs in disease pathogenesis remains to be elucidated.