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The cytolethal distending toxins induce DNA damage and cell cycle arrest

X Cortes-Bratti1, T Frisan, M Thelestam

  • 1Microbiology and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden.

Toxicon : Official Journal of the International Society on Toxinology
|October 12, 2001
PubMed

Insights

Cytolethal distending toxins (CDTs) disrupt the cell cycle, causing cell death. This review explores their effects on mammalian cells and unanswered questions about their molecular mechanisms.

Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • Cytolethal distending toxins (CDTs) are bacterial protein toxins.
  • CDTs interfere with the cell cycle, leading to cell cycle arrest and death.
  • They are encoded by three genes (cdtA, cdtB, cdtC) and produced by Gram-negative bacteria.

Purpose of the Study:

  • To review the effects of CDTs on mammalian cells.
  • To highlight the molecular mechanisms of CDT action.
  • To identify remaining questions regarding CDT function and pathways.

Main Methods:

  • Review of existing literature on CDTs.
  • Analysis of the known functions of CDT components.
  • Comparison of CDT-induced cell cycle arrest with DNA-damaging agents.

Main Results:

  • CDTs are internalized via endocytosis and require the Golgi complex.
  • The CdtB component shows homology to deoxyribonuclease I (DNase I).
  • CDT-induced cell cycle arrest resembles that caused by DNA-damaging agents, suggesting DNA as a target.

Conclusions:

  • The precise molecular mechanism of CDTs is still under investigation.
  • Further research is needed to identify the functions of CdtA and CdtC.
  • Understanding CDT receptors and internalization pathways is crucial.

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