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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Cytolethal Distending Toxin-Increased DNA Damage and Ploidy Involve the YAP/TAZ-TEAD Signaling Pathway.

Ruxue Jia1, Lamia Azzi-Martin1,2, Mariana Saraiva1

  • 1Université de Bordeaux, Inserm, BRIC-Bordeaux Institute of Oncology, U1312, Bordeaux, France.

The Journal of Infectious Diseases
|June 12, 2025
PubMed
Summary

Bacterial genotoxins like CDT and colibactin activate the YAP/TAZ-TEAD pathway, which controls cell ploidy after DNA damage. This pathway is crucial for epithelial cells responding to genotoxic bacterial infections.

Keywords:
HippoK-975TEADXMU-MP-1verteporfin

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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
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Area of Science:

  • Microbiology
  • Molecular Biology
  • Cell Biology

Background:

  • Bacterial genotoxins, including CDT and colibactin, induce significant DNA damage and genomic instability in host cells.
  • These genotoxins disrupt DNA damage response pathways.
  • Observed cellular phenotypes suggest a potential link between genotoxin effects and the Hippo signaling pathway.

Purpose of the Study:

  • To investigate the role of the Hippo signaling pathway in epithelial cells following intoxication with CDT/CdtB and colibactin.
  • To elucidate the molecular mechanisms by which bacterial genotoxins impact host cell signaling and genomic integrity.

Main Methods:

  • Utilized normal and cancer-derived epithelial intestinal and hepatic cell lines.
  • Exposed cells to CDT/CdtB and colibactin.
  • Analyzed Hippo pathway components, including YAP/TAZ and TEAD-mediated transcription.
  • Assessed effects of inhibiting YAP/TAZ-TEAD binding on DNA damage, repair, and ploidy.

Main Results:

  • The active CdtB subunit of CDT modulates YAP/TAZ expression and increases TEAD-mediated transcription.
  • Inhibiting YAP/TAZ-TEAD binding with verteporfin and K-975 reduced DNA damage, impaired repair, and decreased ploidy.
  • Colibactin exposure induced similar effects on the YAP/TAZ-TEAD pathway and cellular phenotypes.
  • YAP/TAZ-TEAD signaling is implicated in increased ploidy in cells surviving CDT/CdtB-induced DNA damage.

Conclusions:

  • Genotoxin-producing bacterial infections engage the YAP/TAZ-TEAD signaling pathway.
  • This pathway plays a critical role in regulating ploidy following DNA damage in epithelial cells.
  • The findings highlight a novel mechanism by which bacteria manipulate host cell processes to promote genomic instability.