Bacterial Toxins and Cell Cycle Dynamics

Bacterial toxins have emerged as critical modulators of eukaryotic cell cycle dynamics, exploiting fundamental checkpoints to favour pathogen survival and propagation. Among these, genotoxins such as cytolethal distending toxins (CDTs), typhoid toxin and colibactin directly inflict DNA damage, activating the DNA damage response (DDR). This leads to cell cycle arrest at the G1 or G2/M transitions, induction of senescence or programmed cell death, and reshaping of the host immune landscape. CDTs, delivered by diverse Gram-negative bacteria, comprise a catalytic CdtB subunit with DNase-like activity and binding subunits that engage membrane microdomains before retrograde vesicular transport to the nucleus. In parallel, cyclomodulins influence cyclin-dependent kinase signalling, subverting proliferation and inflammatory outcomes. The crosstalk between toxin-induced lesions and host repair sensors such as ATM and p53 determines whether cells halt for repair or undergo apoptosis. Recent findings highlight the tissue-specific nature of these interactions, the role of phosphoinositide perturbation in phagocytic evasion and the contribution to chronic inflammation and dysplasia. Deciphering these mechanisms is pivotal for the development of anti-infective strategies, for risk assessment of toxin-producing strains and for exploring toxin derivatives as precision tools in oncology.

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Bacterial Toxins and Cell Cycle Dynamics publication trend

The graph below shows the total number of articles in bacterial toxins and cell cycle dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Genotoxin: Bacterial factor that induces DNA damage, triggering repair pathways and cell cycle checkpoints.

Cytolethal distending toxin (CDT): AB₂ bacterial toxin family whose CdtB subunit causes DNA strand breaks leading to cell cycle arrest.

DNA damage response (DDR): Cellular network that detects DNA lesions, halts the cell cycle and coordinates repair or alternative fates.

Cell cycle arrest: Temporary or permanent halt in cell division at defined checkpoints to allow repair or trigger senescence/apoptosis.

Senescence: Stable exit from the cell cycle in response to damage or stress, often accompanied by secretory changes.

Apoptosis: Programmed cell death executed by conserved molecular pathways to eliminate damaged cells.

References

1. Genotoxin-producing Salmonella enterica induces tissue-specific types of DNA damage and DNA damage response outcomes. Frontiers in Immunology (2024).
2. Aggregatibacter actinomycetemcomitans cytolethal distending toxin modulates host phagocytic function. Frontiers in Cellular and Infection Microbiology (2023).
3. Rab4b Promotes Cytolethal Distending Toxin from Glaesserella parasuis-Induced Cytotoxicity in PK-15 Cells. Toxins (2024).