The polyadenylase PAPI is required for virulence plasmid maintenance in pathogenic bacteria
Katherine Schubert1, Jessica Zhang2,3, Michele E Muscolo4,5
1Department of Molecular, Cell, and Developmental Biology, UC Santa Cruz, Santa Cruz, California, United States of America.
Plos Pathogens
|May 27, 2025
Summary
The chromosomal gene pcnB, encoding polyadenylase PAP I, is crucial for maintaining virulence plasmids in Yersinia and Shigella pathogens. This gene stabilizes plasmids, boosts antibiotic resistance, and enhances bacterial virulence.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Pathogenic bacteria utilize plasmid-encoded virulence factors for infection, with their expression often linked to plasmid replication and copy number.
- The type III secretion system (T3SS) is essential for Yersinia virulence, encoded on the pYV virulence plasmid, and its expression is regulated by temperature and gene dosage.
- The mechanisms governing elevated plasmid copy number and stability at host temperatures remain poorly understood.
Purpose of the Study:
- To investigate the role of the chromosomal gene pcnB, encoding polyadenylase PAP I, in regulating virulence plasmid replication and stability in pathogenic bacteria.
- To determine the impact of pcnB/PAP I on T3SS expression, bacterial virulence, and the maintenance of antimicrobial resistance (AMR) plasmids.
- To explore the broader implications of pcnB/PAP I in the spread and stabilization of virulence and AMR plasmids across bacterial pathogens.
Main Methods:
- Investigated the function of the pcnB gene and its encoded PAP I enzyme in Yersinia and Shigella species.
- Assessed the effect of pcnB/PAP I on pYV plasmid copy number (PCN) and stability at different temperatures.
- Evaluated the impact of pcnB/PAP I on T3SS gene expression, bacterial virulence in a mouse model, and the maintenance of antimicrobial resistance plasmids.
Main Results:
- The chromosomal gene pcnB/PAP I is essential for regulating pYV plasmid copy number, maintaining pYV stability, robust T3SS activity, and Yersinia virulence.
- pcnB/PAP I is also required for robust T3SS expression in Shigella flexneri and for maintaining antimicrobial resistance plasmids, increasing antibiotic resistance tenfold.
- pcnB/PAP I promotes the spread and stabilization of sRNA-regulated virulence and AMR plasmids in bacterial pathogens.
Conclusions:
- The pcnB/PAP I enzyme plays a critical role in stabilizing virulence and antimicrobial resistance plasmids in pathogenic bacteria like Yersinia and Shigella.
- This stabilization directly impacts bacterial virulence and antibiotic resistance by ensuring adequate gene dosage of plasmid-encoded traits.
- The widespread identification of pcnB/PAP I across bacterial species suggests its significant, yet underappreciated, role in bacterial pathogenesis and the dissemination of resistance genes.
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