315: PLE11-encoded Rta restricts ICP1 tail assembly in Vibrio cholerae outbreaks

Mathur Y et al., Nature - Clinical surveillance in Bangladesh shows Vibrio cholerae acquired PLE11 encoding Rta that restricts ICP1 tail assembly, driving a selective sweep of phage-resistant strains. Key terms: Vibrio cholerae, ICP1, PLE11, Rta, phage coevolution.

Study Highlights:
This study analysed clinical Vibrio cholerae and ICP1 isolates from stool in Bangladesh using genomic surveillance, plaque assays, qPCR, experimental phage evolution, TEM and mass spectrometry. The authors identify a newly acquired mobile element, PLE11, whose small protein Rta disrupts ICP1 tail assembly by targeting the phage tape measure protein (TMP), producing genome-filled tailless capsids. PLE11 also encodes a TMP and other tail factors enabling assembly of chimeric virions that incorporate PLE-encoded TMP and BhuB, preserving satellite transmission. Continued surveillance documented natural ICP1 counteradaptation via CRISPR–Cas acquisition and convergent TMP substitutions that restore infectivity.

Conclusion:
Acquisition of PLE11 encoding the tail-targeting protein Rta drove selection of phage-resistant Vibrio cholerae in Bangladesh and prompted convergent ICP1 counteradaptations that restore phage propagation.

Music:
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Article title:
Capturing dynamic phage–pathogen coevolution by clinical surveillance

First author:
Mathur Y

Journal:
Nature

DOI:
10.1038/s41586-026-10136-z

Reference:
Mathur Y., Boyd C. M., Farnham J. E., Monir M. M., Islam M. T., Sultana M., Ahmed T., Alam M. & Seed K. D. Capturing dynamic phage–pathogen coevolution by clinical surveillance. Nature (2026). https://doi.org/10.1038/s41586-026-10136-z

License:
This episode is based on an open-access article published under the Creative Commons Attribution 4.0 International License (CC BY 4.0) - https://creativecommons.org/licenses/by/4.0/

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QC:
This episode was checked against the original article PDF and publication metadata for the episode release published on 2026-03-12.

QC Scope:
- article metadata and core scientific claims from the narration
- excludes analogies, intro/outro, and music
- transcript coverage: Audited the transcript sections that discuss the phage–bacteria arms race, PLE11 and Rta, TMP/TAC/BhuB, chimeric tail assembly, phage counterdefenses (CRISPR–Cas, Odn, Adi), and clinical surveillance data from Bangladesh, including outbreak dynamics and convergent evolution.
- transcript topics: Phage–bacteria arms race overview; Phage satellites (PLEs) and anti-PLE strategies; Rta-mediated tail assembly restriction via TMP targeting; Chimeric tail assembly with PLE11-encoded components; ICP1 counterdefenses (CRISPR–Cas, Odn, Adi) and phage evolution; Clinical surveillance in Bangladesh (BD-1.2 sweep, 2022 outbreak)

QC Summary:
- factual score: 10/10
- metadata score: 10/10
- supported core claims: 7
- claims flagged for review: 0
- metadata checks passed: 4
- metadata issues found: 0

Metadata Audited:
- article_doi
- article_title
- article_journal
- license

Factual Items Audited:
- Rta (PLE11-encoded) restricts ICP1 tail assembly by targeting TMP
- PLE11 encodes its own TMP and tail assembly factors (TAC) and BhuB to form chimeric tails enabling PLE transmission
- BD-1.2 Vibrio cholerae populations acquired PLE11 and reached ~91% prevalence within 9 months
- ICP1 populations shifted from Odn-mediated resistance to CRISPR–Cas–mediated resistance, with TMP substitutions (e.g., L362P, N355S) observed
- TEM and proteomics show PLE11 tails incorporate PLE11 TMP and BhuB and lack ICP1 TMP/BhuB, producing shorter tails (~10 nm)
- Outbreak in Dhaka, Bangladesh in early 2022 involved >42,000 cholera patients

QC result: Pass.