Evidence map›Paper›PMID 24832452›Full record

ArticleCell host & microbe2014

Retracing the evolutionary path that led to flea-borne transmission of Yersinia pestis.

Yi-Cheng Sun, Clayton O Jarrett, Christopher F Bosio, B Joseph Hinnebusch

Abstract read
In one paragraph

Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed.

  1. Review
  2. Article
  3. Emergence, global dispersal, and local adaptations ofApplied and environmental microbiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Molecular turn inEmerging microbes & infections · 2025
    Article
  8. Retracing the path of evolution: polymorphisms ofEmerging microbes & infections · 2025
    Article
  9. Review
  10. Infection and immunity · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Yi-Cheng SunLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4(th) Street, Hamilton, MT 59840, USA.
Clayton O JarrettLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4(th) Street, Hamilton, MT 59840, USA.
Christopher F BosioLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4(th) Street, Hamilton, MT 59840, USA.
B Joseph HinnebuschLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4(th) Street, Hamilton, MT 59840, USA. Electronic address: jhinnebusch@niaid.nih.gov.

Funding

Transmission Of Yersinia Pestis By Fleas: Molecular MechanismsZIAAI000796 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HINNEBUSCH, B J · 2009 to 2023
$9.7M
Intramural NIH HHS ZIA AI000796
6 · The paper itself

Abstract

Yersinia pestis is an arthropod-borne bacterial pathogen that evolved recently from Yersinia pseudotuberculosis, an enteric pathogen transmitted via the fecal-oral route. This radical ecological transition can be attributed to a few discrete genetic changes from a still-extant recent ancestor, thus providing a tractable case study in pathogen evolution and emergence. Here, we determined the genetic and mechanistic basis of the evolutionary adaptation of Y. pestis to flea-borne transmission. Remarkably, only four minor changes in the bacterial progenitor, representing one gene gain and three gene losses, enabled transmission by flea vectors. All three loss-of-function mutations enhanced cyclic-di-GMP-mediated bacterial biofilm formation in the flea foregut, which greatly increased transmissibility. Our results suggest a step-wise evolutionary model in which Y. pestis emerged as a flea-borne clone, with each genetic change incrementally reinforcing the transmission cycle. The model conforms well to the ecological theory of adaptive radiation.

Indexed as

Biological EvolutionAnimalsBacterial ProteinsBiofilmsFemaleHumansInsect VectorsMaleMiceMolecular Sequence DataMutationPhylogenySiphonapteraYersinia InfectionsYersinia pestisYersinia pseudotuberculosisBacterial Proteins

Identifiers

PMID24832452
PMCPMC4084870

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.