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Cell Host Microbe. 2014 May 14;15(5):578-86. doi: 10.1016/j.chom.2014.04.003.

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

Author information

1
Laboratory 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.
2
Laboratory 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.

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.

PMID:
24832452
PMCID:
PMC4084870
DOI:
10.1016/j.chom.2014.04.003
[Indexed for MEDLINE]
Free PMC Article

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