Nature 458, 215-218 (12 March 2009) | doi:10.1038/nature07660; Received 18 August 2008; Accepted 20 November 2008; Published online 1 February 2009

A single regulatory gene is sufficient to alter bacterial host range

Mark J. Mandel1, Michael S. Wollenberg1, Eric V. Stabb2, Karen L. Visick3 & Edward G. Ruby1

  1. Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, 1550 Linden Drive, Madison, Wisconsin 53706, USA
  2. Department of Microbiology, University of Georgia, 828 Biological Sciences, Athens, Georgia 30602, USA
  3. Department of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois 60153, USA

Correspondence to: Mark J. Mandel1 Correspondence and requests for materials should be addressed to M.J.M. (Email: mmandel@wisc.edu).

Microbial symbioses are essential for the normal development and growth of animals1, 2, 3. Often, symbionts must be acquired from the environment during each generation, and identification of the relevant symbiotic partner against a myriad of unwanted relationships is a formidable task4. Although examples of this specificity are well-documented, the genetic mechanisms governing it are poorly characterized5. Here we show that the two-component sensor kinase RscS is necessary and sufficient for conferring efficient colonization of Euprymna scolopes squid by bioluminescent Vibrio fischeri from the North Pacific Ocean. In the squid symbiont V. fischeri ES114, RscS controls light-organ colonization by inducing the Syp exopolysaccharide, a mediator of biofilm formation during initial infection. A genome-level comparison revealed that rscS, although present in squid symbionts, is absent from the fish symbiont V. fischeri MJ11. We found that heterologous expression of RscS in strain MJ11 conferred the ability to colonize E. scolopes in a manner comparable to that of natural squid isolates. Furthermore, phylogenetic analyses support an important role for rscS in the evolution of the squid symbiosis. Our results demonstrate that a regulatory gene can alter the host range of animal-associated bacteria. We show that, by encoding a regulator and not an effector that interacts directly with the host, a single gene can contribute to the evolution of host specificity by switching 'on' pre-existing capabilities for interaction with animal tissue.


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