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Originally published as Genetics Published Articles Ahead of Print on April 3, 2007.
Genetics, Vol. 176, 1013-1022, June 2007, Copyright © 2007
doi:10.1534/genetics.106.064634
High Frequency of Mutations That Expand the Host Range of an RNA Virus
Martin T. Ferris*,
Paul Joyce
and
Christina L. Burch*,1
* Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599 and
Department of Mathematics and Department of Statistics, University of Idaho, Moscow, Idaho 83844
1 Corresponding author: Department of Biology, CB 3280, Coker Hall, University of North Carolina, Chapel Hill, NC 27599-3280.
E-mail: cburch{at}bio.unc.edu
The ability of a virus population to colonize a novel host is predicted to depend on the equilibrium frequency of potential colonists (i.e., genotypes capable of infecting the novel host) in the source population. In this study, we investigated the determinants of the equilibrium frequency of potential colonists in the RNA bacteriophage
6. We isolated 40 spontaneous mutants capable of infecting a novel Pseudomonas syringae host and sequenced their host attachment genes to identify the responsible mutations. We observed 16 different mutations in the host attachment gene and used a new statistical approach to estimate that 39 additional mutations were missed by our screen. Phenotypic and fitness assays confirmed that the proximate mechanism underlying host range expansion was an increase in the ability to attach to the novel host and that acquisition of this ability most often imposed a cost for growth rate on two standard hosts. Considered in a population genetic framework, our data suggest that host range mutations should exist in phage populations at an equilibrium frequency (3 x 104) that exceeds the phage mutation rate by more than two orders of magnitude. Thus, colonization of novel hosts is unlikely to be limited by an inability to produce appropriate mutations.
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