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MBE Advance Access published online on March 18, 2008

Molecular Biology and Evolution, doi:10.1093/molbev/msn059
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© The Author 2008. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Research Article

Evolutionary genomics of host adaptation in vesicular stomatitis virus (VSV)

Susanna K. Remold1, Andrew Rambaut2 and Paul E. Turner3

2 University of Oxford, Department of Zoology, Oxford, OX1 3PS, UK
3 Yale University, Department of Ecology and Evolutionary Biology, New Haven, CT 06520 (where research was done)

1 Corresponding Author, University of Louisville, Department of Biology, Louisville, KY 40292, Email: susanna.remold{at}louisville.edu, Phone: 502-852-0960, Fax: 502- 852-0725

Received for publication February 24, 2007. Revision received February 29, 2008. Accepted for publication March 4, 2008.

Populations experiencing similar selection pressures can sometimes diverge in the genetic architectures underlying evolved complex traits. We used RNA virus populations of large size and high mutation rate to study the impact of historical environment on genome evolution, thus increasing our ability to detect repeatable patterns in the evolution of genetic architecture. Experimental vesicular stomatitis virus (VSV) populations were evolved on HeLa cells, on MDCK cells, or on alternating hosts. Turner and Elena (2000) previously showed that virus populations evolved in single-host environments achieved high fitness on their selected hosts but failed to increase in fitness relative to their ancestor on the unselected host, and that alternating-host-evolved populations had high fitness on both hosts. Here we determined the complete consensus sequence for each evolved population after 95 generations to gauge whether the parallel phenotypic changes were associated with parallel genomic changes. We also analyzed the patterns of allele substitutions to discern whether differences in fitness across hosts arose through true pleiotropy, or the presence of a mutation that is beneficial in both hosts but also one or more mutation(s) at other loci that are costly in the unselected environment (mutation accumulation). We found that ecological history may influence to what extent pleiotropy and mutation accumulation contribute to fitness asymmetries across environments. We discuss the degree to which current genetic architecture is expected to constrain future evolution of complex traits, such as host use by RNA viruses.

Key Words: host adaptation • genetic architecture • epistasis • VSV • antagonistic pleiotropy • mutation accumulation


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