J Brusini1, Y Wang2, L F Matos3, L-S Sylvestre4, B M Bolker5, M L Wayne4. 1. Department of Biology, University of Florida, Gainesville, Florida, USA; Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, California, USA. 2. Department of Biology, University of Florida, Gainesville, Florida, USA; Department of Chemistry, University of California, Irvine, California, USA. 3. Department of Biology, Eastern Washington University, Cheney, Washington, USA. 4. Department of Biology, University of Florida, Gainesville, Florida, USA. 5. Departments of Mathematics & Statistics and Biology, McMaster University, Hamilton, Ontario, Canada.
Abstract
QUESTION: How does virulence evolve in the Drosophila melanogaster/sigma virus (DMelSV) system? ORGANISMS: Drosophila melanogaster (host) and DMelSV (parasite). EMPIRICAL METHODS: Artificial selection on whole-carcass viral titre of infected flies, including two selection regimes (maternal and biparental transmission) and three treatments within each regime (increased titre, decreased titre, and control). The maternal transmission selection regime lasted for six generations, while the biparental transmission selection regime lasted for twelve generations. We further quantified virulence by estimating the fecundity, viability, and development time of infected flies. Finally, we sequenced virus strains at the end of selection. PREDICTIONS AND CONCLUSIONS: Titre is defined here as the number of viral genomes inside a single fly, while virulence is defined as harm to host. We predicted that titre would respond to both increased and decreased selection, that virulence would evolve as a positively correlated response, and that sequence evolution in the viruses would be responsible for these changes. Titre did respond to selection in the biparental regime, although both high and control lines both demonstrated increased titre, while the titre of the low lines did not change. One component of virulence, development time, was positively correlated with titre in the biparental transmission lines (maternal transmission lines were not scored for virulence). However, we detected few (and in some cases, no) genomic changes in the virus, making viral evolution unlikely to be responsible for the response to selection and the association between development time and titre.
QUESTION: How does virulence evolve in the Drosophila melanogaster/sigma virus (DMelSV) system? ORGANISMS: Drosophila melanogaster (host) and DMelSV (parasite). EMPIRICAL METHODS: Artificial selection on whole-carcass viral titre of infected flies, including two selection regimes (maternal and biparental transmission) and three treatments within each regime (increased titre, decreased titre, and control). The maternal transmission selection regime lasted for six generations, while the biparental transmission selection regime lasted for twelve generations. We further quantified virulence by estimating the fecundity, viability, and development time of infected flies. Finally, we sequenced virus strains at the end of selection. PREDICTIONS AND CONCLUSIONS: Titre is defined here as the number of viral genomes inside a single fly, while virulence is defined as harm to host. We predicted that titre would respond to both increased and decreased selection, that virulence would evolve as a positively correlated response, and that sequence evolution in the viruses would be responsible for these changes. Titre did respond to selection in the biparental regime, although both high and control lines both demonstrated increased titre, while the titre of the low lines did not change. One component of virulence, development time, was positively correlated with titre in the biparental transmission lines (maternal transmission lines were not scored for virulence). However, we detected few (and in some cases, no) genomic changes in the virus, making viral evolution unlikely to be responsible for the response to selection and the association between development time and titre.
Authors: Vaughn S Cooper; Michael H Reiskind; Jonathan A Miller; Kirsten A Shelton; Bruno A Walther; Joseph S Elkinton; Paul W Ewald Journal: Proc Biol Sci Date: 2002-06-07 Impact factor: 5.349
Authors: Helen Piontkivska; Luis F Matos; Sinu Paul; Brian Scharfenberg; William G Farmerie; Michael M Miyamoto; Marta L Wayne Journal: Genome Biol Evol Date: 2016-10-05 Impact factor: 3.416