Abstract
It has been proposed that in wild ecosystems viruses are often plant mutualists, whereas agroecosystems favour pathogenicity. We seek evidence for virus pathogenicity in wild ecosystems through the analysis of plant-virus coevolution, which requires a negative effect of infection on the host fitness. We focus on the interaction between Arabidopsis thaliana and Cucumber mosaic virus (CMV), which is significant in nature. We studied the genetic diversity of A. thaliana for two defence traits, resistance and tolerance, to CMV. A set of 185 individuals collected in 76 A. thaliana Iberian wild populations were inoculated with different CMV strains. Resistance was estimated from the level of virus multiplication in infected plants, and tolerance from the effect of infection on host progeny production. Resistance and tolerance to CMV showed substantial genetic variation within and between host populations, and depended on the virus x host genotype interaction, two conditions for coevolution. Resistance and tolerance were co-occurring independent traits that have evolved independently from related life-history traits involved in adaptation to climate. The comparison of the genetic structure for resistance and tolerance with that for neutral traits (QST/FST analyses) indicated that both defence traits are likely under uniform selection. These results strongly suggest that CMV infection selects for defence on A. thaliana populations, and support plant-virus coevolution. Thus, we propose that CMV infection reduces host fitness under the field conditions of the wild A. thaliana populations studied.
Highlights
It is commonly accepted that hosts and pathogens coevolve [1]
We focus on the interaction between Arabidopsis thaliana and Cucumber mosaic virus (CMV), which is significant in nature
We studied the genetic diversity of Arabidopsis thaliana for two defence traits, resistance and tolerance, to Cucumber mosaic virus (CMV) at a regional scale in the Iberian Peninsula
Summary
It is commonly accepted that hosts and pathogens coevolve [1]. This concept rests on the assumption that pathogens are virulent parasites, defining virulence as the negative impact of infection on the host fitness. Coevolution requires certain conditions to be met [1]: i) genetic variation in the relevant host (e.g., resistance, tolerance) and pathogen (e.g., infectivity, virulence) traits; ii) reciprocal effects of the relevant traits of the interaction on the fitness of host and pathogen; iii) dependence of the outcome of the host-pathogen interaction on the combination of host and pathogen genotypes involved. These conditions must be analysed in wild systems, in which the host may evolve in response to environmental pressures, including pathogen infection, at odds with agricultural systems. Evidence for plant-pathogen coevolution from wild pathosystems is limited to a few instances, all involving fungal, oomycete or bacterial pathogens [8,9]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
