Effect of systemic diseases on clonal integration: modelling approach

Systemic disease spread has been suggested as a possible disadvantage of clonal plant integration. As connected ramets have higher risk of being infected, disease should cause a selective pressure against clonality. Since experimental tests of this hypothesis are not easy to perform, we chose a modelling approach, by which we could easily separate different factors influencing the process. We used a spatially explicit model of clonal growth with disease spread implemented and we tested the hypothesis that systemic disease decreases the competitive ability of highly integrated clonal plants when compared to less integrated plants with the same parameters. In contrast to our expectations, the integrator was competitively stronger than the splitter in most cases and it lost only when the disease severity and infection rates were very high. We think that the larger the integrated network is, the better the plant utilises its translocation ability. Even a very small amount of resource sharing greatly increased the relative success of the integrator and larger integrators were competitively stronger than the smaller ones. Our results also indicate that although the same infection rate caused more systemic disease in the integrator than in the splitter population, the disease has only a limited potential to select for the splitter strategy. This is caused not only by the advantages of the clonal integration but also by the fact that there is only a small range of infection rates at which there is sufficient difference in disease impact between the strategies.