1. Widely used methods to assess population genetic structure and differentiation rely on independence of marker loci. Following the assumption, the common metrics, for example FST, evaluate genetic structure by averaging across loci. Common metrics do not use information in the associations among loci at the individual level and are often criticized for failing to measure true differentiation even when loci segregate independently. 2. We introduce a new concept to measure β-variation (Effective Number of Different Populations, ENDP). It requires the following steps: (a) calculation of a proper dissimilarity between genetic profiles of all individuals; (b) calculation of suitable pairwise distances between the samples based on the dissimilarities between individuals; (c) calculation of diversity (in terms of Hill numbers) and dispersion of samples based on the pairwise distances between samples; (d) ENDP is then estimated as a combination of the diversity and dispersion. ENDP estimates β-variation independently of within-sample α-variation. This new concept differs from the existing standard where β-diversity is estimated based on the ‘partition of variation’ scheme (beta=gamma-alpha or beta=gamma/alpha). 3. Estimates of ENDP are obtained by evaluating information in the available genetic profiles of individuals including association of loci. Therefore, ENDP can be used even in an absence of panmixia. 4. We illustrate the use of this concept by analyzing the population genetic structure of a sexual species (a trematode parasite) occupying connected populations across a broad geographic area. Analysis is complicated by two coexisting cryptic sister clades and the potentially mixed-mating system of this hermaphroditic parasite.

Vector-borne parasites often manipulate hosts to attract uninfected vectors. For example, parasites causing malaria alter host odor to attract mosquitoes. Here we discuss the ecology and evolution of fruit-colonizing yeast in a tripartite symbiosis – the so-called “killer yeast” system. “Killer yeast” consists of Saccharomyces cerevisiae yeast hosting two double stranded RNA viruses (M satellite dsRNAs, L-A dsRNA helper virus). When both dsRNA viruses occur in a yeast cell, the yeast converts to lethal toxin‑producing “killer yeast” phenotype that kills uninfected yeasts. Yeasts on ephemeral fruits attract insect vectors to colonize new habitats. As the viruses have no extracellular stage, they depend on the same insect vectors as yeast for their dispersal. Viruses also benefit from yeast dispersal as this promotes yeast to reproduce sexually, which is how viruses can transmit to uninfected yeast strains. We tested whether insect vectors are more attracted to killer yeasts than to non‑killer yeasts. In our field experiment, we found that killer yeasts were more attractive to Drosophila than non-killer yeasts. This suggests that vectors foraging on yeast are more likely to transmit yeast with a killer phenotype, allowing the viruses to colonize those uninfected yeast strains that engage in sexual reproduction with the killer yeast. Beyond insights into the basic ecology of the killer yeast system, our results suggest that viruses could increase transmission success by manipulating the insect vectors of their host.