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Ecological genetics of Bryozoa-Myxozoa host-parasite interactions

Final Report Summary - BRYOZOA (Ecological genetics of Bryozoa-Myxozoa host-parasite interactions)

The objective of this research project was to investigate the population genetics and host-parasite interactions in the highly clonal freshwater bryozoans and their myxozoan parasites that cause the devastating Proliferative Kidney Disease of salmonid fish. We hypothesised that due to the prevalence of asexual modes of reproduction in the bryozoan life-cycle, many populations should show little genetic diversity. However, as the PKD parasite has the potential to exert high virulence (castration) on the bryozoan host, we further hypothesised that antagonistic coevolutionary processes may create local hotspots of bryozoan genotypic diversity and drive local adaptation in this system. To address these hypotheses, we aimed to develop high-resolution, hypervariable population genetic markers, conduct field work to collect F. sultana and monitor the distribution of the PKD parasite, and to conduct field transplant experiments to investigate the adaptive role of genotypic variation with respect to environmental drivers and parasitism.

A) Population genetic markers via next-generation sequencing
Massively parallel sequencing of genomic DNA was used to develop eight hypervariable microsatellite markers for assessing the clonal structure of the bryozoan F. sultana (Hartikainen and Jokela, submitted). This cutting-edge, cost-effective method has quickly become widely used for genetic marker development and our study is the first to use it for development of markers suitable for distinguishing closely related clonal genotypes. Over 900 candidate loci were identified, out of which only the most variable loci were selected. Up to 17 alleles per locus were detected and this high variation allowed clonal identities using multilocus genotypes to be unambiguously determined with only a minimum set of 3 loci. This represents a set of hypervariable markers capable of determining the clonal structure in populations with high levels of inbreeding and asexual propagation.

B) Genotypic diversity of bryozoan populations
F. sultana samples were collected from 10 locations in Switzerland, 8 populations were found to be infected with T. bryosalmonae, showing that this species is widespread especially in the Swiss lowlands. The bryozoan genotypic diversity showed marked spatial variation, from nearly monoclonal stands to populations showing indications of frequent sexual reproduction (Fig 1a). The genotypic evenness (E5) showed that low diversity populations were dominated by very few successful clones (Fig 1b). We had hypothesised that genotypic diversity of bryozoan populations could be driven by antagonistic host-parasite coevolution, given that the parasite shows high virulence by castrating the bryozoan host (Hartikainen and Okamura, in press). Our new results show that genotypic diversity and parasite prevalence are indeed highly correlated, but in an opposite direction to that required by the above hypothesis. Instead we found that bryozoan populations with lowest clonal diversities harboured the most infections (Fig 1c, swiss and other European populations included). This suggests that parasite virulence may be lower than expected, allowing strong local adaptation of the parasite to the most common bryozoan genotype present in the local population. This is supported by the results from the field exposure studies, which showed that susceptible hosts have a window of opportunity for reproduction prior to infection, thus negating the effects of castration by the parasite. Local bryozoan population structure may therefore explain why the incidence of T. bryosalmonae is patchy within bryozoan populations, whereas the disease in fish is generally widespread and outbreaks occur in consecutive years in the same localities. Environmental drivers that potentially reduce the diversity of bryozoan populations, such as habitat modification, dispersal barriers and climate change, may thus indirectly impact PKD occurrence in brown trout populations by provide reservoirs of monoclonal bryozoan populations in which the PKD parasite can multiply and persist.