Genetically based variation of proliferative kidney disease pathology traits
Evolution, Anthropology
Final Report Abstract
Manifestations of diseases usually differ among individuals because of differences in genetic and environmental factors that contribute to the amount of pathogen and the health damage the pathogen can cause. For this project, I joined a research group to quantify genetic and environmental factors of the salmonid-specific proliferative kidney disease (PKD). PKD is triggered by a myxozoan parasite (Tetracapsuloides bryosalmonae) and can be fatal for infected fish, especially at elevated water temperatures, both in aquaculture and in nature. By using mixed animal model methodology on collected field data, we were able to quantify the genetic variation for PKD susceptibility (resistance) and the severity of different PKD-associated traits among wild brown trout (Salmo trutta) individuals from two Estonian rivers with little neutral genetic differentiation between rivers. Most interestingly, genetic variance for PKD resistance differed strongly between the rivers (6.6-fold) with a higher resistance in the colder river. In contrast, PKD manifested more severely and showed a somewhat larger genetic variance based on three correlated traits in the warmer river. Initial goals to identify and quantify transcribed molecular variants (variation in mRNA levels) that either associate with the pathogen resistance or the PKD severity were not reached. This happened because we were unable to sample uninfected individuals that are required as negative control to identify relevant genes, even though we additionally sampled during a second year. Nonetheless, ongoing work of the research group still aims at identifying molecular variants, but different ones than initially planned (DNA sequence variants, SNPs). Preliminary results indicate that a few SNPs can explain about half of the genetic variance present for pathogen resistance within the colder river. We also preliminarily identified one SNP that associates with one disease severity trait (anaemia). These preliminary results, however, still await confirmation using independent samples. Because we detected a relatively high heritability for resistance in the colder river (h2 ± standard error: 0.44 ± 0.14) where we expected weak selection by a low PKD severity, but a low and non-significant h2 in the warmer river (0.10 ± 0.09) where we expect a strong selection by a more severe PKD, we expect that human selection success for T. bryosalmonae resistance to improve aquaculture or conservation programmes may proceed relatively rapidly. However, because relatively few loci appear to underlie the genetically based resistance (which may enable a genetic marker-based selection approach), it is possible that pathogen-host coevolution may rapidly revert any selection successes, as can often be observed when using resistant crop varieties. Our present results on genetic variance differences between rivers exemplify the complexity of pathogen-host system evolution in nature. Furthermore, it suggests that spatio-temporal variability of environmental factors may hamper directional evolution by changing the environmentally governed disease severity, and thus selection intensity, for both pathogen resistance and disease traits.
Publications
- (2017) Quantitative Genetic Variation in, and Environmental Effects on, Pathogen Resistance and Temperature-Dependent Disease Severity in a Wild Trout. The American naturalist 190 (2) 244–265
Debes, Paul Vincent; Gross, Riho; Vasemägi, Anti
(See online at https://doi.org/10.1086/692536) - (2016) Is telomere length a molecular marker of past thermal stress in wild fish? Molecular Ecology 25, 5412-5424
Debes PV, Visse M, Panda B, Ilmonen P, Vasemägi A
(See online at https://doi.org/10.1111/mec.13856)
