|Document Type:||Journal Article|
|Title:||Genetic variation in bacterial kidney disease susceptibility in Lake Michigan Chinook salmon and its progenitor population from the Puget Sound|
|Author:||Maureen K. Purcell, Jeffrey J. Hard, Kathleen Guinevere Neely, Linda K. Park, J. R. Winton, Diane G. Elliott|
|Journal:||Journal of Aquatic Animal Health|
|Keywords:||Renibacterium salmoninarum, heritability, additive genetic variation, pathogen-driven selection, phenotypic plasticity,Disease susceptibility,Genetics,bacterial kidney disease|
Mass mortality events due to infectious disease agents in wild fish populations are troubling, but it is the long-term, population-level consequences which that may be of more significance. Evolutionary theory predicts that populations with sufficient genetic variation will adapt in response to pathogen pressure. Chinook salmon were introduced into Lake Michigan in the late 1960s from a Washington State (WA) hatchery population. In the late 1980s, collapse of the forage base in Lake Michigan was thought to contribute to die-offs of Chinook salmon (Oncorhynchus tshawytscha) due to Renibacterium salmoninarum, the causative agent of bacterial kidney disease (BKD). Previously, we demonstrated that Chinook salmon from Lake Michigan, Wisconsin (WI) have greater survival following BKD challenge relative to its progenitor population. Here, we evaluated whether the phenotypic divergence of these populations in BKD susceptibility was due to selection rather than genetic drift. Comparison of the overall magnitude of quantitative trait divergence to neutral marker divergence between the populations strongly suggested selection had occurred but a direct test of quantitative trait divergence was not significant, preventing the rejection of the null hypothesis of differentiation through genetic drift. Estimates of phenotypic variation (VP), additive genetic variation (VA) and narrow-sense heritability (h2) were consistently higher in the WI relative to the WA population. Our results indicated that if selection had acted on the WI population there was no evidence of a concomitant loss of genetic variation in quantitative traits associated with BKD susceptibility. The R. salmoninarum exposures were conducted at both 14 and 9°C and the warmer temperature accelerated time to death consistently in both populations. There was no evidence of phenotypic plasticity or a genotype by environment (G X E) interaction in mortality or time course of death. Significant levels of additive genetic variation in BKD susceptibility in the WI population are indicative of future adaptive potential and our results suggest that evolutionary changes in BKD susceptibility in this population would be little affected by different temperature regimes.
|Theme:||Sustaining Marine Ecosystem and Human Health|
Characterize the exposure risks and effects of pathogens, chemical contaminants, and biotoxins on human and marine animal health using sentinel species and biomedical models