title: Genetic variation in bacterial kidney disease (BKD) susceptibility in Lake Michigan Chinook Salmon and its progenitor population from the Puget Sound.
abstract: Mass mortality events in wild fish due to infectious diseases are troubling, especially given the potential for long-term, population-level consequences. Evolutionary theory predicts that populations with sufficient genetic variation will adapt in response to pathogen pressure. Chinook Salmon Oncorhynchus tshawytscha were introduced into Lake Michigan in the late 1960s from a Washington State hatchery population. In the late 1980s, collapse of the forage base and nutritional stress in Lake Michigan were thought to contribute to die-offs of Chinook Salmon due to bacterial kidney disease (BKD). Previously, we demonstrated that Lake Michigan Chinook Salmon from a Wisconsin hatchery have greater survival following BKD challenge relative to their 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 to neutral marker divergence between the populations 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 (h (2)) were consistently higher in the Wisconsin relative to the Washington population. If selection had acted on the Wisconsin population there was no evidence of a concomitant loss of genetic variation in BKD susceptibility. The Renibacterium salmoninarum exposures were conducted at both 14°C and 9°C; the warmer temperature accelerated time to death in both populations and there was no evidence of phenotypic plasticity or a genotype-by-environment (G × E) interaction. High h (2) estimates for BKD susceptibility in the Wisconsin population, combined with a lack of phenotypic plasticity, predicts that future adaptive gains in BKD resistance are still possible and that these adaptive gains would be stable under the temperature range evaluated here.
authors.affiliation: a U.S. Geological Survey, Western Fisheries Research Center , 6505 Northeast 65th Street , Seattle , Washington , 98115 , USA.
authors.forename: Maureen K
authors.initials: MK
authors.lastname: Purcell
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Hard
authors.forename: Kathleen G
authors.initials: KG
authors.lastname: Neely
authors.forename: Linda K
authors.initials: LK
authors.lastname: Park
authors.forename: James R
authors.initials: JR
authors.lastname: Winton
authors.forename: Diane G
authors.initials: DG
authors.lastname: Elliott
mesh_terms: D000818:Animals; D005393:Fish Diseases / Q000235:genetics / Q000382:microbiology*; D020022:Genetic Predisposition to Disease; D007674:Kidney Diseases / Q000235:genetics / Q000382:microbiology / Q000662:veterinary*; D010140:Pacific Ocean; D012474:Salmon / Q000235:genetics*; D014861:Washington; D014922:Wisconsin