Abstract
Phenotypic plasticity can increase tolerance to heterogeneous environments but the elevations and slopes of reaction norms are often population specific. Disruption of locally adapted reaction norms through outcrossing can lower individual viability. Here, we sampled five genetically distinct populations of brown trout (Salmo trutta) from within a river network, crossed them in a full-factorial design, and challenged the embryos with the opportunistic pathogen Pseudomonas fluorescens. By virtue of our design, we were able to disentangle effects of genetic crossing distance from sire and dam effects on early life-history traits. While pathogen infection did not increase mortality, it was associated with delayed hatching of smaller larvae with reduced yolk sac reserves. We found no evidence of a relationship between genetic distance (W, FST) and the expression of early-life history traits. Moreover, hybrids did not differ in phenotypic means or reaction norms in comparison to offspring from within-population crosses. Heritable variation in early life-history traits was found to remain stable across the control and pathogen environments. Our findings show that outcrossing within a rather narrow geographical scale can have neutral effects on F1 hybrid viability at the embryonic stage, i.e. at a stage when environmental and genetic effects on phenotypes are usually large.
Highlights
The ability for a genotype to adopt different phenotypes according to environmental conditions permits organisms to maximize fitness in the face of heterogeneous biotic and abiotic risks [1]
There appears to be no clear consensus on how environmental change affects genetic variability in quantitative traits, with indications that it is trait-dependent, and reliant on the stressor in question
To add an additional level of complexity, the effect of ecological stressors on the genetic variability of plastic traits cannot be generalized for a species
Summary
The ability for a genotype to adopt different phenotypes according to environmental conditions permits organisms to maximize fitness in the face of heterogeneous biotic and abiotic risks [1]. As natural populations are increasingly exposed to habitat-altering anthropogenic activities [2,3], this plasticity can be a key factor in increasing tolerance to environmental change [4] The capacity of such traits to evolve in a population relies on the persistence of heritable variation therein [5]. Populations often diverge in the genetic architecture of traits and trait plasticities, as a result of selective pressures varying in type and intensity over space and time [for examples see 19,20] This divergence can indicate local adaptation [21], and as such, changes to the elevation and/or slopes of the reaction norms through outbreeding can have negative effects on fitness. Events including interpopulation hybridization have been shown to bring about such alterations [22,23,24]
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