Abstract
Captive bred individuals are often released into natural environments to supplement resident populations. Captive bred salmonid fishes often exhibit lower survival rates than their wild brethren and stocking measures may have a negative influence on the overall fitness of natural populations. Stocked fish often stem from a different evolutionary lineage than the resident population and thus may be maladapted for life in the wild, but this phenomenon has also been linked to genetic changes that occur in captivity. In addition to overall loss of genetic diversity via captive breeding, adaptation to captivity has become a major concern. Altered selection pressure in captivity may favour alleles at adaptive loci like the Major Histocompatibility Complex (MHC) that are maladaptive in natural environments. We investigated neutral and MHC-linked genetic variation in three autochthonous and three hatchery populations of Austrian brown trout (Salmo trutta). We confirm a positive selection pressure acting on the MHC II β locus, whereby the signal for positive selection was stronger in hatchery versus wild populations. Additionally, diversity at the MHC II β locus was higher, and more uniform among hatchery samples compared to wild populations, despite equal levels of diversity at neutral loci. We postulate that this stems from a combination of stronger genetic drift and a weakening of positive selection at this locus in wild populations that already have well adapted alleles for their specific environments.
Highlights
Animals have been kept under human care since the Neolithic
For comparisons among wild populations, both, FST- and G′ST-values of Major Histocompatibility Complex (MHC) II β were clearly higher than the respective FST- and G′ST-values of neutral SSRs, due to the lack of power, there was no significant difference among those values
We found significantly more variation at adaptive markers (MHC II β and adaptive SSRs) in hatchery versus wild populations
Summary
The environmental conditions in captivity often differ drastically from natural surroundings and include altered diet, increased or reduced populations sizes, different pathogen stress and the release from ecological forces such as competition or predation. These changes manifest themselves in behavioural (Price 1999; Reinhardt 2001), morphological (O’Regan and Kitchener 2005; Stringwell et al 2014) and physiological changes (Quispe et al 2014; Roznere et al 2014). The causes of reintroduction failures have been linked to ecological factors or mismanagement, but genetic factors have been suggested (Fischer and Lindenmayer 2000; Jiménez et al 1994)
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