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One of the most well-known life-history continuums is the fast-slow axis, where 'fast' individuals mature earlier than 'slow' individuals. 'Fast' individuals are predicted to be more active than 'slow' individuals because high activity is required to maintain a fast life-history strategy. Recent meta-analyses revealed mixed evidence for such integration. Here, we test whether known life-history genotypes differ in activity expression by using Atlantic salmon (

Organisms utilize varying lipid resource allocation strategies as a means to survive seasonal environmental changes and life-history stage transitions. In Atlantic salmon, a certain lipid threshold is needed to initiate sexual maturation. Because of this, an individual’s maturation schedule may be affected by changes in temperature and food availability across the seasons that create natural fluctuations of lipid reserves.Recent studies have found a genome region, including the genevgll3,that explains a large proportion of variation for size and age at maturity. Vgll3encodes a transcription co-factor that acts as an inhibitor of adipogenesis in mice and also affects condition factor and other phenotypes in juvenile salmon. However, even with many studies investigating varying temperature effects, there is a lack of temporal studies examining the effects of seasonality on such phenotypes, nor have the effects ofvgll3genotype on condition factor and maturation in different temperatures at different life stages.Here, we investigate the influence of different larval and juvenile incubation temperatures,vgll3genotype and their interactions on juvenile salmon phenotypes including body condition, and sexual maturation rate. We reared Atlantic salmon for 2 years in varying temperatures with an average 1.76 °C difference between warm and cold treatments in four different larval-juvenile phase treatment groups (Warm-Warm, Warm-Cold, Cold-Warm, and Cold-Cold) until the first occurrence of maturation in males.We found no effect of larval temperature on the measured phenotypes or maturation rate, suggesting the occurrence of growth compensation over the course of the experiment. Agreeing with previous studies, an increased maturation rate was observed in individuals of the warm juvenile temperature treatment.In addition, we observed differences in condition factor associated withvgll3genotype, wherebyvgll3*EEindividuals (the genotype associated with early maturation) had a less variable condition factor across the seasons compared to thevgll3*LL(associated with late maturation) individuals.This result suggests avgll3influence on resource acquisition and allocation strategies, possibly linked with the early maturation process, with individuals carrying the early maturationvgll3genotype having a higher early maturation rate and a higher condition factor in the spring.

Age at maturity can vary dramatically within some species. We show that, when raised in controlled conditions, Atlantic salmon age at maturity is affected greatly by temperature as well as a recently discovered age-at-maturity gene. The influence of temperature on age at maturity differed between two populations, but the effect of the age-at-maturity gene was similar in both temperatures and populations.Age at maturity is a key life history trait involving a trade-off between survival risk and reproductive investment, and is an important factor for population structures. In ectotherms, a warming environment may have a dramatic influence on development and life history, but this influence may differ between populations. While an increasing number of studies have examined population-dependent reactions with temperature, few have investigated this in the context of maturation timing. Atlantic salmon, a species of high conservation relevance, is a good study species for this topic as it displays considerable variation in age at maturity, of which a large proportion has been associated with a genomic region including the strong candidate gene vgll3. Until now, the effect of this gene in the context of different environments and populations has not been studied. Using a large-scale common-garden experiment, we find strong effects of temperature, population-of-origin, and vgll3 genotype on maturation in 2-year-old male Atlantic salmon (Salmo salar). With a temperature difference of 1.8 degrees C, maturation probability was 4.8 times higher in the warm treatment than the cold treatment. This temperature effect was population-specific and was higher in the southern (60.48 degrees N) compared to the northern (65.01 degrees N) population. The early maturation vgll3*E allele was associated with a significantly higher maturation probability, but there was no vgll3 interaction with temperature or population. Both body condition and body mass associated with maturation. The body mass association was only present in the warm treatment. Our findings demonstrate that (i) populations can vary in their response to temperature change in terms of age at maturity, (ii) high intrinsic growth could be associated with higher thermal sensitivity for life history variation and (iii) vgll3 effects on age at maturity might be similar between populations and different thermal environments.

Populations may counteract lasting temperature changes or recurrent extremes through plasticity or adaptation. However, it remains underexplored how outbreeding, either naturally, unintentionally, or facilitated, may modify a local response potential and whether genotype-by-environment interactions or between-trait correlations can restrict this potential. We quantified population differences and outbreeding effects, within-population genetic variation, and plasticity of these, for thermal performance proxy traits using 32 pedigreed wild, domesticated, and wild-domesticated Atlantic salmon families reared under common-garden conditions. Following exposure to ambient cold (11.6 °C) or ~4° and ~8° warmer summer temperatures, populations differed notably for body length and critical thermal maximum (CT(max)) and for thermal plasticity of length, condition, and CT(max), but not for haematocrit. Line-cross analysis suggested mostly additive and some dominant outbreeding effects on means and solely additive outbreeding effects on plasticity. Heritability was detected for all traits. However, with increasing acclimation temperature, differences in CT(max) between populations and CT(max) heritability diminished, and CT(max) breeding values re-ranked. Furthermore, CT(max) and body size were negatively correlated at the genetic and phenotypic levels, and there was indirect evidence for a positive correlation between growth potential and thermal performance breadth for growth. Thus, population differences (including those between wild and domesticated populations) in thermal performance and plasticity may present a genetic resource in addition to the within-population genetic variance to facilitate, or impede, thermal adaptation. However, unfavourable genotype-by-environment interactions and negative between-trait correlations may generally hamper joint evolution in response to an increase in average temperature and temporary extremes.

One of the most well-known life-history continuums is the fast–slow axis, where ‘fast’ individuals mature earlier than ‘slow’ individuals. ‘Fast’ individuals are predicted to be more active than ‘slow’ individuals because high activity is required to maintain a fast life-history strategy. Recent meta-analyses revealed mixed evidence for such integration. Here, we test whether known life-history genotypes differ in activity expression by using Atlantic salmon ( Salmo salar ) as a model. In salmon, variation in Vgll3, a transcription cofactor, explains approximately 40% of variation in maturation timing. We predicted that the allele related to early maturation ( vgll3 *E) would be associated with higher activity. We used an automated surveillance system to follow approximately 1900 juveniles including both migrants and non-migrants (i.e. smolt and parr fish, respectively) in semi-natural conditions over 31 days (approx. 580 000 activity measurements). In migrants, but not in non-migrants, vgll3 explained variation in activity according to our prediction in a sex-dependent manner. Specifically, in females the vgll3 *E allele was related to increasing activity, whereas in males the vgll3 *L allele (later maturation allele) was related to increasing activity. These sex-dependent effects might be a mechanism maintaining within-population genetic life-history variation.

The myxozoan Tetracapsuloides bryosalmonae is a widely spread endoparasite that causes proliferative kidney disease (PKD) in salmonid fish. We developed an in silico pipeline to separate transcripts of T. bryosalmonae from the kidney tissue of its natural vertebrate host, brown trout (Salmo trutta). After stringent filtering, we constructed a partial transcriptome assembly T. bryosalmonae, comprising 3427 transcripts. Based on homology-restricted searches of the assembled parasite transcriptome and Atlantic salmon (Salmo salar) proteome, we identified four protein targets (Endoglycoceramidase, Legumain-like protease, Carbonic anhydrase 2, Pancreatic lipase-related protein 2) for the development of anti-parasitic drugs against T. bryosalmonae. Earlier work of these proteins on parasitic protists and helminths suggests that the identified anti-parasitic drug targets represent promising chemotherapeutic candidates also against T. bryosalmonae, and strengthen the view that the known inhibitors can be effective in evolutionarily distant organisms. In addition, we identified differentially expressed T. bryosalmonae genes between moderately and severely infected fish, indicating an increased abundance of T. bryosalmonae sporogonic stages in fish with low parasite load. In conclusion, this study paves the way for future genomic research in T. bryosalmonae and represents an important step towards the development of effective drugs against PKD.

One of the most important life-history continuums is the fast–slow axis, where “fast” individuals mature earlier than “slow” individuals. “Fast” individuals are predicted to be more active than “slow” individuals; high activity is required to maintain a fast life-history strategy. Recent meta-analyses revealed mixed evidence for such integration. Here, we test whether known life-history genotypes differ in activity expression by using Atlantic salmon (Salmo salar) as a model. In salmon, variation in Vgll3, a transcription co-factor, explains ∼40% of variation in maturation timing. We predicted that the allele related to early maturation (vgll3*E) would be associated with increased activity. We used an automated surveillance system to follow ∼1900 juveniles including both migrants and non-migrants (i.e. smolt and parr fish, respectively) in semi-natural conditions over 31 days (∼580 000 activity measurements). Against our prediction, vgll3 did not explain variation in activity in pooled migrant and non-migrant data. However, in migrants, vgll3 explained variation in activity according to our prediction in a sex-dependent manner. Specifically, in females the vgll3*E allele was related to increasing activity, whereas in males the vgll3*L allele (later maturation allele) was related to increasing activity. These sex-dependent effects might be a mechanism maintaining within-population genetic life-history variation.

Sexual maturation timing is a life-history trait central to the balance between mortality and reproduction. Maturation may be triggered when an underlying compound trait, called liability, exceeds a threshold. In many different species and especially fishes, this liability is approximated by growth and body condition. However, environmental vs. genetic contributions either directly or via growth and body condition to maturation timing remain unclear. Uncertainty exists also because the maturation process can reverse this causality and itself affect growth and body condition. In addition, disentangling the contributions of polygenic and major loci can be important. In many fishes, males mature before females, enabling the study of associations between male maturation and maturation-unbiased female liability traits. Using 40 Atlantic salmon families, longitudinal common-garden experimentation, and quantitative genetic analyses, we disentangled environmental from polygenic and major locus (vgll3) effects on male maturation, and sex-specific growth and condition. We detected polygenic heritabilities for maturation, growth, and body condition, and vgll3 effects on maturation and body condition but not on growth. Longitudinal patterns for sex-specific phenotypic liability, and for genetic variances and correlations between sexes suggested that early growth and condition indeed positively affected maturation initiation. However, towards spawning time, causality appeared reversed for males whereby maturation affected growth negatively and condition positively via both the environmental and genetic effects. Altogether, the results indicate that growth and condition are useful traits to study liability for maturation initiation, but only until maturation alters their expression, and that vgll3 contributes to maturation initiation via condition.

The Atlantic salmon has been studied extensively, particularly as a model for understanding the genetic and environmental contributions to the evolution and development of life history traits. Expression pattern analysis in situ, however, is mostly lacking in salmon. We examine the embryonic developmental expression of six6, a candidate gene previously identified to be associated with spawning ecotypes and age at sexual maturity, in Atlantic salmon. Six6 is a member of the sine oculis homeobox family of transcription factors and is known to regulate eye and brain development in other vertebrates. We assay the expression of this gene in embryonic Atlantic salmon Salmo salar by whole-mount in situ hybridization. In line with earlier studies in other vertebrate species, we find conserved expression in the developing brain and sensory organs, including optic and olfactory primordia. However, we also find previously unreported domains of expression that suggest additional roles in axial and appendicular development, cardiovascular, intestinal, and sensory organogenesis. Each of these systems are important in the sensory ecology of Atlantic salmon, suggesting it is plausible that six6 may have pleiotropic roles in this complex phenotype.

A major goal in biology is to understand how evolution shapes variation in individual life histories. Genome-wide association studies have been successful in uncovering genome regions linked with traits underlying life history variation in a range of species. However, lack of functional studies of the discovered genotype-phenotype associations severely restrains our understanding how alternative life history traits evolved and are mediated at the molecular level. Here, we report a cis-regulatory mechanism whereby expression of alternative isoforms of the transcription co-factor vestigial-like 3 (vgll3) associate with variation in a key life history trait, age at maturity, in Atlantic salmon (Salmo salar). Using a common-garden experiment, we first show that vgll3 genotype associates with puberty timing in one-year-old salmon males. By way of temporal sampling of vgll3 expression in ten tissues across the first year of salmon development, we identify a pubertal transition in vgll3 expression where maturation coincided with a 66% reduction in testicular vgll3 expression. The late maturation allele was not only associated with a tendency to delay puberty, but also with expression of a rare transcript isoform of vgll3 pre-puberty. By comparing absolute vgll3 mRNA copies in heterozygotes we show that the expression difference between the early and late maturity alleles is largely cis-regulatory. We propose a model whereby expression of a rare isoform from the late allele shifts the liability of its carriers towards delaying puberty. These results exemplify the potential importance of regulatory differences as a mechanism for the evolution of life history traits., Author summary Alternative life history strategies are an important source of diversity within populations and promote the maintenance of adaptive capacity and population resilience. However, in many cases the molecular basis of different life history strategies remains elusive. Age at maturity is a key adaptive life history trait in Atlantic salmon and has a relatively simple genetic basis. Using salmon age at maturity as a model, we report a mechanism whereby different transcript isoforms of the key age at maturity gene, vestigial-like 3 (vgll3), associate with variation in the timing of male puberty. Our results show how gene regulatory differences in conjunction with variation in gene transcript structure can encode for complex alternative life histories.

Sexual maturation is a pivotal life-history trait that balances the probabilities between mortality and reproduction. Environmental vs. genetic contributions to maturation component traits, such as somatic growth and body condition, remain uncertain because of difficulties in determining causality. In Atlantic salmon, maturation timing associates with a large-effect locus around vgll3, which also links with growth, condition, and maturation in mammals. We investigate environmental vs. genetic contributions to maturation and its component traits by combining controlled breeding with common-garden experimentation in two temperatures. We test whether vgll3 associates with first-year maturation of male salmon and, to avoid reverse causality, whether vgll3 effects express via growth or condition in the males’ non-maturing female relatives. Across 41 families, 4% of males matured in the cold vs. 39% in the warm environment. Maturation rate differed 3.3- to 4.6-fold between vgll3 genotypes, which also explained around 30% of maturation heritability. Female condition differed up to 2% between vgll3 genotypes, which also explained 6-17% of condition heritability. Non-significant vgll3 effects on female length were antagonistic to those for condition but of equal proportional size. When accounting for vgll3 effects, positive genetic correlations between male maturation and female growth increased, whereas those between male maturation and condition decreased, supporting an antagonistic effect of vgll3 on growth and condition. The results indicate that large vgll3 effects on maturation are mediated via large condition effects and suggest vgll3 as a candidate locus for controlling the resource allocation trade-off between somatic growth and body condition. Significance Statement Identifying traits that affect sexual maturation timing and quantifying their relative environmental and genetic importance is a major goal in evolutionary research because of their strong links to fitness. However, cause and effect between maturation timing and such traits often remain unknown. We conducted a common-garden quantitative genetic study using Atlantic salmon to test for genetic contributions of body length and body condition expressed in immature females on maturation of their male relatives. We show that the detection of genetic associations between maturation and length or condition depends on both genetic and environmental factors and suggest that the genetic association with condition chiefly underlies a candidate gene with large effect on maturation that is mediated via variation in body condition.

Despite recent taxonomic diversification in studies linking genotype with phenotype, follow-up studies aimed at understanding the molecular processes of such genotype-phenotype associations remain rare. The age at which an individual reaches sexual maturity is an important fitness trait in many wild species. However, the molecular mechanisms regulating maturation timing processes remain obscure. A recent genome-wide association study in Atlantic salmon (Salmo salar) identified large-effect age-at-maturity-associated chromosomal regions including genesvgll3,akap11andsix6, which have roles in adipogenesis, spermatogenesis and the hypothalamic-pituitary-gonadal (HPG) axis, respectively. Here, we determine expression patterns of these genes during salmon development and their potential molecular partners and pathways. Using Nanostring transcription profiling technology, we show development- and tissue-specific mRNA expression patterns forvgll3,akap11andsix6. Correlated expression levels ofvgll3andakap11, which have adjacent chromosomal location, suggests they may have shared regulation. Further,vgll3correlating witharhgap6andyap1, andakap11withlats1andyap1suggests that Vgll3 and Akap11 take part in actin cytoskeleton regulation. Tissue-specific expression results indicate thatvgll3andakap11paralogs have sex-dependent expression patterns in gonads. Moreover,six6correlating withslc38a6andrtn1, and Hippo signaling genes suggests that Six6 could have a broader role in the HPG neuroendrocrine and cell fate commitment regulation, respectively. We conclude that Vgll3, Akap11 and Six6 may influence Atlantic salmon maturation timing via affecting on adipogenesis and gametogenesis by regulating cell fate commitment and the HPG axis. These results may help to unravel general molecular mechanisms behind maturation.

Health after pathogen contact varies among individuals because of differences in pathogen load (which is limited by resistance) and disease severity in response to pathogen load (which is limited by tolerance). To understand pathogen-induced host evolution, it is critical to know not only the relative contributions of nongenetic and genetic variation to resistance and tolerance but also how they change environmentally. We quantified nongenetic and genetic variation in parasite load and the associated temperature-dependent disease among trout siblings from two rivers. We detected a genetic variance for parasite load 6.6 times as large in the colder river. By contrast, genetic variance for disease traits tended to be larger in the warmer river, where the disease was manifested more severely. The relationships between disease severity and pathogen load (tolerance) exhibited plateaus at low pathogen load and stronger steepening slopes at high pathogen load in the warmer river. Our study demonstrates the environmental influence on disease severity, nongenetic and genetic variance for health-damage-limiting host abilities, and the shape of tolerance curves. Environmental variability is predicted to govern the presence and intensity of selection, change the relative contributions of nongenetic and genetic variance, and therefore hamper evolution toward more resistant and tolerant hosts.

Telomeres protect eukaryotic chromosomes; variation in telomere length has been linked (primarily in homoeothermic animals) to variation in stress, cellular ageing, and disease risk. Moreover, telomeres have been suggested to function as molecular markers for quantifying past environmental stress, but studies in wild animals remain rare. Environmental stress, such as extreme environmental temperatures in poikilothermic animals, may result in oxidative stress that accelerates telomere attrition. However, growth, which may depend on temperature, can also contribute to telomere attrition. To test for associations between multi-tissue telomere length and past water temperature while accounting for the previous individual growth, we used quantitative PCR to analyse samples from 112 young-of-the-year brown trout from 10 natural rivers with average water-temperature differences of up to 6°C (and an absolute maximum of 23 °C). We found negative associations between relative telomere length (RTL) and both average river temperature and individual body size. We found no indication of RTL-temperature association differences among six tissues, but we did find indications for differences among the tissues for associations between RTL and body size; size trends, albeit non-significant in their differences, were strongest in muscle and weakest in fin. Although causal relationships among temperature, growth, oxidative stress, and cross-sectional telomere length remain largely unknown, our results indicate that telomere-length variation in a poikilothermic wild animal is associated with both past temperature and growth. This article is protected by copyright. All rights reserved.

The alternative respiratory chain (aRC), comprising the alternative NADH dehydrogenases (NDX) and quinone oxidases (AOX), is found in microbes, fungi and plants, where it buffers stresses arising from restrictions on electron flow in the oxidative phosphorylation system. The aRC enzymes are also found in species belonging to most metazoan phyla, including some chordates and arthropods species, although not in vertebrates or in Drosophila. We postulated that the aRC enzymes might be deployed to alleviate pathological stresses arising from mitochondrial dysfunction in a wide variety of disease states. However, before such therapies can be contemplated, it is essential to understand the effects of aRC enzymes on cell metabolism and organismal physiology. Here we report and discuss new findings that shed light on the functions of the aRC enzymes in animals, and the unexpected benefits and detriments that they confer on model organisms. In Ciona intestinalis, the aRC is induced by hypoxia and by sulfide, but is unresponsive to other environmental stressors. When expressed in Drosophila, AOX results in impaired survival under restricted nutrition, in addition to the previously reported male reproductive anomalies. In contrast, it confers cold resistance to developing and adult flies, and counteracts cell signaling defects that underlie developmental dysmorphologies. The aRC enzymes may also influence lifespan and stress resistance more generally, by eliciting or interfering with hormetic mechanisms. In sum, their judicious use may lead to major benefits in medicine, but this will require a thorough characterization of their properties and physiological effects.

The between-population genetic architecture for growth and maturation has not been examined in detail for many animal species despite its central importance in understanding hybrid fitness. We studied the genetic architecture of population divergence in: (i) maturation probabilities at the same age; (ii) size at age and growth, while accounting for maturity status and sex; and (iii) growth plasticity in response to environmental factors, using divergent wild and domesticated Atlantic salmon (Salmo salar). Our work examined two populations and their multigenerational hybrids in a common experimental arrangement in which salinity and quantity of suspended sediments were manipulated to mimic naturally occurring environmental variation. Average specific growth rates across environments differed among crosses, maturity groups, and cross-by-maturity groups, but a growth-rate reduction in the presence of suspended sediments was equal for all groups. Our results revealed both additive and nonadditive outbreeding effects for size at age and for growth rates that differed with life stage, as well as the presence of different sex- and size-specific maturation probabilities between populations. The major implication of our work is that estimates of the genetic architecture of growth and maturation can be biased if one does not simultaneously account for temporal changes in growth and for different maturation probabilities between populations. Namely, these correlated traits interact differently within each population and between sexes and among generations, due to nonadditive effects and a level of independence in the genetic control for traits. Our results emphasize the challenges to investigating and predicting phenotypic changes resulting from between-population outbreeding.

Captive-breeding programs can be implemented to preserve the genetic diversity of endangered populations such that the controlled release of captive-bred individuals into the wild may promote recovery. A common difficulty, however, is that programs are founded with limited wild broodstock, and inbreeding can become increasingly difficult to avoid with successive generations in captivity. Program managers must choose between maintaining the genetic purity of populations, at the risk of inbreeding depression, or interbreeding populations, at the risk of outbreeding depression. We evaluate these relative risks in a captive-breeding program for 3 endangered populations of Atlantic salmon (Salmo salar). In each of 2 years, we released juvenile F(1) and F(2) interpopulation hybrids, backcrosses, as well as inbred and noninbred within-population crosstypes into 9 wild streams. Juvenile size and survival was quantified in each year. Few crosstype effects were observed, but interestingly, the relative fitness consequences of inbreeding and outbreeding varied from year to year. Temporal variation in environmental quality might have driven some of these annual differences, by exacerbating the importance of maternal effects on juvenile fitness in a year of low environmental quality and by affecting the severity of inbreeding depression differently in different years. Nonetheless, inbreeding was more consistently associated with a negative effect on fitness, whereas the consequences of outbreeding were less predictable. Considering the challenges associated with a sound risk assessment in the wild and given that the effect of inbreeding on fitness is relatively predictable, we suggest that risk can be weighted more strongly in terms of the probable outcome of outbreeding. Factors such as genetic similarities between populations and the number of generations in isolation can sometimes be used to assess outbreeding risk, in lieu of experimentation.

The study of population differentiation in the context of ecological speciation is commonly assessed using populations with obvious discreteness. Fewer studies have examined diversifying populations with occasional adaptive variation and minor reproductive isolation, so factors impeding or facilitating the progress of early stage differentiation are less understood. We detected non-random genetic structuring in lake trout (Salvelinus namaycush) inhabiting a large, pristine, postglacial lake (Mistassini Lake, Canada), with up to five discernible genetic clusters having distinctions in body shape, size, colouration and head shape. However, genetic differentiation was low (FST = 0.017) and genetic clustering was largely incongruent between several population- and individual-based clustering approaches. Genotype- and phenotype-environment associations with spatial habitat, depth and fish community structure (competitors and prey) were either inconsistent or weak. Striking morphological variation was often more continuous within than among defined genetic clusters. Low genetic differentiation was a consequence of relatively high contemporary gene flow despite large effective population sizes, not migration-drift disequilibrium. Our results suggest a highly plastic propensity for occupying multiple habitat niches in lake trout and a low cost of morphological plasticity, which may constrain the speed and extent of adaptive divergence. We discuss how factors relating to niche conservatism in this species may also influence how plasticity affects adaptive divergence, even where ample ecological opportunity apparently exists.

Outbreeding between segregating populations can be important from an evolutionary, conservation and economical-agricultural perspective. Whether and how outbreeding influences maternal effects in wild populations has rarely been studied, despite both the prominent maternal influence on early offspring survival and the known presence of fitness effects resulting from outbreeding in many taxa. We studied several traits during the yolk-feeding stage in multigenerational crosses between a wild and a domesticated Atlantic salmon (Salmo salar) population up to their third-generation hybrid in a common laboratory environment. Using cross-means analysis, we inferred that maternal additive outbreeding effects underlie most offspring traits but that yolk mass also underlies maternal dominant effects. As a consequence of the interplay between additive and dominant maternally controlled traits, offspring from first-generation hybrid mothers expressed an excessive proportion of residual yolk mass, relative to total mass, at the time of first feeding. Their residual yolk mass was 23–97% greater than those of other crosses and 31% more than that predicted by a purely additive model. Offspring additive, epistatic and epistatic offspring-by-maternal outbreeding effects appeared to further modify this largely maternally controlled cross-means pattern, resulting in an increase in offspring size with the percentage of domesticated alleles. Fitness implications remain elusive because of unknown phenotype-by-environment interactions. However, these results suggest how mechanistically co-adapted genetic maternal control on early offspring development can be disrupted by the effects of combining alleles from divergent populations. Complex outbreeding effects at both the maternal and offspring levels make the prediction of hybrid phenotypes difficult.

Geographic distributions of most temperate marine fishes are affected by postglacial recolonisation events, which have left complex genetic imprints on populations of marine species. This study investigated population structure and demographic history of European sprat (Sprattus sprattus L.) by combining inference from both mtDNA and microsatellite genetic markers throughout the species' distribution. We compared effects from genetic drift and mutation for both genetic markers in shaping genetic differentiation across four transition zones. Microsatellite markers revealed significant isolation by distance and a complex population structure across the species' distribution (overall θ(ST)=0.038, P0.01). Across transition zones markers indicated larger effects of genetic drift over mutations in the northern distribution of sprat contrasting a stronger relative impact of mutation in the species' southern distribution in the Mediterranean region. These results were interpreted to reflect more recent divergence times between northern populations in accordance with previous findings. This study demonstrates the usefulness of comparing inference from different markers and estimators of divergence for phylogeographic and population genetic studies in species with weak genetic structure, as is the case in many marine species.

Captive-breeding programs can be implemented to preserve the genetic diversity of endangered populations such that the controlled release of captive-bred individuals into the wild may promote recovery. A common difficulty, however, is that programs are founded with limited wild broodstock, and inbreeding can become increasingly difficult to avoid with successive generations in captivity. Program managers must choose between maintaining the genetic purity of populations, at the risk of inbreeding depression, or interbreeding populations, at the risk of outbreeding depression. We evaluate these relative risks in a captive-breeding program for 3 endangered populations of Atlantic salmon (Salmo salar). In each of 2 years, we released juvenile F(1) and F(2) interpopulation hybrids, backcrosses, as well as inbred and noninbred within-population crosstypes into 9 wild streams. Juvenile size and survival was quantified in each year. Few crosstype effects were observed, but interestingly, the relative fitness consequences of inbreeding and outbreeding varied from year to year. Temporal variation in environmental quality might have driven some of these annual differences, by exacerbating the importance of maternal effects on juvenile fitness in a year of low environmental quality and by affecting the severity of inbreeding depression differently in different years. Nonetheless, inbreeding was more consistently associated with a negative effect on fitness, whereas the consequences of outbreeding were less predictable. Considering the challenges associated with a sound risk assessment in the wild and given that the effect of inbreeding on fitness is relatively predictable, we suggest that risk can be weighted more strongly in terms of the probable outcome of outbreeding. Factors such as genetic similarities between populations and the number of generations in isolation can sometimes be used to assess outbreeding risk, in lieu of experimentation.

Sequence variation in the mitochondrial control region was studied in the Mediterranean rainbow wrasse (Coris julis), a species with pronounced pelagic larval phase inhabiting the Mediterranean Sea and the adjacent coastal eastern Atlantic Ocean. A total of 309 specimens from 19 sampling sites were analysed with the aim of elucidating patterns of molecular variation between the Atlantic and the Mediterranean as well as within the Mediterranean Sea. Phylogeographic analyses revealed a pronounced structuring into a Mediterranean and an Atlantic group. Samples from a site at the Moroccan Mediterranean coast in the Alboran Sea showed intermediate frequencies of “Mediterranean” and “Atlantic” haplotypes. We recognised a departure from molecular neutrality and a star-like genealogy for samples from the Mediterranean Sea, which we propose to have happened due to a recent demographic expansion. The results are discussed in the light of previous studies on molecular variation in fish species between the Atlantic and the Mediterranean and within the Mediterranean.

Theory predicts that hybrid fitness should decrease as population divergence increases. This suggests that the effects of human-induced hybridization might be adequately predicted from the known divergence among parental populations. We tested this prediction by quantifying trait differentiation between multigenerational crosses of farmed Atlantic salmon (Salmo salar) and divergent wild populations from the Northwest Atlantic; the former escape repeatedly into the wild, while the latter are severely depleted. Under common environmental conditions and at the spatiotemporal scale considered (340 km, 12 000 years of divergence), substantial cross differentiation had a largely additive genetic basis at behavioral, life history, and morphological traits. Wild backcrossing did not completely restore hybrid trait distributions to presumably more optimal wild states. Consistent with theory, the degree to which hybrids deviated in absolute terms from their parental populations increased with increasing parental divergence (i.e., the collective environmental and life history differentiation, genetic divergence, and geographic distance between parents). Nevertheless, while these differences were predictable, their implications for risk assessment were not: wild populations that were equally divergent from farmed salmon in the total amount of divergence differed in the specific traits at which this divergence occurred. Combined with ecological data on the rate of farmed escapes and wild population trends, we thus suggest that the greatest utility of hybridization data for risk assessment may be through their incorporation into demographic modeling of the short- and long-term consequences to wild population persistence. In this regard, our work demonstrates that detailed hybridization data are essential to account for life-stage-specific changes in phenotype or fitness within divergent but interrelated groups of wild populations. The approach employed here will be relevant to risk assessments in a range of wild species where hybridization with domesticated relatives is a concern, especially where the conservation status of the wild species may preclude direct fitness comparisons in the wild.

We examined the genetic structure of the European sprat (Sprattus sprattus) by means of a 530-bp sequence of the mitochondrial control region from 210 fish originating from seven sampling localities of its distributional range. Phylogeographical analysis of 128 haplotypes showed a phylogenetic separation into two major clades with the Strait of Sicily acting as a barrier to gene flow between them. While no population differentiation was observed based on analysis of molecular variance and net nucleotide differences between samples of the Baltic Sea, the North Sea and the Bay of Biscay nor between the Black Sea and the Bosporus, a strong population differentiation between these samples and two samples from the Mediterranean Sea was found. Further, the biggest genetic distance was observed within the Mediterranean Sea between the populations of the Gulf of Lyon and the Adriatic Sea, indicating genetic isolation of these regions. Low genetic diversities and star-like haplotype networks of both Mediterranean Sea populations point towards recent demographic expansion scenarios after low population size, which is further supported by negative F(S) values and unimodal mismatch distributions with a low mean. Along the northeast Atlantic coast, a northwards range expansion of a large and stable population can be assumed. The history of a diverse but differentiated Black Sea population remains unknown due to uncertainties in the palaeo-oceanography of this sea. Our genetic data did not confirm the presently used classification into subspecies but are only preliminary in the absence of nuclear genetic analyses.

Whether and how habitat fragmentation and population size jointly affect adaptive genetic variation and adaptive population differentiation are largely unexplored. Owing to pronounced genetic drift, small, fragmented populations are thought to exhibit reduced adaptive genetic variation relative to large populations. Yet fragmentation is known to increase variability within and among habitats as population size decreases. Such variability might instead favour the maintenance of adaptive polymorphisms and/or generate more variability in adaptive differentiation at smaller population size. We investigated these alternative hypotheses by analysing coding-gene, single-nucleotide polymorphisms associated with different biological functions in fragmented brook trout populations of variable sizes. Putative adaptive differentiation was greater between small and large populations or among small populations than among large populations. These trends were stronger for genetic population size measures than demographic ones and were present despite pronounced drift in small populations. Our results suggest that fragmentation affects natural selection and that the changes elicited in the adaptive genetic composition and differentiation of fragmented populations vary with population size. By generating more variable evolutionary responses, the alteration of selective pressures during habitat fragmentation may affect future population persistence independently of, and perhaps long before, the effects of demographic and genetic stochasticity are manifest.

Energy allocation in juvenile fish can have important implications for future life-history progression. Inherited and environmental factors determine when and where individuals allocate energy, and timely and sufficient energy reserves are crucial for reaching key life stages involved in the timing of maturation and sea migration. In Atlantic salmon, lipid reserves are predominantly found in the viscera and myosepta in the muscle and have been shown to play a key role in determining the timing of maturity. This life-history trait is tightly linked to fitness in many species and can be different between males and females, however, the details of relative energy allocation in juveniles of different sexes is not well understood. Therefore, the aim of this study was to investigate the effects of sex, genetics and environment during juvenile development of salmon on the amount and composition of their lipid reserves. To do so, juvenile salmon were fed one of two different lipid food contents during their first summer and autumn under common-garden conditions. Muscle lipid composition and concentrations were determined by thin layer chromatography. The muscle lipid class concentrations covaried negatively with body length and males showed higher concentrations than females for phosphatidylcholine, cholesterol, sphingomyelin, and triacylglycerol. This sex-specific difference in major lipid classes presents a new scope for understanding the regulation of lipids during juvenile development and gives direction for understanding how lipids may interact and influence major life-history traits in Atlantic salmon.