3 Populations and Pathways
95
• cis regulation: the linkage between heterozygosity at the candidate locus and
expression level should remain unchanged.
• trans regulation: recombination between the candidate locus and trans-acting
elements (i.e. a possible cause of epistasis) should eliminate or reduce overexpression in heterozygotes.
The likely importance of trans-acting elements in regulating many non-additive
patterns of gene expression would suggest that growth heterosis may largely result
from epistatic gene interactions. Besides the importance of this study in identifying
the main causes of hybrid vigour, further analysis suggested ≈350 candidate genes
were involved in growth heterosis and exhibited concordant non-additive expression in reciprocal hybrids. This represented only ≈1.5% of the total transcripts and
approximately matched the number of genes that regulate the physiology of life span
and lipid accumulation in C. elegans (Ashrafi et al. 2003). This is clearly only one
example of the investigation of heterosis, but given the success using new technologies, additional studies, in different organisms, are certain to follow, particularly
driven by the commercial interests of the aquaculture industry.
3.3.4 Gene Polymorphism and Population Adaptation
Sequencing the same gene many times in different individuals of the same species
does not correspond to the traditional view of population genetics (Ellegren and
Sheldon (2008) and Stinchcombe and Hoekstra (2008)). Indeed it would more generally be viewed as phylogeny or as a sort of bar-coding. However, nucleotide
changes in a particular gene (polymorphisms) can explain within- and amongpopulation differences related to the observed phenotypic scope (or within and
among species differences) (reviewed in Yang and Bielawski 2002).
For example, Streelman and Kocher (2002) reported a microsatellite polymorphism in the proximal promoter of the prolactin (prl) gene in the Nile tilapia
(Oreochromis niloticus). They demonstrated that distinct microsatellite genotypes
were associated with differences in PRL expression and that the growth performance of tilapia challenged by various salinities was, at least partly, reflected by
changes in growth patterns (assessed by body mass) across a salinity gradient. Also
in the sea bass, prolactin gene expression was demonstrated to differ among habitats
(Boutet et al. 2007). This suggests that that other regulatory mechanisms (potentially due to polymorphisms) at this locus could be involved in more generalised
adaptations rather than purely salinity as described in the case of tilapia. Similarly,
Almuly et al. (2008) also reported results that described the role of polymorphisms
and minisatellites in the regulation of the growth hormone gene (GH). GH genotypes of one of these loci in seabream (Sparus aurata) have been shown to correlate
with populations inhabiting distinct environments (open sea vs lagoon) (L. Chaoui
and F. Bonhomme, pers. obs.). Finally, using the basis of a pedigree-based analysis, Tao and Boulding (2003) reported that a SNP marker located in one intron of
95
• cis regulation: the linkage between heterozygosity at the candidate locus and
expression level should remain unchanged.
• trans regulation: recombination between the candidate locus and trans-acting
elements (i.e. a possible cause of epistasis) should eliminate or reduce overexpression in heterozygotes.
The likely importance of trans-acting elements in regulating many non-additive
patterns of gene expression would suggest that growth heterosis may largely result
from epistatic gene interactions. Besides the importance of this study in identifying
the main causes of hybrid vigour, further analysis suggested ≈350 candidate genes
were involved in growth heterosis and exhibited concordant non-additive expression in reciprocal hybrids. This represented only ≈1.5% of the total transcripts and
approximately matched the number of genes that regulate the physiology of life span
and lipid accumulation in C. elegans (Ashrafi et al. 2003). This is clearly only one
example of the investigation of heterosis, but given the success using new technologies, additional studies, in different organisms, are certain to follow, particularly
driven by the commercial interests of the aquaculture industry.
3.3.4 Gene Polymorphism and Population Adaptation
Sequencing the same gene many times in different individuals of the same species
does not correspond to the traditional view of population genetics (Ellegren and
Sheldon (2008) and Stinchcombe and Hoekstra (2008)). Indeed it would more generally be viewed as phylogeny or as a sort of bar-coding. However, nucleotide
changes in a particular gene (polymorphisms) can explain within- and amongpopulation differences related to the observed phenotypic scope (or within and
among species differences) (reviewed in Yang and Bielawski 2002).
For example, Streelman and Kocher (2002) reported a microsatellite polymorphism in the proximal promoter of the prolactin (prl) gene in the Nile tilapia
(Oreochromis niloticus). They demonstrated that distinct microsatellite genotypes
were associated with differences in PRL expression and that the growth performance of tilapia challenged by various salinities was, at least partly, reflected by
changes in growth patterns (assessed by body mass) across a salinity gradient. Also
in the sea bass, prolactin gene expression was demonstrated to differ among habitats
(Boutet et al. 2007). This suggests that that other regulatory mechanisms (potentially due to polymorphisms) at this locus could be involved in more generalised
adaptations rather than purely salinity as described in the case of tilapia. Similarly,
Almuly et al. (2008) also reported results that described the role of polymorphisms
and minisatellites in the regulation of the growth hormone gene (GH). GH genotypes of one of these loci in seabream (Sparus aurata) have been shown to correlate
with populations inhabiting distinct environments (open sea vs lagoon) (L. Chaoui
and F. Bonhomme, pers. obs.). Finally, using the basis of a pedigree-based analysis, Tao and Boulding (2003) reported that a SNP marker located in one intron of