136
T.F. Cross et al.
A more recently demonstrated indirect genetic effect appears to be mediated by
disease organisms, which can be transferred from reared to wild fish species. This
effect is observed in the Major Histocompatibility Complex (MHC) genes of wild
Salmo salar and Salmo trutta putatively challenged by diseases carried by reared
salmon (Box 4.2). Because of high-density rearing conditions, reared fish and
invertebrates often have much higher disease challenges and/or loads than their
wild conspecifics or congenerics, but these diseases can be controlled in captivity
using anti-bacterial compounds or vaccination. However, when such individuals
escape or are introduced into the wild, they may act as highly virulent carriers and
cause outbreaks of the disease in wild fish or invertebrates, with subsequent demonstrateable effects at MHC genes (at least in salmonid fishes). The example
described in Box 4.2 constitutes another potentially damaging effect of aquaculture,
which should be investigated in other cultured species.
Box 4.2 MHC genes in interaction studies between reared strains and wild
populations of teleost fish
In teleost fish, MHC Class I and II loci are not physically linked (Sato et al.
2000) and thus can evolve independently (hence termed MH). Members of the
genus Salmo are found to possess single classical Class I (UBA) and II (DAA/
DAB) loci (Shum et al. 2001; Stet et al. 2002; Aoyagi et al. 2002; Grimholt
et al. 2002; Miller et al. 2006) greatly simplifying salmonid MHC studies.
Pathogen-driven balancing selection, with overdominance or heterozygote
advantage, is believed to underpin high levels of polymorphism observed in
MHC loci (Wegner et al. 2003). Challenge experiments in which domesticated
salmonid stocks were exposed to a number of pathogens (Langefors et al.
1998; Lohm et al. 2002; Arkush et al. 2002; Grimholt et al. 2003) uncovered
differential survival rates mediated primarily by MH heterozygosity and/or
overdominant selection.
Grimholt et al. (2003) deliberately infected two distinct groups of post-smolt
S. salar with furunculosis bacteria and ISAV virus, respectively. MH genotyping
of mortalities and survivors demonstrated genotypic and allele effects, at class I
for ISAV challenge and at class II for furunculosis. Mass screening was
facilitated by the use of polymorphic VNTRs located in the 3’UTRs of the SasaUBA and Sasa-DAA genes (Grimholt et al. 2002; Stet et al. 2002), which exhibited simple linkage.
These findings led to an EU project (Salimpact) on MH genes in wild
S. salar and brown trout, Salmo trutta, populations, where diseases carried by
co-habiting, reared salmon were considered as challenge agents. Simultaneous
screening of several neutral loci, (unaffected by disease challenge), with the
MH-linked marker loci provided the opportunity to examine for selective
effects on the MH marker loci in a number of interaction situations in Ireland
T.F. Cross et al.
A more recently demonstrated indirect genetic effect appears to be mediated by
disease organisms, which can be transferred from reared to wild fish species. This
effect is observed in the Major Histocompatibility Complex (MHC) genes of wild
Salmo salar and Salmo trutta putatively challenged by diseases carried by reared
salmon (Box 4.2). Because of high-density rearing conditions, reared fish and
invertebrates often have much higher disease challenges and/or loads than their
wild conspecifics or congenerics, but these diseases can be controlled in captivity
using anti-bacterial compounds or vaccination. However, when such individuals
escape or are introduced into the wild, they may act as highly virulent carriers and
cause outbreaks of the disease in wild fish or invertebrates, with subsequent demonstrateable effects at MHC genes (at least in salmonid fishes). The example
described in Box 4.2 constitutes another potentially damaging effect of aquaculture,
which should be investigated in other cultured species.
Box 4.2 MHC genes in interaction studies between reared strains and wild
populations of teleost fish
In teleost fish, MHC Class I and II loci are not physically linked (Sato et al.
2000) and thus can evolve independently (hence termed MH). Members of the
genus Salmo are found to possess single classical Class I (UBA) and II (DAA/
DAB) loci (Shum et al. 2001; Stet et al. 2002; Aoyagi et al. 2002; Grimholt
et al. 2002; Miller et al. 2006) greatly simplifying salmonid MHC studies.
Pathogen-driven balancing selection, with overdominance or heterozygote
advantage, is believed to underpin high levels of polymorphism observed in
MHC loci (Wegner et al. 2003). Challenge experiments in which domesticated
salmonid stocks were exposed to a number of pathogens (Langefors et al.
1998; Lohm et al. 2002; Arkush et al. 2002; Grimholt et al. 2003) uncovered
differential survival rates mediated primarily by MH heterozygosity and/or
overdominant selection.
Grimholt et al. (2003) deliberately infected two distinct groups of post-smolt
S. salar with furunculosis bacteria and ISAV virus, respectively. MH genotyping
of mortalities and survivors demonstrated genotypic and allele effects, at class I
for ISAV challenge and at class II for furunculosis. Mass screening was
facilitated by the use of polymorphic VNTRs located in the 3’UTRs of the SasaUBA and Sasa-DAA genes (Grimholt et al. 2002; Stet et al. 2002), which exhibited simple linkage.
These findings led to an EU project (Salimpact) on MH genes in wild
S. salar and brown trout, Salmo trutta, populations, where diseases carried by
co-habiting, reared salmon were considered as challenge agents. Simultaneous
screening of several neutral loci, (unaffected by disease challenge), with the
MH-linked marker loci provided the opportunity to examine for selective
effects on the MH marker loci in a number of interaction situations in Ireland