Functional implication of an Arg307Gly substitution in corticosteroid-binding globulin, a candidate gene for a quantitative trait locus associated with cortisol variability and obesity in pig.

V. Guyonnet-Duperat
Genetics. 2006-05-15; 173(4): 2143-2149
DOI: 10.1534/genetics.105.053983

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1. Genetics. 2006 Aug;173(4):2143-9. Epub 2006 May 15.

Functional implication of an Arg307Gly substitution in corticosteroid-binding
globulin, a candidate gene for a quantitative trait locus associated with
cortisol variability and obesity in pig.

Guyonnet-Dupérat V(1), Geverink N, Plastow GS, Evans G, Ousova O, Croisetière C,
Foury A, Richard E, Mormède P, Moisan MP.

Author information:
(1)Laboratoire de Neurogénétique et Stress, INRA UMR1243-Université Victor
Ségalen Bordeaux, France.

We previously reported that corticosteroid-binding globulin gene (Cbg) may be the
causal gene of a quantitative trait locus associated with cortisol levels, fat
deposition, and muscle content in a pig intercross. Sequence analysis of parental
animals allowed us to identify four amino-acid substitutions. Here we have
examined if any of these single amino acid substitutions could be responsible for
the difference in CBG binding and affinity for cortisol between the parental
breeds, using in vitro assays of Cbg variants after transfection of mammalian
cells. Additionally, the Cbg coding region was analyzed in samples from a
synthetic pig line to study association between polymorphism and CBG biochemical
properties, carcass composition, and meat quality. Both in vitro transfection
assays and the association studies suggest a role of the Arg307Gly mutation in
increasing CBG capacity (by >70%) and decreasing CBG affinity for cortisol (by
30%). The Ile265Val substitution may also have an effect on decreasing CBG
affinity for cortisol by 25%. The mutations Ser15Ile and Thr257Met do not seem to
have an effect on CBG parameters. The Arg307Gly substitution was the only
mutation associated with a parameter of meat quality and no mutation was linked
to carcass composition.

DOI: 10.1534/genetics.105.053983
PMCID: PMC1569726
PMID: 16702435 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus