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      The influence of gene-environment interactions on GHR and IGF-1 expression and their association with growth in brook charr, Salvelinus fontinalis (Mitchill)

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      1 , , 2 , 3 , 1
      BMC Genetics
      BioMed Central

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          Abstract

          Background

          Quantitative reaction norm theory proposes that genotype-by-environment interaction (GxE) results from inter-individual differences of expression in adaptive suites of genes in distinct environments. However, environmental norms for actual gene suites are poorly documented. In this study, we investigated the effects of GxE interactions on levels of gene transcription and growth by documenting the impact of rearing environment (freshwater vs. saltwater), sex and genotypic (low vs. high estimated breeding value EBV) effects on the transcription level of insulin-like growth factor (IGF-1) and growth hormone receptor (GHR) in brook charr ( Salvelinus fontinalis).

          Results

          Males grew faster than females (μ = 1.20 ± 0.07 g·d -1, μ = 1.46 ± 0.06 g·d -1) and high-EBV fish faster than low-EBV fish (μ LOW = 0.97 ± 0.05 g·d -1, μ HIGH = 1.58 ± 0.07 g·d -1; p < 0.05). However, growth was markedly lower in saltwater-reared fish than freshwater sibs (μ FW = 1.52 ± 0.07 g·d -1, μ SW = 1.15 ± 0.06 g·d -1), yet GHR mRNA transcription level was significantly higher in saltwater than in freshwater (μ SW = 0.85 ± 0.05, μ FW = 0.61 ± 0.05). The ratio of actual growth to units in assayed mRNA ('individual transcript efficiency', iTE; g·d -1·u -1) also differed among EBV groups (μ LOW = 2.0 ± 0.24 g·d -1·u -1; μ HIGH = 3.7 ± 0.24 g·d -1·u -1) and environments (μ SW = 2.0 ± 0.25 g·d -1·u -1; μ FW = 3.7 ± 0.25 g·d -1·u -1) for GHR. Males had a lower iTE for GHR than females (μ = 2.4 ± 0.29 g·d -1·u -1; μ = 3.1 ± 0.23 g·d -1·u -1). There was no difference in IGF-1 transcription level between environments (p > 0.7) or EBV groups (p > 0.15) but the level of IGF-1 was four times higher in males than females (μ = 2.4 ± 0.11, μ = 0.58 ± 0.09; p < 0.0001). We detected significant sexual differences in iTE (μ = 1.3 ± 0.59 g·d -1·u -1; μ = 3.9 ± 0.47 g·d -1·u -1), salinities (μ SW = 2.3 ± 0.52 g·d -1·u -1; μ FW = 3.7 ± 0.53 g·d -1·u -1) and EBV-groups (μ LOW = 2.4 ± 0.49 g·d -1·u -1; μ HIGH = 3.8 ± 0.49 g·d -1·u -1). Interaction between EBV-group and environment was detected for both GHR (p = 0.027) and IGF-1 (p = 0.019), and for iTE in the two genes (p < 0.0001; p < 0.05, respectively), where increased divergence in levels of GHR and IGF-1 transcription occurred among EBV-groups in the saltwater environment.

          Conclusion

          Our results show that both environment and sex have major impacts on the expression of mRNA for two key genes involved in the physiological pathway for growth. We also demonstrate for the first time, at least in fish, genotype-by-environment interaction at the level of individual gene transcription. This work contributes significantly to ongoing efforts towards documenting environmentally and sexually induced variance of gene activity and understanding the resulting phenotypes.

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          Estimating genetic parameters in natural populations using the "animal model".

          Estimating the genetic basis of quantitative traits can be tricky for wild populations in natural environments, as environmental variation frequently obscures the underlying evolutionary patterns. I review the recent application of restricted maximum-likelihood "animal models" to multigenerational data from natural populations, and show how the estimation of variance components and prediction of breeding values using these methods offer a powerful means of tackling the potentially confounding effects of environmental variation, as well as generating a wealth of new areas of investigation.
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            Role of insulin-like growth factors in embryonic and postnatal growth.

            A developmental analysis of growth kinetics in mouse embryos carrying null mutations of the genes encoding insulin-like growth factor I (IGF-I), IGF-II, and the type 1 IGF receptor (IGF1R), alone or in combination, defined the onset of mutational effects leading to growth deficiency and indicated that between embryonic days 11.0 and 12.5, IGF1R serves only the in vivo mitogenic signaling of IGF-II. From E13.5 onward, IGF1R interacts with both IGF-I and IGF-II, while IGF-II recognizes an additional unknown receptor (XR). In contrast with the embryo proper, placental growth is served exclusively by an IGF-II-XR interaction. Additional genetic data suggested that the type 2IGF/mannose 6-phosphate receptor is an unlikely candidate for XR. Postnatal growth curves indicated that surviving Igf-1(-/-) mutants, which are infertile and exhibit delayed bone development, continue to grow with a retarded rate after birth in comparison with wild-type littermates and become 30% of normal weight as adults.
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              Evolutionary Quantitative Genetics

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                Author and article information

                Journal
                BMC Genet
                BMC Genetics
                BioMed Central
                1471-2156
                2007
                21 December 2007
                : 8
                : 87
                Affiliations
                [1 ]Département de biologie, Université Laval, Québec, Québec, Canada
                [2 ]Department of Biological Sciences, University of Southern California, 3616 Trousdale Pkwy, Los Angeles, CA, USA
                [3 ]Département de biologie et de chimie, UQAR, Rimouski, QC, Canada
                Article
                1471-2156-8-87
                10.1186/1471-2156-8-87
                2257973
                18154679
                7da77a91-5da3-4a47-a99b-890b1f50e1b3
                Copyright © 2007 Côté et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 July 2007
                : 21 December 2007
                Categories
                Research Article

                Genetics
                Genetics

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