Structural characterization of the mouse high growth deletion and discovery of a novel fusion transcript between suppressor of cytokine signaling-2 ( Socs-2 ) and viral encoded semaphorin receptor ( Plexin C1 )

Wong, Marisa L.; Islas‐Trejo, Alma; Medrano, Juan F.

doi:10.1016/s0378-1119(02)01052-1

Cited by 22 publications

(25 citation statements)

References 26 publications

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“…Note that the B6 hg/hg strain was isogenic to B6, except for the high-growth (hg) mutation on mouse chromosome 10 Wong et al 2002) and a stretch of AKR/J sequence around this mutation (Horvat and Medrano 1996). This cross originated 596 F 2 heterozygote mice for the hg mutation (+/hg), 262 with genotype hg/hg and 274 with genotype +/+.…”

Section: Examples From Simulated Datamentioning

confidence: 99%

Genome Scans for Transmission Ratio Distortion Regions in Mice

et al. 2012

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Transmission ratio distortion (TRD) is the departure from the expected genotypic frequencies under Mendelian inheritance. This departure can be due to multiple physiological mechanisms during gametogenesis, fertilization, fetal and embryonic development, and early neonatal life. Although a few TRD loci have been reported in mouse, inheritance patterns have never been evaluated for TRD. In this article, we developed a Bayesian binomial model accounting for additive and dominant deviation TRD mechanisms. Moreover, this model was used to perform genome-wide scans for TRD quantitative trait loci (QTL) on six F 2 mouse crosses involving between 296 and 541 mice and between 72 and 1854 genetic markers. Statistical significance of each model was checked at each genetic marker with Bayes factors. Genome scans revealed overdominance TRD QTL located in mouse chromosomes 1, 2, 12, 13, and 14 and additive TRD QTL in mouse chromosomes 2, 3, and 15, although these results did not replicate across mouse crosses. This research contributes new statistical tools for the analysis of specific genetic patterns involved in TRD in F 2 populations, our results suggesting a relevant incidence of TRD phenomena in mouse with important implications for both statistical analyses and biological research.

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Section: Examples From Simulated Datamentioning

confidence: 99%

Genome Scans for Transmission Ratio Distortion Regions in Mice

et al. 2012

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“…The hg mutation is due to a 460 kb deletion in mouse chromosome 10 that includes three known genes, Suppressor of cytokine signaling 2 (Socs-2), RIP-associated ICDH-1/ CED-3-homologous protein with a death domain (Raidd/Cradd), and Plexin C1 [7]. The HG phenotype results from the lack of expression of Socs-2 [8], which negatively regulates GH signal transduction.…”

Section: Introductionmentioning

confidence: 99%

Diet effects on female reproduction in high growth (hg/hg) mice that are deficient in the Socs-2 gene

et al. 2004

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-The detrimental effect of larger body size on reproductive performance has been well documented in mouse models of overgrowth, such as Growth Hormone (GH) transgenics. This study describes the reproductive performance of the High Growth (HG) mouse model of overgrowth. The HG mouse model exhibits overgrowth due to a partially recessive autosomal mutation that increases growth rate and mature body size. The HG phenotype results from the lack of expression of Socs-2, which negatively regulates GH signaling. C57BL/6J (C57) and congenic C57BL/6J-hg/hg (HG) female mice were fed four diets differing in protein and energy content, starting at 8 weeks of age. A complete reproductive cycle from mating to weaning was evaluated. HG mice were 40% larger than C57 and had a higher feed intake throughout the experiment. Significant genotype × diet interactions were detected for growth, body composition and reproductive traits. HG females showed poor reproductive performance compared to controls as demonstrated by their lower fertility during mating, which was not overcome by changes in the diet. No differences were detected in litter size, but HG animals exhibited a longer gestation length and heavier pup weaning weights compared to controls. Reproductive impairment in HG seems to be the consequence of the lack of Socs-2 independent of the effects of increased body size on reproduction. genetics / overgrowth / genotype-nutrition interaction / reproduction

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“…The HG strain lacks expression of the Socs2 gene (a negative inhibitor of growth hormone signaling) due to a spontaneously arising 500-kbp deletion on mouse chromosome (MMU) 10 Wong et al 2002). In the above cross, MMU2 and MMU11 harbored QTL with significant affects on weight gain (Wg2 on MMU2 and Wg4 on MMU11), carcass ash (Cara1 on MMU2 and Cara2 on MMU11), and carcass protein (Carp1 on MMU2 and Carp2 on MMU11).…”

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Fine Mapping Reveals Sex Bias in Quantitative Trait Loci Affecting Growth, Skeletal Size and Obesity-Related Traits on Mouse Chromosomes 2 and 11

Farber¹,

Medrano

2007

Genetics

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Previous speed congenic analysis has suggested that the expression of growth and obesity quantitative trait loci (QTL) on distal mouse chromosomes (MMU) 2 and 11, segregating between the CAST/EiJ (CAST) and C57BL/6J-hg/hg (HG) strains, is dependent on sex. To confirm, fine map, and further evaluate QTL 3 sex interactions, we constructed congenic by recipient F 2 crosses for the HG.CAST-(D2Mit329-D2Mit457)N(6) (HG2D) and HG.CAST-(D11Mit260-D11Mit255)N(6) (HG11) congenic strains. Over 700 F 2 mice were densely genotyped and phenotyped for a panel of 40 body and organ weight, skeletal length, and obesity-related traits at 9 weeks of age. Linkage analysis revealed 20 QTL affecting a representative subset of phenotypes in HG2DF 2 and HG11F 2 mice. The effect of sex was quantified by comparing two linear models: the first model included sex as an additive covariate and the second incorporated sex as an additive and an interactive covariate. Of the 20 QTL, 8 were sex biased, sex specific, or sex antagonistic. Most traits were regulated by single QTL; however, two closely linked loci were identified for five traits in HG2DF 2 mice. Additionally, the confidence intervals for most QTL were significantly reduced relative to the original mapping results, setting the stage for quantitative trait gene (QTG) discovery. These results highlight the importance of assessing the contribution of sex in complex trait analyses.

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Structural characterization of the mouse high growth deletion and discovery of a novel fusion transcript between suppressor of cytokine signaling-2 ( Socs-2 ) and viral encoded semaphorin receptor ( Plexin C1 )

Cited by 22 publications

References 26 publications

Genome Scans for Transmission Ratio Distortion Regions in Mice

Genome Scans for Transmission Ratio Distortion Regions in Mice

Diet effects on female reproduction in high growth (hg/hg) mice that are deficient in the Socs-2 gene

Fine Mapping Reveals Sex Bias in Quantitative Trait Loci Affecting Growth, Skeletal Size and Obesity-Related Traits on Mouse Chromosomes 2 and 11

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