Thehigh growth(hg) Locus Maps to a Deletion in Mouse Chromosome 10

doi:10.1006/geno.1996.0504

Genomics

Volume 36, Issue 3, 15 September 1996, Pages 546-549

https://doi.org/10.1006/geno.1996.0504 Get rights and content

Abstract

Thehigh growth(hg) locus in mice produces a 30–50% increase in weight gain of homozygous individuals. Here we report that the microsatellite markerD10Mit69is deleted in high growth mice. The deletion ofD10Mit69was uncovered in a screen of the high growth mouse and its progenitor strains for available markers in thehgregion. We demonstrate thathgandD10Mit69cosegregate in a cross of congenic strains C57BL/6J-hghg× C57BL/6J. These results suggest that deletion of a region aroundD10Mit69is responsible for the high growth effect. MarkerD10Mit69will be utilized as an entry point to physical cloning of thehg-containing segment. A dense map of markers aroundhgconstructed here should allow identification of markers in homologous regions in domestic animals and humans, which may be utilized to assess the role of thehglocus in these other species.

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Cited by (18)

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2000, Domestic Animal Endocrinology
Growth process of animals is regulated by a multitude of physiological pathways among which components of the somatotropic axis play a key role. A number of severe, simply inherited growth disturbances have been identified in humans, laboratory and farm animals. These disorders are controlled by defective alleles at major loci referring to hormones or hormone receptors, e.g. growth hormone receptor for the recessive sex-linked dwarfism (dw) in chickens and the recessive autosomal Laron-type dwarfism in man, and growth hormone releasing hormone receptor for the recessive “little” mutation (lit) in mice. Apart from these particular cases, growth rate is a quantitative polygenic trait which has a moderate heritability (close to 0.30) and is influenced by prenatal and postnatal maternal effects. Increase in the average coefficient of inbreeding in a population is also known to result in lower growth rate. Divergent selection experiments have shown that upward or downward selection on growth is effective, sometimes with asymmetrical responses, but patterns of changes in underlying physiological traits appear to differ among experiments.
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IGFs are important positive modulators of overall body and muscle growth in different species. Genetic variation in IGF-I gene expression exists as shown by the possibility of genetic selection for high or low circulating IGF-I concentrations in mice and the associated variations in growth potential. Targeted over-expression of IGF-I in transgenic mice results in muscle hypertrophy, but it is yet unknown whether genetic variability in muscle IGF-I gene expression exists. Much less data are available in birds. This review is focussed on the potential role of IGFs on chicken muscle development. Apart from the absence of a type 2 IGF receptor (IGF-II receptor), the general characteristics of the chicken IGF system seem to be similar to mammalian species. In different genetic models with altered growth rates or body composition, differences in the IGF system are observed suggesting its importance in regulating body growth in those species. The components for a paracrine action of IGF are also present in chicken muscle but it has not yet been demonstrated if they contribute to differences in muscle development.
A 500-kb YAC and BAC contig encompassing the high-growth deletion in mouse chromosome 10 and identification of the murine Raidd/Cradd gene in the candidate region
1998, Genomics
The mousehigh growth(hg) gene was identified in a selection experiment for rapid growth. It produces a 30–50% increase in weight gain of homozygous individuals without resulting in obesity. Recently,hgwas mapped to a deletion around markerD10Mit69.Here we report a map of yeast artificial chromosome and bacterial artificial chromosome clones spanning the entire region deleted in high-growth mice. The size of the deletion estimated from the clone lengths is approximately 500 kb. Using exon trapping, the murineRaidd/Craddgene was identified in thehgregion, and its cDNA sequence and expression pattern were determined. The human RAIDD/CRADD was mapped using radiation hybrid mapping to human chromosome 12, 2.9 cR distal to marker AFMB311WC5. The identifiedRaidd/Craddgene, which is deleted in high-growth mice, presents a potential candidate forhg.
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¹: Present address: Roslin Institute (Edinburgh), Division of Molecular Biology, Roslin EH25 9PS, United Kingdom.

²: To whom correspondence should be addressed. Telephone: (916) 752-6786. Fax: (916) 752-0175. E-mail: [email protected].

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Short CommunicationThehigh growth(hg) Locus Maps to a Deletion in Mouse Chromosome 10

Abstract

Short Communication
Thehigh growth(hg) Locus Maps to a Deletion in Mouse Chromosome 10