Mapping modifiers affecting muscularity of the myostatin mutant (Mstn Cmpt-dl1Abc) compact mouse

László Varga, Géza Müller, Gyula Szabó, Orsolya Pinke, Edit Korom, Balázs Kovács, László Patthy, Morris Soller

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

The hypermuscular Compact phenotype was first noted in a line of mice selected for high body weight and protein content. A new line, based on mice showing the Compact phenotype, was formed and selected for maximum expression of the Compact phenotype. Previously we mapped and identified a 12-bp deletion in the myostatin gene, denoted MstnCmpt-dl1Abc, which can be considered as a major gene responsible for the hypermuscular phenotype. Genetic analysis revealed that full expression of the hypermuscular phenotype requires the action of modifier loci in addition to MstnCmpt-dl1Abc. To map these modifier loci, an interspecific F2 population was generated between Comp9, an inbred line homozygous for MstnCmpt-dl1Abc, and CAST/Ei, an inbred line generated from Mus musculus castaneus. Selective DNA pooling and genotyping, separately by gender, was carried out within a subpopulation of the F2 consisting of individuals homozygous for MstnCmpt-dl1Abc. Significant association with hypermuscularity at a false discovery rate (FDR) of 0.05 was found for markers on chromosomes 3, 5, 7, 11, 16, and X. In all cases, the marker allele derived from the Comp9 parent showed a higher frequency in the hypermuscular group and the CAST/Ei allele in the normal group. The modifier loci apparently exerted their effects on muscularity only in the presence of MstnCmpt-dl1Abc.

Original languageEnglish
Pages (from-to)257-267
Number of pages11
JournalGenetics
Volume165
Issue number1
Publication statusPublished - Sep 1 2003

ASJC Scopus subject areas

  • Genetics

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    Varga, L., Müller, G., Szabó, G., Pinke, O., Korom, E., Kovács, B., Patthy, L., & Soller, M. (2003). Mapping modifiers affecting muscularity of the myostatin mutant (Mstn Cmpt-dl1Abc) compact mouse. Genetics, 165(1), 257-267.