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Marker-assisted introgression of the Compact mutant myostatin allele MstnCmpt-dl1Abc into a mouse line with extreme growth effects on body composition and muscularity

Published online by Cambridge University Press:  14 January 2005

LUTZ BÜNGER
Affiliation:
Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK Current address: Scottish Agricultural College, SLS, GGS, Sir Stephen Watson Building, Bush Estate, Penicuik, Midlothian, EH26 0PH, UK.
GERHARD OTT
Affiliation:
Fachhochschule Lippe – University of Applied Sciences, Liebigstrasse 87, 32657 Lemgo, Germany
LÁSZLÓ VARGA
Affiliation:
Agricultural Biotechnology Center, PO Box 411, H-2101 Gödöllö, Hungary
WERNER SCHLOTE
Affiliation:
Humboldt-Universität zu Berlin, Institut für Nutztierwissenschaften, Landwirtschaftlich-Gärtnerische Fakultät, Unter den Linden 6, D-10099 Berlin, Germany
CHARLOTTE REHFELDT
Affiliation:
Research Institute for Biology of Farm Animals, Department of Muscle Biology and Growth, Wilhelm-Stahl-Allee 2, D-18196 Dummerstorf, Germany
ULLA RENNE
Affiliation:
Research Institute for Biology of Farm Animals, Department of Muscle Biology and Growth, Wilhelm-Stahl-Allee 2, D-18196 Dummerstorf, Germany
JOHN L. WILLIAMS
Affiliation:
Roslin Institute (Edinburgh), Roslin, Midlothian, EH25 9PS, UK
WILLIAM G. HILL
Affiliation:
Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK
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Abstract

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Myostatin is a negative regulator of muscle growth and mutations in its gene lead to muscular hypertrophy and reduced fat. In cattle, this is seen in ‘double muscled’ breeds. We have used marker-assisted introgression to introduce a murine myostatin mutation, MstnCmpt-dl1Abc [Compact (C)], into an inbred line of mice (DUHi) that had been selected on body weight and had exceptional growth. Compared with homozygous wild-type mice, homozygous (C/C) mice of this line were ~4–5% lighter, had ~7–8% shorter tails, substantially increased muscle weights (e.g. quadriceps muscle in males was 59% heavier) and an increased ‘dressing percentage’ (~49% vs 39%), an indicator of overall muscularity. The weights of several organs (e.g. liver, kidney, heart and digestive tract) were significantly reduced, by 12–20%. Myostatin deficiency also resulted in drastic reductions of total body fat and of various fat depots, total body fat proportion falling from ~17·5% in wild-type animals of both sexes to 9·5% and 11·6% in homozygous (C/C) females and males, respectively. Males with a deficiency in myostatin had higher gains in muscle traits than females. Additionally, there was a strong distortion of the segregation ratio on the DUHi background. Of 838 genotyped pups from inter se matings 29%, 63% and 8% were homozygous wild type (+/+), heterozygous (C/+) and homozygous (C/C), respectively, showing that MstnCmpt-dl1Abc has lower fitness on this background. This line, when congenic, will be a useful resource in gene expression studies and for finding modifying genes.

Type
Research Article
Copyright
© 2004 Cambridge University Press