A deletion in the bovine myostatin gene causes the double–muscled phenotype in cattle View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-09

AUTHORS

Luc Grobet, Luis José Royo Martin, Dominique Poncelet, Dimitri Pirottin, Benoit Brouwers, Juliette Riquet, Andreina Schoeberlein, Susana Dunner, François Ménissier, Julio Massabanda, Ruedi Fries, Roger Hanset, Michel Georges

ABSTRACT

An exceptional muscle development commonly referred to as ‘double-muscled’ (Fig. 1) has been seen in several cattle breeds and has attracted considerable attention from beef producers. Double-muscled animals are characterized by an increase in muscle mass of about 20%, due to general skeletal-muscle hyperplasia—that is, an increase in the number of muscle fibers rather than in their individual diameter1. Although the hereditary nature of the double-muscled condition was recognized early on, the precise mode of inheritance has remained controversial; monogenic (dominant and recessive), oligogenic and polygenic models have been proposed2. In the Belgian Blue cattle breed (BBCB)4, segregation analysis performed both in experimental crosses3 and in the outbred population suggested an autosomal recessive inheritance. This was confirmed when the muscular hypertrophy (mh) locus was mapped 3.1 cM from microsatellite TGLA44 on the centromeric end of bovine chromosome 2 (ref. 5). We used a positional candidate approach to demonstrate that a mutation in bovine MSTN, which encodes myostatin, a member of the TGFβ superfamily, is responsible for the double-muscled phenotype. We report an 11-bp deletion in the coding sequence for the bioactive carboxy-termihal domain of the protein causing the muscular hypertrophy observed in Belgian Blue cattle. More... »

PAGES

71-74

Journal

TITLE

Nature Genetics

ISSUE

1

VOLUME

17

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng0997-71

    DOI

    http://dx.doi.org/10.1038/ng0997-71

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1013716618

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9288100


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