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The IGF2-intron3-G3072A substitution explains a major imprinted QTL effect on backfat thickness in a Meishan×European white pig intercross

Published online by Cambridge University Press:  26 November 2004

BART J. JUNGERIUS ,
ANNE-SOPHIE VAN LAERE ,
MARINUS F. W. TE PAS ,
BERNARD A. VAN OOST ,
LEIF ANDERSSON  and
MARTIEN A. M. GROENEN
BART J. JUNGERIUS
Affiliation:
Department of Animal Breeding and Genetics, Wageningen University, P.O. Box 40, 6700 AH Wageningen, The Netherlands
ANNE-SOPHIE VAN LAERE
Affiliation:
Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Sweden
MARINUS F. W. TE PAS
Affiliation:
Animal Sciences Group, Wageningen University and Research Centre, Lelystad, The Netherlands
BERNARD A. VAN OOST
Affiliation:
Department of Laboratory Animal Sciences, Utrecht University, Utrecht, The Netherlands
LEIF ANDERSSON
Affiliation:
Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Sweden Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden
MARTIEN A. M. GROENEN
Affiliation:
Department of Animal Breeding and Genetics, Wageningen University, P.O. Box 40, 6700 AH Wageningen, The Netherlands

Abstract

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A paternally expressed QTL for muscle growth and backfat thickness (BFT) has previously been identified near the IGF2 locus on the distal tip of pig chromosome 2 (SSC2p) in three experimental F2 populations. Recently, a mutation in a regulatory element of the IGF2 gene was identified as the quantitative trait nucleotide (QTN) underlying the major QTL effect on muscle growth and BFT in crosses between Large White and Wild Boar or Pietrain. This study demonstrates that the IGF2 mutation also controls the paternally expressed QTL for backfat thickness in a cross between Meishan and European Whites. In addition, a comparison of QTL of backfat thickness measured by Hennessy grading probe (HGP) and by ultrasound measurement (USM) was made. In the USM analyses, the IFG2 mutation explains the entire QTL effect on SSC2p, whereas in the HGP analysis the presence of a second minor QTL can not be excluded. Finally, this study shows that this particular IGF2 mutation does not cause the paternally expressed QTL for teat number mapping to the same region of SSC2p as the BFT QTL.

Type
Research Article
Information
Genetics Research , Volume 84 , Issue 2 , October 2004 , pp. 95 - 101
Copyright
© 2004 Cambridge University Press