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Mutation in bone morphogenetic protein receptor-IB is associated with increased ovulation rate in Booroola Mérino
1Institut National de la Recherche Agronomique, Laboratoire de Génétique Cellulaire, BP, 27, 31326 Castanet-Tolosan, France. mulsant@toulouse.inra.fr
Summary
The FecB(B) allele in Booroola sheep enhances ovulation and litter size by altering the bone morphogenetic protein receptor IB (BMPR-IB) gene. This genetic change affects ovarian cell function, leading to increased fertility.
Area of Science:
- Genetics
- Reproductive Biology
- Animal Science
Background:
- Booroola Merino ewes exhibit a high ovulation rate and litter size.
- This hyperprolificacy is attributed to the FecB(B) allele of the FecB gene.
Purpose of the Study:
- To genetically map the FecB locus.
- To identify the specific gene and mutation responsible for the hyperprolificacy phenotype in Booroola sheep.
Main Methods:
- Genetic analysis of 31 half-sib families.
- Localization of the FecB locus to ovine chromosome 6, syntenic to human chromosome 4q22-23.
- Sequencing of the bone morphogenetic protein receptor IB (BMPR-IB) gene.
Main Results:
- The FecB locus was mapped to ovine chromosome 6.
- A specific mutation (Q249R) in the BMPR-IB gene was identified and fully associated with the hyperprolificacy phenotype.
- Ovarian granulosa cells from FecB(B)/FecB(B) ewes showed reduced responsiveness to BMPR-IB ligands.
Conclusions:
- The Q249R substitution in BMPR-IB is the causative mutation for hyperprolificacy in Booroola sheep.
- This mutation likely leads to partial inactivation of BMPR-IB, affecting granulosa cell differentiation and follicle maturation.
- Understanding this mechanism offers insights into mammalian reproductive potential.