scholarly journals Mutation in bone morphogenetic protein receptor-IB is associated with increased ovulation rate in Booroola Merino ewes

2001 ◽  
Vol 98 (9) ◽  
pp. 5104-5109 ◽  
Author(s):  
P. Mulsant ◽  
F. Lecerf ◽  
S. Fabre ◽  
L. Schibler ◽  
P. Monget ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Ovulation Rate ◽  
Bone Morphogenetic Protein Receptor ◽  
Protein Receptor ◽  
Morphogenetic Protein

scholarly journals Oocytes in sheep homozygous for a mutation in bone morphogenetic protein receptor 1B express lower mRNA levels of bone morphogenetic protein 15 but not growth differentiation factor 9

Reproduction ◽  
2011 ◽  
Vol 142 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Janet L Crawford ◽  
Derek A Heath ◽  
Karen L Reader ◽  
Laurel D Quirke ◽  
Norma L Hudson ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Cumulus Cell ◽  
Ovulation Rate ◽  
Mrna Levels ◽  
Camp Production ◽  
Expression Levels ◽  
Bone Morphogenetic Protein Receptor ◽  
Protein Receptor ◽  
Morphogenetic Protein ◽  
Validation Experiment

The aim of this study was to test the hypothesis that the high ovulation rate in ewes (BB) homozygous for a mutation in the bone morphogenetic protein receptor type 1B (BMPR1B) gene is linked to lower BMP15 and/or GDF9 mRNA in oocytes compared with those in wild-type (++) ewes. Cumulus cell–oocyte complexes (COC) and granulosa cells (GC) were recovered from ≥1 mm diameter follicles of BB and ++ ewes during a prostaglandin-induced follicular phase. Expression levels of GDF9 and BMP15 were measured by multiplex qPCR from individual COC. The gonadotropin-induced cAMP responses of the GC from each non-atretic follicle were measured following treatment with FSH or human chorionic gonadotropin. In a separate validation experiment, GDF9 and BMP15 expression was present only in oocytes and not in cumulus cells. There was no effect of follicular diameter on oocyte-derived GDF9 or BMP15 mRNA levels. The mean expression levels of BMP15, but not GDF9, were significantly lower in all non-atretic follicles, including the subsets containing either FSH- or LH-responsive GC in BB, compared with ++, ewes. No genotype effects were noted for FSH-induced cAMP production by GC either with respect to dose of, or number of follicles responding to, FSH. However, ovaries from BB ewes contained significantly more follicles responsive to LH, with respect to cAMP production in GC. We propose that these findings are consistent with the hypothesis that the higher ovulation rate in BB sheep is due, at least in part, to lower oocyte-derived BMP15 mRNA levels together with the earlier onset of LH-responsiveness in GC.

scholarly journals Identification of a Lysosomal Pathway Regulating Degradation of the Bone Morphogenetic Protein Receptor Type II

2010 ◽  
Vol 285 (48) ◽  
pp. 37641-37649 ◽  
Author(s):  
Hannah J. Durrington ◽  
Paul D. Upton ◽  
Simon Hoer ◽  
Jessica Boname ◽  
Benjamin J. Dunmore ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Receptor Type ◽  
Type Ii ◽  
Bone Morphogenetic Protein Receptor ◽  
Protein Receptor ◽  
Morphogenetic Protein

scholarly journals Case study of a Hungarian breeding program using imported Booroola rams

2004 ◽  
Vol 47 (4) ◽  
pp. 359-366
Author(s):  
M. Árnyasi ◽  
A. Zsolnai ◽  
I. Komlósi ◽  
L. Fésüs ◽  
A. Jávor
Keyword(s):  
Major Gene ◽  
Ovulation Rate ◽  
Dna Testing ◽  
Bone Morphogenetic Protein Receptor ◽  
Long Period ◽  
Protein Receptor ◽  
Morphogenetic Protein ◽  
Pcr Rflp ◽  
Phenotype Measurement

Abstract. The first major gene for prolificacy identified in sheep was the Booroola (FecB) gene. Since the recognition of its existence, the Booroola Merino has spread all over the world. In Hungary, a new breed – called Hungarian Prolific Merino – had been established based on the crossing of Hungarian Merino ewes and Booroola Merino rams, and was acknowledged in 1992. The only way to determine the FecB genotypes has been the measurement of the ovulation rate over a long period. In 2001, the Booroola mutation was identified. Mutation on the bone morphogenetic protein receptor – 1B gene was found to be associated with the increased ovulation rate in the Booroola Merino ewes. 138 ewes and 46 rams in the Hungarian Prolific Merino population were tested for this mutation by PCR-RFLP and their FecB genotypes were determined. One copy of the FecB allele increased (P < 0,05) the ovulation rate by 0.89 ova and two copies increased by an average of 2.27 ova. Effectiveness of the FecB genotype estimation based on phenotype measurement was also compared to the results of direct DNA testing, and was found to have up to 80% accuracy.

scholarly journals Cercosporamide inhibits bone morphogenetic protein receptor type I kinase activity in zebrafish

2020 ◽  
Vol 13 (9) ◽  
pp. dmm045971 ◽  
Author(s):  
Jelmer Hoeksma ◽  
Gerard C. M. van der Zon ◽  
Peter ten Dijke ◽  
Jeroen den Hertog
Keyword(s):  
Bone Morphogenetic Protein ◽  
Mammalian Cells ◽  
Kinase Activity ◽  
Fibrodysplasia Ossificans Progressiva ◽  
Type I ◽  
Developmental Defects ◽  
Bone Morphogenetic Protein Receptor ◽  
Protein Receptor ◽  
Morphogenetic Protein ◽  
Constitutively Active

ABSTRACTZebrafish models are well-established tools for investigating the underlying mechanisms of diseases. Here, we identified cercosporamide, a metabolite from the fungus Ascochyta aquiliqiae, as a potent bone morphogenetic protein receptor (BMPR) type I kinase inhibitor through a zebrafish embryo phenotypic screen. The developmental defects in zebrafish, including lack of the ventral fin, induced by cercosporamide were strikingly similar to the phenotypes caused by renowned small-molecule BMPR type I kinase inhibitors and inactivating mutations in zebrafish BMPRs. In mammalian cell-based assays, cercosporamide blocked BMP/SMAD-dependent transcriptional reporter activity and BMP-induced SMAD1/5-phosphorylation. Biochemical assays with a panel of purified recombinant kinases demonstrated that cercosporamide directly inhibited kinase activity of type I BMPRs [also called activin receptor-like kinases (ALKs)]. In mammalian cells, cercosporamide selectively inhibited constitutively active BMPR type I-induced SMAD1/5 phosphorylation. Importantly, cercosporamide rescued the developmental defects caused by constitutively active Alk2 in zebrafish embryos. We believe that cercosporamide could be the first of a new class of molecules with potential to be developed further for clinical use against diseases that are causally linked to overactivation of BMPR signaling, including fibrodysplasia ossificans progressiva and diffuse intrinsic pontine glioma.This article has an associated First Person interview with the first author of the paper.

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