scholarly journals Association of polymorphisms in bone morphogenetic protein receptor-1B gene exon-9 with litter size in Dorset, Mongolian, and Small Tail Han ewes

2019 ◽  
Vol 32 (7) ◽  
pp. 949-955 ◽  
Author(s):  
Jianlei Jia ◽  
Qian Chen ◽  
Linsheng Gui ◽  
Jipeng Jin ◽  
Yongyuan Li ◽  
...  
2010 ◽  
Vol 285 (48) ◽  
pp. 37641-37649 ◽  
Author(s):  
Hannah J. Durrington ◽  
Paul D. Upton ◽  
Simon Hoer ◽  
Jessica Boname ◽  
Benjamin J. Dunmore ◽  
...  

2020 ◽  
Vol 13 (4) ◽  
pp. 614-621
Author(s):  
Sara E. Ibrahim Mohamed ◽  
Romaz M. Ahmed ◽  
Khaleel I. Z. Jawasreh ◽  
M. A. M. Salih ◽  
Dalia Mursi Abdelhalim ◽  
...  

Background and Aim: The Watish sheep is a strain of desert sheep of smaller size compared to other desert sheep ecotypes, and there is anecdotal evidence that it is endowed with high litter size. The present study was designed for screening for polymorphisms in the known fecundity genes (bone morphogenetic protein receptor type 1B A<G in exon 6, bone morphogenetic protein 15 (BMP15) (FecXB, FecXG, FecXH, and FecXI) in exon2, growth differentiation factor 9 (GDF9) – G1 in exon1 and G8 in exon2 and PRLG<A in intron2) and their association with litter size in Watish. Materials and Methods: The study involved 156 Watish ewes of 2-6 years of age, along with data on litter size in the first, second, and third parity from Sinnar state and contiguous Blue Nile State. Genomic DNA was isolated and genotyped using polymerase chain reaction-restriction fragment length polymorphism. Allele and genotype frequencies were calculated by direct counting. Chi-square test for goodness of fit was performed for agreement with Hardy-Weinberg expectations and association testing. Results: The results demonstrated that all individuals were non-carriers for the target mutations of FecB, BMP15 (FecXB, FecXH, and FecXI), and GDF9-G8. With regard to the GDF9-G1 gene, the genotypic frequencies were 0.07% (G+) and 0.93% (++), in FecXG gene they were 0.993% (++) and 0.006% (B+), in PRL gene 0.516(++), 0.347(B+), and 0.137(BB). The Chi-square test showed a non-significant association between ewe's type of birth and the detected mutations genotypes. Conclusion: These results preliminarily indicated that GDF9-G1, BMP15 (FecXG), and PRL genes might have had some contribution for improving litter size in Watish Sudanese sheep. However, further studies using larger samples are needed to detect the effects of those mutations on Watish sheep litter size.


2020 ◽  
Vol 13 (9) ◽  
pp. dmm045971 ◽  
Author(s):  
Jelmer Hoeksma ◽  
Gerard C. M. van der Zon ◽  
Peter ten Dijke ◽  
Jeroen den Hertog

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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