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Copy number variation (CNV) as an important source of genetic phenotypic and variation is related to complex phenotypic traits. The aim of this study was to investigate the potential associations of BAG4 (Bcl-2-associated athanogene 4) copy numbers variations with sheep growth traits in three Chinese sheep breeds (CKS, STHS, and HS). BAG4 is located within the stature and udder attachment quantitative trait loci (QTL) in sheep. Expression profiling revealed that the BAG4 gene was widely expressed in the tissues of sheep. The distribution of BAG4 gene copy number showed that the loss of copy number was more dominant in CKS and HS which was different from that in STHS. Statistical analysis revealed that the BAG4 CNV was significantly associated with body height in CKS (p < 0.05), with body slanting length in HS (p < 0.05), and with body height and hip cross height in STHS (p < 0.05). The χ2 values showed significant differences in the BAG4 CNV distribution frequency between varieties. In conclusion, the results establish the association between BAG4 CNV and sheep traits and suggest that BAG4 CNV may be a promising marker for the molecular breeding of Chinese sheep. [ABSTRACT FROM AUTHOR]

Copy number variations (CNVs) are gains and losses of genomic sequence of more than 50 bp between two individuals of a species. Also, CNV is considered to be one of the main elements affecting the phenotypic diversity and evolutionary adaptation of animals. ORMDL sphingolipid biosynthesis regulator 1 (ORMDL1) is a protein-coding gene associated with diseases and development. In our study, the polymorphism of ORMDL1 gene copy numbers in four Chinese sheep breeds (abbreviated CK, HU, STH, and LTH) was detected. In addition, we analyzed the transcriptional expression level of ORMDL1 gene in different tissues of sheep and examined the association of ORMDL1 CNV with growth traits. The statistical analysis revealed that ORMDL1 CNV was remarkably correlated with body height, heart girth, and circumference of cannon bone in HU sheep (P<0.05), and there are significant effects on body weight, body height, body length, chest depth, and height of hip cross in STH sheep (P<0.05). In conclusion, our results provide a basis for the relationship between CNV of ORMDL1 gene and sheep growth traits, suggesting that ORMDL1 CNV may be considered a promising marker for the molecular breeding of Chinese sheep. [ABSTRACT FROM AUTHOR]

Skeletal muscle is the most abundant tissue in the body. The development of skeletal muscle cell is complex and affected by many factors. A sea of microRNAs (miRNAs) have been identified as critical regulators of myogenesis. MiR‐208b, a muscle‐specific miRNA, was reported to have a connection with fiber type determination. However, whether miR‐208b has effect on proliferation of muscle cell was under ascertained. In our study, cyclin‐dependent kinase inhibitor 1A (CDKN1A), which participates in cell cycle regulation, was predicted and then validated as one target gene of miR‐208b. We found that overexpression of miR‐208b increased the expression of cyclin D1, cyclin E1, and cyclin‐dependent kinase 2 at the levels of messenger RNA and protein in cattle primary myoblasts in vivo and in vitro. Flow cytometry showed that forced expression of miR‐208b increased the percentage of cells at the S phase and decreased the percentage of cells at the G0/G1 phase. These results indicated that miR‐208b participates in the cell cycle regulation of cattle primary myoblast cells. 5‐Ethynyl‐20‐deoxyuridine and 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assays showed that overexpression of miR‐208b promoted the proliferation of cattle primary myoblasts. Therefore, we conclude that miR‐208b participates in the cell cycle and proliferation regulation of cattle primary skeletal muscle cell through the posttranscriptional downregulation of CDKN1A. Our data demonstrated that cyclin‐dependent kinase inhibitor 1A (CDKN1A) is a target gene of microRNA (miR)‐208b. MiR‐208b participates in the cell cycle and proliferation regulation of cattle primary skeletal muscle cell through the posttranscriptional downregulation of CDKN1A. [ABSTRACT FROM AUTHOR]