Previously, was identified as a candidate gene associated with sheep growth traits. This study aimed to investigate the direct role of in regulating myogenesis in embryonic myoblast cells and to investigate the association between single-nucleotide polymorphisms (SNPs) in its promoter region and sheep growth traits. The function of in myoblast proliferation and differentiation was detected after small interfering RNAs (siRNAs) knocked down the expression of . Cell proliferation was detected using CCK-8 assay, EdU proliferation assay, and flow cytometry cell cycle analysis. Cell differentiation was detected via cell immunofluorescence and the quantification of myogenic regulatory factors (MRFs). SNPs in the promoter region were detected using Sanger sequencing and genotyped using the improved multiplex ligation detection reaction (iMLDR) technique. As a result, a notable decrease ( < 0.01) in the percentage of EdU-positive cells in the siRNA-694-treated group was observed. A significant decrease ( < 0.01) in cell viability after treatment with siRNA-694 for 48 h and 72 h was detected using the CCK-8 method. The quantity of S-phase cells in the siRNA-694 treatment group was significantly decreased ( < 0.01). After interfering with in myoblasts during induced differentiation, the relative expression levels of MRFs were markedly ( < 0.05 or < 0.01) reduced compared with the control group on days 5-7. The myoblast differentiation in the siRNA-694 treatment group was obviously suppressed compared with the control group. SNP1, SNP2, SNP3, and SNP4 were significantly ( < 0.05) associated with all traits except body weight measured at birth and one month of age. SNP5 was significantly ( < 0.05) associated with body weight, body height, and body length in six-month-old sheep. In conclusion, interfering with can inhibit the proliferation and differentiation of ovine embryonic myoblasts. SNPs in its promoter region can serve as potential useful markers for selecting sheep growth traits.
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http://dx.doi.org/10.3390/ani13203173 | DOI Listing |
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Engineering Research Center of National Forestry and Grassland Administration for Rosa Roxburghii, Agricultural College, Guizhou University, Guiyang, 550025, People's Republic of China.
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January 2025
Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA.
Studies of the genetics of Alzheimer's disease (AD) have largely focused on single nucleotide variants and short insertions/deletions. However, most of the disease heritability has yet to be uncovered, suggesting that there is substantial genetic risk conferred by other forms of genetic variation. There are over one million short tandem repeats (STRs) in the genome, and their link to AD risk has not been assessed.
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January 2025
Endoscopy Center, Zhongshan Hospital of Fudan University, Shanghai 200032, China; Endoscopy Research Institute of Fudan University, Shanghai 200032, China. Electronic address:
Dysfunction of lipid metabolism is important for the development and progression of colorectal cancer, but the underlying mechanisms remain unclear. Here, HDAC2 was identified as highly expressed in both adenoma and colorectal cancer. We aimed to explore the roles and mechanisms of HDAC2 in lipid metabolism in colorectal cancer.
View Article and Find Full Text PDFGene
January 2025
School of Public Health, North China University of Science and Technology, Tangshan, China; College of Life Sciences, North China University of Science and Technology, Tangshan, China; Hebei Key Laboratory of Occupational Health and Safety for Coal Industry, Tangshan, China. Electronic address:
Background: Genome-wide association studies (GWAS) have identified susceptibility loci for colorectal cancer (CRC), but the underlying mechanisms remain unclear. This study investigates functional genetic variants in promoter regions of Leucine Rich Repeat Containing 6 (LRRC6) at 8q24 and Myotubularin Related Protein 10 (MTMR10) at 15q13.3 and their association with CRC susceptibility.
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January 2025
Department of Geriatrics, Peking University Shenzhen Hospital, Shenzhen, China.
Insulin resistance, a hallmark of type 2 diabetes, accelerates muscle breakdown and impairs energy metabolism. However, the role of Ubiquitin Specific Peptidase 2 (USP2), a key regulator of insulin resistance, in sarcopenia remains unclear. Peroxisome proliferator activated receptor γ (PPARγ) plays a critical role in regulating muscle atrophy.
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