Genomic Insights Into the Multiple Factors Controlling Abdominal Fat Deposition in a Chicken Model

Genetic selection for an increased growth rate in meat-type chickens has been accompanied by excessive fat accumulation particularly in abdominal cavity. These progressed to indirect and often unhealthy effects on meat quality properties and increased feed cost. Advances in genomics technology over recent years have led to the surprising discoveries that the genome is more complex than previously thought. Studies have identified multiple-genetic factors associated with abdominal fat deposition. Meanwhile, the obesity epidemic has focused attention on adipose tissue and the development of adipocytes. The aim of this review is to summarize the current understanding of genetic/epigenetic factors associated with abdominal fat deposition, or as it relates to the proliferation and differentiation of preadipocytes in chicken. The results discussed here have been identified by different genomic approaches, such as QTL-based studies, the candidate gene approach, epistatic interaction, copy number variation, single-nucleotide polymorphism screening, selection signature analysis, genome-wide association studies, RNA sequencing, and bisulfite sequencing. The studies mentioned in this review have described multiple-genetic factors involved in an abdominal fat deposition. Therefore, it is inevitable to further study the multiple-genetic factors in-depth to develop novel molecular markers or potential targets, which will provide promising applications for reducing abdominal fat deposition in meat-type chicken

Gga-miR-205a Affecting Myoblast Proliferation and Differentiation by Targeting CDH11

Non-coding RNAs especially miRNAs have been found to play important roles during skeletal muscle development. Our previous RNA-Seq performed on breast muscle tissue from 7 weeks old Recessive White Rock and Xinhua Chicken and leg muscle tissue from female Xinghua Chicken at three development time points (11 embryo age, 16 embryo age, and 1 day post hatch) (accession number GSE62971 and GSE89355, respectively) showed that miR-205a and CDH11 were differentially expressed genes. In this study, we found that overexpression of CDH11 significantly facilitated Quail muscle clone (QM7) and chicken primary myoblast (CPM) proliferation and hampered CPM differentiation. MiR-205a can directly binding to the 3′UTR of CDH11 and the overexpression of miR-205a could inhibit both cell lines (QM7) and CPM proliferation, at the meantime promote the differentiation of myoblasts. The Dual-Luciferase Reporter Assay results and qRT-PCR results showed that myogenin (MyoG) could regulate the expression of miR-205a by binding to the active region of miR-205a. Altogether our data suggest that MyoG could stimulate miR-205a expression to suppress CDH11, which promotes myoblasts proliferation while represses the differentiation

A Novel Dnmt3a1 Transcript Inhibits Adipogenesis

DNA (cytosine-5)-methyltransferase 3a (Dnmt3a) is an enzyme that catalyzes the transfer of methyl groups to specific CpG forms in DNA. In mammals, two variant transcripts of Dnmt3a have been successfully identified. To the best of our knowledge, no Dnmt3a transcripts in an avian have been successfully identified. This study was performed to detect different transcripts of Dnmt3a in chickens and to examine whether a novel Dnmt3a transcript named Dnmt3a1 may regulate adipogenesis. In addition to cloning, sequencing, transcript detection, and expression studies, a novel Dnmt3a1 transcript overexpression and knockdown were conducted to explore the potential role of Dnmt3a1 in preadipocyte proliferation and the early stage of adipocyte differentiation. In chicken abdominal fat tissue, we detected a novel Dnmt3a1 transcript that differs from Dnmt3a by lacking 23 amino acids at the exon-1/exon-2 border. Dnmt3a1 mRNA was ubiquitously expressed in a variety of tissues or cells and highly expressed in chicken adipose tissue/cells. The expression of Dnmt3a1 was regulated under different physiological conditions including aging, fasting, and high-fat diet. In addition, overexpression of Dnmt3a1 significantly decreased preadipocyte proliferation and induced cell-cycle arrest while its inhibition increased cell proliferation and S-phase cells. Furthermore, the overexpression of Dnmt3a1 significantly upregulated the mRNA level of cell-cycle-related genes, such as CDKN1A, CDKN1B, CCNB3, CCND2, CCNG2, CDKN2B, and CDK9, or the protein level of CDKN1A, CDKN1B, and CCNG2. Conversely, the knockdown of Dnmt3a1 by siRNA had the opposite effects. Moreover, during early adipocyte differentiation, the overexpression of Dnmt3a1 significantly decreased the mRNA and the protein levels of PPAR-γ, C/EBP-α, ADIPOR1, and STAT3, and the mRNA levels of FAS, LEPR, LPL, PRKAB2, and ATGL. In contrast, their expression was significantly increased after the knockdown of Dnmt3a1. Taken together, we identified a novel transcript of Dnmt3a, and it played a potential role in adipogenesis

The genetic regulation of skeletal muscle development: insights from chicken studies

Skeletal muscle development is a complex multi-process trait regulated by various genetic factors. The chicken embryo is an ideal model system for studying skeletal muscle development. However, only a small proportion of the genetic factors affecting skeletal muscle development have been identified in chicken. The aim of this review is to summarize recent knowledge about the genetic factors involved in the regulation of skeletal muscle development in the chicken, such as gene polymorphisms, epigenetic modification, noncoding RNAs and transcription factors, which can influence skeletal muscle development at the genome, epigenome, transcriptome and proteome levels. Research on the regulation of skeletal muscle development in chicken is not yet comprehensive and most of the candidate genes and single nucleotide polymorphisms related to chicken muscle growth remain to be verified in experimental studies. In addition, the data derived from transcriptome sequencing and genome-wide association studies still require further investigation and analysis and comprehensive studies on the regulation of chicken skeletal muscle development will continue as a major research focus

Identification, expression and variation of the GNPDA2 gene, and its association with body weight and fatness traits in chicken

Background. The GNPDA2 (glucosamine-6-phosphate deaminase 2) gene is a member of Glucosamine-6-phosphate (GlcN6P) deaminase subfamily, which encoded an allosteric enzyme of GlcN6P. Genome-wide association studies (GWAS) have shown that variations of human GNPDA2 are associated with body mass index and obesity risk, but its function and metabolic implications remain to be elucidated.The object of this study was to characterize the gene structure, expression, and biological functions of GNPDA2 in chickens. Methods. Variant transcripts of chicken GNPDA2 and their expression were investigated using rapid amplification of cDNA ends (RACE) system and real-time quantitative PCR technology. We detected the GNPDA2 expression in hypothalamic, adipose, and liver tissue of Xinghua chickens with fasting and high-glucose-fat diet treatments, and performed association analysis of variations of GNPDA2 with productive traits in chicken. The function of GNPDA2 was further studied by overexpression and small interfering RNA (siRNA) methods in chicken preadipocytes. Results.Four chicken GNPDA2 transcripts (cGNPDA2-a∼cGNPDA2-d) were identified in this study. The complete transcript GNPDA2-a was predominantly expressed in adipose tissue (subcutaneous fat and abdominal fat), hypothalamus, and duodenum. In fasting chickens, the mRNA level of GNPDA2 was decreased by 58.8% (P < 0.05) in hypothalamus, and returned to normal level after refeeding. Chicken fed a high-glucose-fat diet increased GNPDA2 gene expression about 2-fold higher in adipose tissue (P < 0.05) than that in the control (fed a basal diet), but decreased its expression in hypothalamus. Two single-nucleotide polymorphisms of the GNPDA2 gene were significantly associated with body weight and a number of fatness traits in chicken (P < 0.05). Conclusion. Our findings indicated that the GNPDA2 gene has a potential role in the regulation of body weight, fat and energy metabolism in chickens