Abstract
Sex-linked dwarf (SLD) chicken, which is caused by a recessive mutation of the growth hormone receptor (GHR), has been widely used in the Chinese broiler industry. However, it has been found that the SLD chicken has more abdominal fat deposition than normal chicken. Excessive fat deposition not only reduced the carcass quality of the broilers but also reduced the immunity of broilers to diseases. To find out the key genes and the precise regulatory pathways that were involved in the GHR mutation-induced excessive fat deposition, we used high-fat diet (HFD) and normal diet to feed the SLD chicken and normal chicken and analyzed the differentially expressed genes (DEGs) among the four groups. Results showed that the SLD chicken had more abdominal fat deposition and larger adipocytes size than normal chicken and HFD can promote abdominal fat deposition and induce adipocyte hypertrophy. RNA sequencing results of the livers and abdominal fats from the above chickens revealed that many DEGs between the SLD and normal chickens were enriched in fat metabolic pathways, such as peroxisome proliferator-activated receptor (PPAR) signaling, extracellular matrix (ECM)-receptor pathway, and fatty acid metabolism. Importantly, by constructing and analyzing the GHR-downstream regulatory network, we found that suppressor of cytokine signaling 2 (SOCS2) and cytokine-inducible SH2-containing protein (CISH) may involve in the GHR mutation-induced abdominal fat deposition in chicken. The ectopic expression of SOCS2 and CISH in liver-related cell line leghorn strain M chicken hepatoma (LMH) cell and immortalized chicken preadipocytes (ICP) revealed that these two genes can regulate fatty acid metabolism, adipocyte differentiation, and lipid droplet accumulation. Notably, overexpression of SOCS2 and CISH can rescue the hyperactive lipid metabolism and excessive lipid droplet accumulation of primary liver cell and preadipocytes that were isolated from the SLD chicken. This study found some genes and pathways involved in abdominal fat deposition of the SLD chicken and reveals that SOCS2 and CISH are two key genes involved in the GHR mutation-induced excessive fat deposition of the SLD chicken.
Highlights
Broiler consumption accounts for a large part of global meat consumption
These results demonstrated that the Sex-linked dwarf (SLD) chickens have more abdominal fat deposition and larger adipocytes size than normal chickens, and that high-fat diet (HFD) can increase abdominal fat deposition and enlarge adipocytes size in chicken
Co-transfection of Suppressor of cytokine signaling 2 (SOCS2) and CISH decreased more lipid droplet accumulation than individual transfection of SOCS2, suggesting a complementary role between SOCS2 and CISH (Figure 7C). These results indicate that cooverexpression of SOCS2 and CISH can make the lipid droplet accumulation of the SLD chicken return to the level of normal chicken, suggesting that SOCS2 and CISH are important in growth hormone receptor (GHR) mutation-induced fat deposition in the SLD chicken
Summary
Sex-linked dwarf (SLD) chicken is caused by deletion or point mutations of the growth hormone receptor (GHR) gene located in the Z chromosome (Tahara et al, 2009). Homozygous SLD chicken has smaller muscle fiber diameter and higher intramuscular fat deposition, which plays an essential role in meat quality (Knížetová, 1993; Melesse et al, 2013; Ye et al, 2014; Ferdaus et al, 2016; Luo et al, 2016; Cui et al, 2019). Organism to study human inherited diseases caused by GHR gene mutations. The symptoms of those diseases are similar to the SLD chicken, which has short shape, obesity, high level of serum growth hormone (GH), and low level of serum IGF-1 (Berg et al, 1993)
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