VNN1 Gene Expression and Polymorphisms Associated with Chicken Carcass Traits.

This study aimed to investigate the association between hepatic VNN1 expression and carcass traits in Mahuang chickens as well as to identify polymorphisms in the upstream and downstream regions of VNN1 that could potentially be associated with these carcass traits. The study revealed that VNN1 expression levels in liver correlated with various carcass traits such as dressed weight, eviscerated weight, and abdominal fat weight. A total of 39 polymorphic sites were identified, among which 23 were found to be associated with 15 different carcass traits. These polymorphic sites were organized into three distinct haplotype blocks, with BLOCK2 and BLOCK3 being associated with various eviscerated weight percentages, thigh weight, breast muscle weight, wing weight, and other traits. The study underscores the significant role of VNN1 in influencing the carcass traits of Mahuang chickens and sheds light on the genetic foundations of these traits. The findings provide valuable insights that could inform breeding strategies aimed at optimizing traits relevant to market demands and slaughtering efficiency.

Metagenomic analysis reveals the microbiome and antibiotic resistance genes in indigenous Chinese yellow-feathered chickens.

Yellow-feathered chickens have great nutritional value and are widely and traditionally used in China, on an industrial scale as broilers. The presence of intestinal microbes has been shown to correlate with poultry performance and serves as an essential reservoir of antibiotic resistance genes (ARGs). Antibiotic resistance is a major public health concern. Here, we investigated functional characteristics of the gut microbiome of indigenous Chinese yellow-feathered chickens (the Huiyang Bearded, Xinghua, Huaixiang, Zhongshan Shanlan, Qingyuan Partridge, and Yangshan chickens) through metagenomic sequencing and reconstructed 409 draft genomes, including 60 novel species and 6 novel genera. Furthermore, we assessed the functions of the intestinal microbial communities and examined the ARGs within them. The results showed that the microbial populations of yellow-feathered broilers were primarily dominated by Bacteroidetes and Firmicutes at the phylum level and Bacteroides at the genus level. Furthermore, the Qingyuan Partridge chicken showed a significantly higher abundance of Prevotella than the other five breeds of chicken. Principal coordinates analysis indicated significant differences in the structures of microbial communities and ARGs, based on the binary Jaccard distance, among the six chicken breeds. Moreover, 989 ARGs conferring tetracycline, multidrug, and aminoglycoside resistance were identified, which represented more than 80% of the faecal resistomes; the most abundant gene in the yellow-feathered chickens was tet(Q). In addition, we found the greatest abundance of resistance genes in Xinghua chickens, indicating that Xinghua chickens are highly resistant to antibiotics. Overall, our findings revealed differences in the gut microbial community structure of indigenous Chinese yellow-feathered broiler breeds and the composition and characteristics of ARGs and antibiotic resistance that enabled us to reconstruct the yellow-feathered chicken gut microbial community genomes. The current data significantly improves our knowledge of the gut microbiome and antibiotic resistance of popular broiler breeds in China.

Chicken Protein S Gene Regulates Adipogenesis and Affects Abdominal Fat Deposition.

(1) Background: Excessive abdominal fat deposition in broilers not only causes feed waste but also leads to a series of metabolic diseases. It has gradually become a new breeding goal of the broiler industry to improve growth rates and to reduce abdominal fat rates. In a previous study, PROS1 was highly expressed in low-abdominal fat broilers, suggesting a potential role in broilers adipogenesis. However, the function of PROS1 in preadipocytes and its association with abdominal fat traits need to be characterized. (2) Methods: qRT-PCR and Western Blot were used to quantify gene expression at the RNA and protein levels; flow cytometry and EdU were carried out to detect cell proliferation; and a GLM analysis was used to determine the association between PROS1 SNPs and carcass traits. (3) Results: PROS1 was downregulated in high-abdominal fat chicken; PROS1 contributed preadipocyte proliferation but suppressed preadipocyte differentiation; and the SNPs in the PROS1 5' flank were significantly associated with the abdominal fat weight rate. (4) Conclusions: Chicken PROS1 is able to suppress adipogenesis, and its polymorphisms are associated with the abdominal fat weight rate, which can be considered the molecular markers for chicken breeding, indicating that PROS1 is an effective potential gene in regulating abdominal fat deposition.

CircDCLRE1C Regulated Lipopolysaccharide-Induced Inflammatory Response and Apoptosis by Regulating miR-214b-3p/STAT3 Pathway in Macrophages.

The immune cell inflammation response is closely related to the occurrence of disease, and much evidence has shown that circular RNAs (circRNAs) play vital roles in the occurrence of disease. However, the biological function and regulatory mechanisms of circRNAs in the immune cell inflammation response remain poorly understood. In this study, we constructed an inflammatory model using lipopolysaccharide (LPS)-stimulated chicken macrophage lines (also known as HD11) to verify the function and mechanism of the novel circDCLRE1C (ID: gga_circ_0001674), which was significantly upregulated in spleen tissues infected by coccidia and the macrophage cells exposed to LPS. The results showed that circDCLRE1C aggravated LPS-induced inflammation and apoptosis in HD11 cells. Systemically, circDCLRE1C acted as a sponge for miR-214b-3p binding sites thereby regulating the expression of STAT3. The overexpression of miR-214b-3p rescued the pro-inflammatory effect of circDCLRE1C in HD11 cells stimulated with LPS, and rescued the high expression of STAT3. In conclusion, our study showed that circDCLRE1C could aggravate LPS-induced inflammation and apoptosis through competitive adsorption of miR-214b-3p, thereby increasing the expression of STAT3.