(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.

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.

Excessive abdominal fat deposition reduces feed efficiency and edible carcass yield in chickens, yet its developmental and regional specialization remains poorly understood. We generated 93 bulk RNA sequencing (RNA-seq) libraries from 15 fat-associated anatomical regions at embryonic day 16 (E16) and 16 regions at 2 weeks post-hatch (2w) in six Xinghua chickens. Exploratory single-nucleus RNA sequencing was additionally performed on abdominal region (AR) tissue from one individual at each stage. Repeated-measures-aware analysis identified developmental stage as the major source of transcriptomic variation, with 4556 genes expressed at higher levels at E16 and 4528 at 2w. E16-associated programs were enriched for proliferation, morphogenesis, and structural development, whereas postnatal programs were dominated by immune and stimulus-response processes. Stage-specific weighted gene co-expression network analysis (WGCNA) identified substantial regional heterogeneity. AR showed stage-dependent signatures, including higher developmental and morphogenetic programs and lower lipid-metabolic programs at E16, and higher cell-cycle-related and lower developmental and fatty-acid-metabolic programs at 2w. Single-nucleus analysis identified adipose-lineage and multiple non-adipocyte populations, and cross-omics mapping showed that AR-associated signatures were distributed across multiple cellular compartments. These results suggest stage-dependent, multicellular transcriptional specialization of chicken AR tissue.

Accurate identification of indigenous chicken breeds is fundamental for the conservation and utilization of poultry genetic resources. To enable reliable identification of Wannan Yellow-feathered (WN) chickens, we developed a genomic framework based on whole-genome resequencing data. Comparative analyses of WN (n = 10) and 12 reference populations (n = 60) revealed clear population structure and identified 119 candidate selective regions containing 34,036 SNPs and 41 genes related to metabolism, reproduction, muscle development and behavior. Using these loci, a Random Forest model was constructed to prioritize informative markers, resulting in a compact panel of 41 SNPs. Validation on an independent cohort (n = 40) achieved 92.5% accuracy and an AUC of 0.995. Our results demonstrate that reliable breed identification requires integration of multiple frequency-variable loci rather than reliance on single markers. This study provides both biological insights into WN genetic architecture and a practical tool for breed authentication and conservation.

Escherichia coli (E. coli)-induced enteritis impairs intestinal barrier function, immune homeostasis, and growth performance in broilers. This study investigated whether dietary curcumin alleviates E. coli-induced intestinal injury by modulating macrophage-mediated inflammatory responses through the p38 MAPK signaling pathway. Broilers were fed either a basal or curcumin-supplemented diet and challenged with E. coli. Growth performance, intestinal inflammatory cytokines, morphology, barrier-related gene expression, goblet cell density, and ileal macrophage responses were evaluated. Lipopolysaccharide (LPS)-stimulated HD11 cells were used to examine the underlying mechanism. Curcumin supplementation increased body weight, average daily feed intake, and average daily gain in E. coli-challenged broilers, without significantly affecting the feed conversion ratio. Curcumin also reduced jejunal and ileal IL-1β, IL-6, and TNF-α levels; improved villus morphology and the villus height-to-crypt depth ratio; and upregulated CLDN1, OCLN, ZO-1, and MUC2 expression. In addition, curcumin restored goblet cell density and ileal macrophage abundance while suppressing macrophage-derived pro-inflammatory cytokine expression. In HD11 cells, curcumin inhibited LPS-induced inflammatory cytokine expression and secretion and reduced p38 MAPK phosphorylation, whereas pharmacological activation of p38 partially reversed these effects. In conclusion, dietary curcumin alleviated E. coli-induced enteritis in broilers by suppressing intestinal inflammation, preserving intestinal barrier function, and modulating macrophage-mediated immune responses. In vitro findings further suggest that inhibition of p38 MAPK signaling may contribute to the anti-inflammatory effects of curcumin on chicken macrophages.