Keel bone damage (KBD) is a prominent concern within the realm of the egg-laying industry, exerting substantial impacts on the welfare and productivity of laying hens. This comprehensive review undertakes a detailed exploration of the diverse factors contributing to KBD, such as inadequate calcium sources in the medullary bone, genetic factors, nutritional deficiencies, and physical stressors. The consequences of KBD on production performance, stress and inflammation levels, and the physical and chemical properties of the keel are meticulously examined. Additionally, the review evaluates the existing methods for assessing KBD, including keel curvature scoring, imaging techniques, palpation, biomechanical testing, behavioral observations, and biochemical markers. Finally, management strategies, including nutritional adjustments, genetic selection, and environmental modifications, are proposed to potentially mitigate the prevalence and severity of KBD, thereby aiming to enhance the welfare and productivity of laying hens.

Pigeons serve as important model animals and commercial poultry. The Tarim pigeon, as a breed of Columba livia, is a locally indigenous breed unique to China. While the genome of C. livia was published in 2013, its assembly was fragmented and incomplete. In this study, we generated a near telomere-to-telomere assembly of the pigeon genome using the sequencing platform of PacBio HiFi, Nanopore long reads and Hi-C. The assembled genome spans 1295.8 Mb, with a contig N50 size of 49 Mb and a scaffold N50 size of 85 Mb. Approximately 98.4% of the assembly is anchored onto 41 chromosomes, with a BUSCO assessment indicating a completeness of 97.2%. And telomeres were identified at both ends of the four chromosomes. A total of 21,450 genes were annotated. The genome assembly of C. livia lays the foundation for understanding their genetic composition and evolutionary history and contributes to the pigeon breeding industry. Additionally, it will provide a basis for further management and conservation of pigeon breed diversity.

Clutch persistence, defined as the ability to sustain consecutive egg-laying cycles, is a pivotal determinant of profitability in the poultry industry, particularly for aging laying hens (≥65 weeks). However, the molecular mechanisms governing this trait remain elusive, largely due to the traditional “ovary-centric” paradigm that overlooks systemic regulation by the gut microbiota. To address this knowledge gap, the present study aimed to dissect the comprehensive regulatory network governing clutch persistence using integrated multi-omics analyses. A total of 20 sixty-five-week-old Rhode Island Red (RIR) laying hens with cumulative egg production exceeding 300 eggs but distinct clutch persistence were stratified into a high-clutch persistence group (HCP, ≥25 clutches, n = 10) and a low-clutch persistence group (LCPLCP, ≤15 clutches, n = 10). Multi-omics profiling, including ovarian transcriptomics, proteomics, and metabolomics; serum metabolomics; and cecal microbiota 16S rRNA sequencing was performed. Data integration and association mining were conducted via Spearman correlation analysis with stringent thresholds (r > 0.6, p < 0.01). Integrated analyses revealed a “gut–ovary axis” regulatory model mediated by a lipid mediator network, operating through a three-tiered mechanism: (1) Gut Initiation: The HCP group exhibited enriched cecal γ-Proteobacteria, which promoted biosynthesis of lipid precursors. (2) Serum Transport: Key serum lipid mediators, most notably LysoPC (22:6) (VIP = 4.5) and cholesterol ester CE (20:4), served as critical carriers transducing gut-derived signals to the ovary. (3) Ovarian Execution: These lipid signals activated a core ovarian metabolic pathway centered on the PLA2G6-ALOX15B-AGPAT3 axis, which coordinated follicular development and ovulation by supplying steroid hormone synthesis substrates, exerting anti-inflammatory effects, and stabilizing membrane structures. Collectively, this study demonstrates that gut microbiota modulates clutch persistence in aging laying hens via lipid mediators, orchestrating a systemic “gut–serum–ovary” regulatory cascade. These findings provide a novel molecular framework for extending the economic egg-laying cycle through the targeted manipulation of intestinal microbiota or serum lipid metabolism.

Objective: This study aimed to elucidate the molecular and microbial mechanisms underlying feather coverage in laying hens, with implications for understanding epithelial homeostasis and potential translational applications in tissue regeneration. By integrating multi-omics approaches, we sought to identify key genetic and microbial determinants of feather morphology and their synergistic effects on host physiology.Methods: A retrospective analysis was conducted on 400 laying hens classified into high (H) and low (L) feather coverage groups using a standardized 4-point scoring system. Transcriptomic profiling of cecal tissue was performed via RNA sequencing, while gut microbiota composition was analyzed using 16S rRNA amplicon sequencing. Differential gene expression and pathway enrichment were assessed using DESeq2 and clusterProfiler. Microbial community structure was evaluated through LEfSe analysis, and interplay between host transcripts and microbiota was examined via coinertia analysis.Results: Key findings revealed distinct microbial signatures in the L group, characterized by elevated Bacteroidetes (P < 0.01) and reduced Firmicutes (P < 0.01) abundance compared with the H group. Transcriptomic analysis identified dysregulation of pathways involved in epithelial remodeling (Wnt/β-catenin, TGF-β) and structural integrity (BMP and keratin family genes). Integration of multi-omics data demonstrated significant correlations between microbial composition and host gene expression (P < 0.05), highlighting the synergistic regulation of feather morphogenesis via microbial-metabolite crosstalk.Conclusions: This study elucidates the intricate interplay between host genetics and gut microbiota in regulating feather coverage, providing insights into epithelial biology and potential therapeutic targets for tissue homeostasis disorders. The findings underscore the importance of microbiome modulation in optimizing physiological traits relevant to avian health and agricultural productivity.

Fatty acid composition is crucial for determining meat quality. Pigeon meat, renowned for its tender texture, high protein content, and abundant polyunsaturated fatty acid (PUFAs), yet the developmental dynamics and molecular mechanisms of intramuscular fatty acid deposition remain unclear. Previous studies suggest that lipid metabolism is often governed by coordinated gene expression programs. Therefore, we hypothesized that fatty acid profiles in pigeon muscle are regulated by gene co-expression modules identifiable via weighted gene co-expression network analysis (WGCNA). To test this, we analyzed pectoral muscles from pigeons at five developmental stages (28 days to 48 months) using gas chromatography–mass spectrometry (GC–MS) and transcriptomic sequencing. A total of 39 fatty acids were identified, with key PUFAs such as DHA increasing and EPA decreasing over time, while overall MUFAs declined and PUFAs peaked at 6 months, revealing distinct stage-dependent patterns in fatty acid composition. WGCNA revealed that three gene modules (green, yellow, turquoise) were significantly associated with fatty acid traits. GO Enrichment analysis indicated their involvement in ribosome activity, mitochondrial pathways, and unsaturated fatty acid biosynthesis, while KEGG pathway highlighted oxidative phosphorylation and phosphatidylinositol signaling. Protein-protein interaction (PPI) analysis pinpointed hub genes, including RPS16, NDUFS6, RHOJ, and NUDT12 as key regulators of fatty acid metabolism. This study provides the first co-expression network linking fatty acid composition with transcriptional regulation in pigeons, broadening WGCNA application in avian lipid metabolism. The findings offer new insights into gene networks underlying lipid deposition and suggest targets for improving meat quality through molecular breeding.