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Gamecock chickens are one of the earliest recorded birds in China, and have accumulated some unique morphological and behavioral signatures such as large body size, muscularity and aggressive behavior, whereby being excellent breeding materials and a good model for studying bird muscular development and behavior. In this study, we sequenced 126 chicken genomes from 19 populations, including four commercial chicken breeds that are commonly farmed in China, 13 nationwide Chinese typical indigenous chicken breeds (including two Chinese gamecock breeds), one red jungle fowl from Guangxi Province of China and three gamecock chickens from Laos. Combined with 31 published chicken genomes from three populations, a comparative genomics analysis was performed across 157 chickens. We found a severe confounding effect on potential cold adaptation exerted by introgression from commercial chickens into Chinese indigenous chickens, and argued that the genetic introgression from commercial chickens into indigenous chickens should be seriously considered for identifying selection footprint in indigenous chickens. LX gamecock chickens might have played a core role in recent breeding and conservation of other Chinese gamecock chickens. Importantly, AGMO ( Alkylglycerol monooxygenase ) and CPZ ( Carboxypeptidase Z ) might be crucial for determining the behavioral pattern of gamecock chickens, while ISPD ( Isoprenoid synthase domain containing ) might be essential for the muscularity of gamecock chickens. Our results can further the understanding of the evolution of Chinese gamecock chickens, especially the genetic basis of gamecock chickens revealed here was valuable for us to better understand the mechanisms underlying the behavioral pattern and the muscular development in chicken.

Metabolites from intestinal microbes modulate the mucosal immune system by regulating the polarization and expansion of T cells. Whether the microbial metabolites influence macrophage polarization, however, is poorly understood. Here, we show that the large bowel microbial fermentation product, butyrate, facilitates M2 macrophage polarization, in vitro and in vivo . The supernatant from butyrate-treated M2 macrophage increased the migration and enhanced the wound closure rate of MLE-12 cells. Butyrate attenuated intestinal inflammation in mice with dextran sulfate sodium (DSS)-induced colitis, with a significant increase in colonic expression of the M2 macrophage-associated protein, Arg1. M2 macrophage treated with butyrate, had increased activation of the H3K9/STAT6 signaling pathway, suggesting a mechanism for butyrate facilitated M2 macrophage polarization. Collectively, our study indicated that commensal microbe-derived butyrate is a novel activator of STAT6-mediated transcription through H3K9 acetylation driving M2 macrophage polarization and delineated new insights into the immune interplay underlying inflammatory bowel disease.

Complex traits exhibit a highly polygenic architecture that complicates gene mapping and molecular characterization. As a model organism for birds, chickens possess high-quality reference panels, functional annotations, and molecular quantitative trait locus maps. However, the genetic mechanisms underlying growth traits have not been systematically analyzed. Here, we develop a 16-generation advanced intercross line of chickens to enhance informative recombination and identify 154 single-gene quantitative trait loci. We use multiple co-localization methods to establish a network landscape of tissue-specific regulatory mutations and functional gene relationships. We leverage gene-clustering and restoration quantitative trait loci within the omnigenic model framework to elucidate the genetic regulation system of growth traits. Cross-species comparisons show the conserved functions of growth-related genes and divergent features of regulatory mechanisms in mammals and birds. Complex traits present challenges for gene mapping and molecular characterization. Here, the authors develop a 16-generation intercross line of chickens to explore the genetic architecture of complex traits in chicken.

Newcastle disease (ND) is one of the most serious viral diseases affecting chickens and is caused by Newcastle disease virus (NDV), an avian paramyxovirus serotype-1. The virus contains five structural proteins and two nonstructural proteins that interact with the host proteins involved in viral infection and host antiviral responses. Currently, several NDV strains have been molecularly characterized; however, a comprehensive overview of NDV in chickens that addresses recent findings is lacking. This review summarizes the current report of the molecular structure of NDV, including candidate genes and genomic regions, virulence and route of infection, mechanisms of resistance, host immune response, disease resistance mechanisms and effects of NDV on chicken immune performance. Therefore, this review can be used by researchers seeking a comprehensive understanding that can be applied in future breeding programs aimed at enhancing disease resistance.

Carotenoid consumption decreases the risk of cancer, osteoporosis, or neurodegenerative diseases through interrupting the formation of free radicals. The deposition of carotenoids in chicken skin makes the skin color turn from white into yellow. The enzyme β-carotene oxygenase 2 (BCO2) plays a key role during the degradation process of carotenoids in skin. How the BCO2 affects the skin color of the chicken and whether it is the key factor that results in the phenotypic difference between yellow- and white-skin chickens are still unclear. In this research, the measurement of the concentration of carotenoids in chicken skin by HPLC showed that the carotenoid concentration in chickens with a yellow skin was significantly higher than that in white-skin chickens. Moreover, there were significant differences in BCO2 gene expression in the back skin between yellow- and white-skin chickens. Scanning the SNPs in BCO2 gene revealed a G/A mutation in exon 6 of the BCO2 gene in white and yellow skin chicken. Generally, one SNP c.890A>G was found to be associated with the chicken skin color and may be used as a genetic marker in breeding for yellow skin in Chinese indigenous chickens.

Background Globally, the Newcastle disease virus (NDV) is a seriously important pathogen and results in substantial economic losses in the poultry industry. To mitigate this pathogen, the poultry industry has employed intensive breeding programs aimed at selecting genetic Lines that promote resistance and enhance immune response. Resistance to infection occurs at multiple levels and involves genotype-specific polymorphisms in the host. To date, the influence of genetic variations on the immune response within the same chicken Lines at the genotype-specific level is not fully understood. Therefore, it is important to understand the host genetic resistance that plays a role after NDV infection. This study aimed to investigate genotype-specific immune responses in chicken spleens following NDV infection at 7 days post-infection (7dpi), Samples were analyzed for differentially expressed genes (DEGs) using high-throughput RNA sequencing approaches. Results Twelve cDNA Libraries from LNH chicken spleens were compared with those of NDV-infected birds across the AA and GG genotypes. A total of 9886 genes were compared, of which 1348 were upregulated (833) and downregulated (515). Of these, 552 genes, with 415 upregulated and 137 downregulated genes, were differentially expressed (DE) between the two pairwise comparison groups: Control_AA vs. Immune_AA (AA group) and Control_GG vs. Immune_GG (GG group). Higher number of differentially expressed genes (407 DEGs), with 349 upregulated and 58 downregulated genes, were identified in chickens with the GG genotype, whereas 142 genes, with 63 upregulated and 79 downregulated genes, were observed in chickens with the AA genotype. In this study, a set of seven candidate genes (LECT1, MR1, MYH3, USH1C, NMU, BG8, and CCN3) was identified associated with the immune response in chickens. Further analysis revealed that DEGs in the spleen were enriched in various signaling pathways, such as neuroactive ligand-receptor interactions, tight junctions, and glycolysis/gluconeogenesis pathways, suggesting their potential role in immune resilience. Conclusions RNA-seq analysis revealed immune-related genes and pathways involved in the immune response in the chicken spleen. The results indicate that chickens with the GG genotype exhibited higher levels of differentially expressed genes (DEGs), potentially linked to NDV responses. Our findings also offer valuable transcriptomic insights for the comparative analysis of molecular mechanisms underlying immune response in LNH chickens and have practical implications for enhancing chicken breeding programs.

Avian leukosis virus (ALV) causes high mortality associated with tumor formation and decreased fertility, and results in major economic losses in the poultry industry worldwide. Recently, a putative novel ALV subgroup virus named ALV-K was observed in Chinese local chickens. In this study, a novel ALV strain named GD14LZ was isolated from a Chinese local yellow broiler in 2014. The proviral genome was sequenced and phylogenetically analyzed. The replication ability and pathogenicity of this virus were also evaluated. The complete proviral genome sequence of GD14LZ was 7482 nt in length, with a genetic organization typical of replication-competent type C retroviruses lacking viral oncogenes. Sequence analysis showed that the gag , pol and gp37 genes of GD14LZ have high sequence similarity to those of other ALV strains (A–E subgroups), especially to those of ALV-E. The gp85 gene of the GD14LZ isolate showed a low sequence similarity to those other ALV strains (A–E subgroups) but showed high similarity to strains previously described as ALV-K. Phylogenetic analysis of gp85 also suggested that the GD14LZ isolate was related to ALV-K strains. Further study showed that this isolate replicated more slowly and was less pathogenic than other ALV strains. These results indicate that the GD14LZ isolate belongs to the novel subgroup ALV-K and probably arose by recombination of ALV-K with endogenous viruses with low replication and pathogenicity. This virus might have existed in local Chinese chickens for a long time.

In depth studies of quantitative trait loci (QTL) can provide insights to the genetic architectures of complex traits. A major effect QTL at the distal end of chicken chromosome 1 has been associated with growth traits in multiple populations. This locus was fine-mapped in a fifteen-generation chicken advanced intercross population including 1119 birds and explored in further detail using 222 sequenced genomes from 10 high/low body weight chicken stocks. We detected this QTL that, in total, contributed 14.4% of the genetic variance for growth. Further, nine mosaic precise intervals (Kb level) which contain ancestral regulatory variants were fine-mapped and we chose one of them to demonstrate the key regulatory role in the duodenum. This is the first study to break down the detail genetic architectures for the well-known QTL in chicken and provides a good example of the fine-mapping of various of quantitative traits in any species. Yuzhe Wang, Xuemin Cao et al. report the fine-mapping of a major growth trait QTL in chicken using genome-wide association and haplotype association analyses. They discover multiple mutations cumulatively contribute to the previously-reported QTL and identify one of a regulatory mutation that contributes to the variation in the measured traits.

Background During domestication, remarkable changes in behavior, morphology, physiology and production performance have taken place in farm animals. As one of the most economically important poultry, goose owns a unique appearance characteristic called knob, which is located at the base of the upper bill. However, neither the histomorphology nor the genetic mechanism of the knob phenotype has been revealed in geese. Results In the present study, integrated radiographic, histological, transcriptomic and genomic analyses revealed the histomorphological characteristics and genetic mechanism of goose knob. The knob skin was developed, and radiographic results demonstrated that the knob bone was obviously protuberant and pneumatized. Histologically, there were major differences in structures in both the knob skin and bone between geese owing knob (namely knob-geese) and those devoid of knob (namely non-knob geese). Through transcriptome analysis, 592 and 952 genes differentially expressed in knob skin and bone, and significantly enriched in PPAR and Calcium pathways in knob skin and bone, respectively, which revealed the molecular mechanisms of histomorphological differences of the knob between knob- and non-knob geese. Furthermore, integrated transcriptomic and genomic analysis contributed to the identification of 17 and 21 candidate genes associated with the knob formation in the skin and bone, respectively. Of them, DIO2 gene could play a pivotal role in determining the knob phenotype in geese. Because a non-synonymous mutation (c.642,923 G > A, P265L) changed DIO2 protein secondary structure in knob geese, and Sanger sequencing further showed that the AA genotype was identified in the population of knob geese, and was prevalent in a crossing population which was artificially selected for 10 generations. Conclusions This study was the first to uncover the knob histomorphological characteristics and genetic mechanism in geese, and DIO2 was identified as the crucial gene associated with the knob phenotype. These data not only expand and enrich our knowledge on the molecular mechanisms underlying the formation of head appendages in both mammalian and avian species, but also have important theoretical and practical significance for goose breeding.

Avian leukosis is a neoplastic disease caused in part by subgroup J avian leukosis virus J (ALV-J). Micro ribonucleic acids (miRNAs) play pivotal oncogenic and tumour-suppressor roles in tumour development and progression. However, little is known about the potential role of miRNAs in avian leukosis tumours. We have found a novel tumour-suppressor miRNA, gga-miR-375, associated with avian leukosis tumorigenesis by miRNA microarray in a previous report. We have also previously studied the biological function of gga-miR-375; Overexpression of gga-miR-375 significantly inhibited DF-1 cell proliferation, and significantly reduced the expression of yes-associated protein 1 (YAP1) by repressing the activity of a luciferase reporter carrying the 3'-untranslated region of YAP1. This indicates that gga-miR-375 is frequently downregulated in avian leukosis by inhibiting cell proliferation through YAP1 oncogene targeting. Overexpression of gga-miR-375 markedly promoted serum starvation induced apoptosis, and there may be the reason why the tumour cycle is so long in the infected chickens. In vivo assays, gga-miR-375 was significantly downregulated in chicken livers 20 days after infection with ALV-J, and YAP1 was significantly upregulated 20 days after ALV-J infection (P<0.05). We also found that expression of cyclin E, an important regulator of cell cycle progression, was significantly upregulated (P<0.05). Drosophila inhibitor of apoptosis protein 1 (DIAP1), which is related to caspase-dependent apoptosis, was also significantly upregulated after infection. Our data suggests that gga-miR-375 may function as a tumour suppressor thereby regulating cancer cell proliferation and it plays a key role in avian leukosis tumorigenesis.