11 research outputs found
Whole-genome resequencing of Xishuangbanna fighting chicken to identify signatures of selection
International audienceAbstractBackgroundSelective breeding for genetic improvement is expected to leave distinctive selection signatures within genomes. The identification of selection signatures can help to elucidate the mechanisms of selection and accelerate genetic improvement. Fighting chickens have undergone extensive artificial selection, resulting in modifications to their morphology, physiology and behavior compared to wild species. Comparing the genomes of fighting chickens and wild species offers a unique opportunity for identifying signatures of artificial selection.ResultsWe identified selection signals in 100-kb windows sliding in 10-kb steps by using two approaches: the pooled heterozygosity (Hp)\documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\usepackage{upgreek}\setlength{\oddsidemargin}{-69pt}\begin{document}\end{document} and the fixation index (FST)\documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\usepackage{upgreek}\setlength{\oddsidemargin}{-69pt}\begin{document}\end{document} between Xishuangbanna fighting chicken (YNLC) and Red Jungle Fowl. A total of 413 candidate genes were found to be putatively under selection in YNLC. These genes were related to traits such as growth, disease resistance, aggressive behavior and energy metabolism, as well as the morphogenesis and homeostasis of many tissues and organs.ConclusionsThis study reveals mechanisms and targets of artificial selection, which will contribute to improve our knowledge about the evolution of fighting chickens and facilitate future quantitative trait loci mapping
Effects of Caponization on Expression of Gonadotropin-Releasing Hormone-I and Gonadotropin Subunits Genes in Roosters
We evaluated the effects of caponization on mRNA levels of gonadotropin-releasing hormone-I (GnRH-I), gonadotropin subunit and other hypothalamic and hypophyseal peptide genes in male chicken. Thirty roosters (25 d) with similar weight were equally divided into the experimental (capons) and control (sham-operated males) groups randomly. Caponization was performed at 28 days of age and birds were slaughtered at 140 days of age. Caponization resulted in increasing levels of luteinizing hormone β (LHβ) and follicle-stimulating hormone β (FSHβ) mRNA in the pituitary gland and levels of LH and FSH in serum (P<0.05 or P<0.01). There were no significant differences in levels of GnRH-I, Gonadotropin releasing hormone receptor (GnRHR), neuropeptide Y (NPY) and Proopiomelanocortin (POMC) mRNA between the two groups. Capons exhibited lower levels of follistatin (FS), estrogen receptor α (ERα) and higher levels of androgen receptor (AR) mRNA in the pituitary gland compared with sham-operated males (P<0.05). These results suggest that increased LH and FSH concentrations in serum and LHβ and FSHβ mRNA levels in pituitary after castration are not depended on GnRH synthesis. And changed expression of ERα, AR and FS genes in the pituitary gland may be important components of regulating gonadotropin in capons
Identification of central regulators related to abdominal fat deposition in chickens based on weighted gene co-expression network analysis
ABSTRACT: Abdominal fat (AF) is one of the most important economic traits in chickens. Excessive AF in chickens will reduce feed utilization efficiency and negatively affect reproductive performance and disease resistance. However, the regulatory network of AF deposition needs to be further elucidated. In the present study, 300 one-day-old female Wannan chickens were reared to 17 wk of age, and 200 Wannan hens were selected to determine the abdominal fat percentage (AFP). Twenty AF tissue samples with the lowest AFP were selected as the low abdominal fat group (L-AFG), and 20 AF tissue samples with the highest AFP were selected as the high abdominal fat group (H-AFG). Eleven samples from L-AFG and 14 samples from H-AFG were selected for RNA-seq and used for weighted gene co-expression network analysis (WGCNA). Among the 25 RNA-seq samples, 5 samples with the lowest and highest AFP values were selected for differential expression gene analysis. Compared with the L-AFG, 225 and 101 genes were upregulated and downregulated in the H-AFG, respectively. A total of 20,503 genes were used to construct the WGCNA, and 44 co-expression gene modules were identified. Among these modules, 3 modules including turquoise, darkorange2, and floralwhite were identified as significantly associated with AFP traits. Furthermore, several genes including acyl-CoA oxidase 1 (ACOX1), stearoyl-CoA desaturase (SCD), aldehyde dehydrogenase 6 family member A1 (ALDH6A1), jun proto-oncogene, AP-1 transcription factor subunit (JUN), and fos proto-oncogene, AP-1 transcription factor subunit (FOS) involved in the “PPAR signaling pathway,” “fatty acid metabolism,” and “MAPK signaling pathway” were identified as central regulators that contribute to AF deposition. These results provide valuable information for further understanding of the gene expression and regulation of AF traits and contribute to future molecular breeding for AF in chickens
Parallel Evolution of Polydactyly Traits in Chinese and European Chickens.
Polydactyly is one of the most common hereditary congenital limb malformations in chickens and other vertebrates. The zone of polarizing activity regulatory sequence (ZRS) is critical for the development of polydactyly. The causative mutation of polydactyly in the Silkie chicken has been mapped to the ZRS; however, the causative mutations of other chicken breeds are yet to be established. To understand whether the same mutation decides the polydactyly phenotype in other chicken breeds, we detected the single-nucleotide polymorphism in 26 different chicken breeds, specifically, 24 Chinese indigenous breeds and 2 European breeds. The mutation was found to have fully penetrated chickens with polydactyly in China, indicating that it is causative for polydactyly in Chinese indigenous chickens. In comparison, the mutation showed no association with polydactyly in Houdan chickens, which originate from France, Europe. Based on the different morphology of polydactyly in Chinese and European breeds, we assumed that the trait might be attributable to different genetic foundations. Therefore, we subsequently performed genome-wide association analysis (GWAS) to locate the region associated with polydactyly. As a result, a ~0.39 Mb genomic region on GGA2p was identified. The region contains six candidate genes, with the causative mutation found in Chinese indigenous breeds also being located in this region. Our results demonstrate that polydactyly in chickens from China and Europe is caused by two independent mutation events that are closely located in the chicken genome
Variation in X-ray digital radiography with respect to Beijing-You foot polydactyly.
<p><b>A-D</b> show the different foot phenotypes of Beijing-You chicken, <b>E-H</b> show the X-ray digital radiography coordinately with <b>A–D</b>. <b>A & E:</b> non-polydactylous foot with four digits, identified from anterior to posterior (1, 2, 3, 4). <b>B & F</b>: Beijing-You foot with four digits, with a polyphalange in digit “1” making it digit “2” (2, 2, 3, 4). <b>C & G</b>: polydactylous Beijing-You foot with five digits (2, 1, 2, 3, 4). <b>D & H</b>: polydactylous Beijing-You foot with six digits (1, 2, 1, 2, 3, 4).</p
Genotypes of causative SNP loci detected by sequencing and diagnostic PCR.
<p>The genotypes shown on the left side are wild type (CC), mutation heterozygote (AC), and derived homozygote (AA), from top to bottom. The mutation genotypes were fully associated with polydactyly in Chinese chickens, regardless of whether the mutation was homozygotic or heterozygotic. PCR products digested by restriction enzyme BsrDI are presented on the right.</p
Principal polydactyly subtypes in Beijing-You, Silkie, and Houdan chickens.
<p>Two subtypes of polydactyly were found in the three chicken breeds, but with difference prevalence. Subtype I: principal subtype of Beijing-You (A) and Silkie (B), in which an extra toe was separated from the second phalanx in the most anterior toe; Subtype II: principal subtype of Houdan (C), with extra toe separation occurring from the first phalanx.</p
Genome-wide scan for polydactyly in Houdan chickens.
<p>Manhattan plot showing the association of all SNPs with the polydactyly trait of Houdan chickens. SNPs were plotted on the x-axis according to their position on each chromosome against their association with these traits on the y-axis (shown as -log10 P-value). The green line and black line indicate the genome-wide suggestive and significant association with P-values of 1.73 × 10<sup>−5</sup> (1.00/57,657) and 8.67 × 10<sup>−7</sup> (0.05/57,657), respectively.</p