Contribution of both positive selection and relaxation of selective constraints to degeneration of flyability during geese domestication

<div><p>Flyability is the most discrepant trait between modern-day geese and their wild ancestors, and the degeneration of flyability is a key marker of the successful domestication of wild geese. In light of the relatively short history of domestic geese, intense artificial selection is thought to play an important role in the degeneration of flyability. However, the underlying mechanism behind this phenomenon has seldom been investigated. In this study, we applied a molecular evolutionary approach to the evaluation of partial breeds of domestic geese in order to look for genes involved in the selection pressure toward degeneration of flyability. The haplotype networks, pairwise fixation index (<i>F</i>_<i>ST</i>) values, and analysis of molecular variance results all clearly illustrated a population variance between Landes geese and partial Chinese domestic geese. We also detected signatures of positive artificial selection in the <i>COX2</i> and <i>COX3</i> genes, and related selection in the <i>HBB</i> gene. Our results support the independent origins of partial European domestic geese and Chinese domestic geese. In addition, both positive artificial selection and the relaxation of functional constraints appeared to play important roles in the degeneration of flyability in domestic geese.</p></div

Genotypes for the association panel

Genotypes for the association pane

The Identification of Loci for Immune Traits in Chickens Using a Genome-Wide Association Study

<div><p>The genetic improvement of disease resistance in poultry continues to be a challenge. To identify candidate genes and loci responsible for these traits, genome-wide association studies using the chicken 60k high density single nucleotide polymorphism (SNP) array for six immune traits, total serum immunoglobulin Y (IgY) level, numbers of, and the ratio of heterophils and lymphocytes, and antibody responses against Avian Influenza Virus (AIV) and Sheep Red Blood Cell (SRBC), were performed. RT-qPCR was used to quantify the relative expression of the identified candidate genes. Nine significantly associated SNPs (<i>P</i> < 2.81E-06) and 30 SNPs reaching the suggestively significant level (<i>P</i> < 5.62E-05) were identified. Five of the 10 SNPs that were suggestively associated with the antibody response to SRBC were located within or close to previously reported QTL regions. Fifteen SNPs reached a suggestive significance level for AIV antibody titer and seven were found on the sex chromosome Z. Seven suggestive markers involving five different SNPs were identified for the numbers of heterophils and lymphocytes, and the heterophil/lymphocyte ratio. Nine significant SNPs, all on chromosome 16, were significantly associated with serum total IgY concentration, and the five most significant were located within a narrow region spanning 6.4kb to 253.4kb (<i>P</i> = 1.20E-14 to 5.33E-08). After testing expression of five candidate genes (<i>IL4I1</i>, <i>CD1b</i>, <i>GNB2L1</i>, <i>TRIM27</i> and <i>ZNF692</i>) located in this region, changes in <i>IL4I1</i>, <i>CD1b</i> transcripts were consistent with the concentrations of IgY, while abundances of <i>TRIM27</i> and <i>ZNF692</i> showed reciprocal changes to those of IgY concentrations. This study has revealed 39 SNPs associated with six immune traits (total serum IgY level, numbers of, and the ratio of heterophils and lymphocytes, and antibody responses against AIV and SRBC) in Beijing-You chickens. The narrow region spanning 247kb on chromosome 16 is an important QTL for serum total IgY concentration. Five candidate genes related to IgY level validated here are novel and may play critical roles in the modulation of immune responses. Potentially useful candidate SNPs for marker-assisted selection for disease resistance are identified. It is highly likely that these candidate genes play roles in various aspects of the immune response in chickens.</p></div

Suggestively Associated SNPs for five immune traits.

<p>Suggestively Associated SNPs for five immune traits.</p

Matrix of pairwise <i>F</i>_<i>ST</i> for each gene across populations. (A) <i>COX2</i>, (B) <i>COX3</i>, (C) <i>HBA1</i>, (D) <i>HBA2</i>, and (E) <i>HBB</i>.

<p>Matrix of pairwise <i>F</i>_<i>ST</i> for each gene across populations. (A) <i>COX2</i>, (B) <i>COX3</i>, (C) <i>HBA1</i>, (D) <i>HBA2</i>, and (E) <i>HBB</i>.</p

Values of the Hudson-Kreitman-Aguade test for each gene across populations^a.

<p>Values of the Hudson-Kreitman-Aguade test for each gene across populations<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0185328#t002fn001" target="_blank">^a</a>.</p

Manhattan plots showing association of all SNPs with six immune traits.

<p>SNPs are plotted on the x-axis according to their position on each chromosome against association with these traits on the y-axis (shown as-log10 <i>p</i>-value). The red dashed line indicates suggestive genome-wise significance (<i>p</i>-value = 5.62E-05), and the black dashed line shows genome-wise 5% significance with a p-value threshold of 2.81E-06. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117269#pone.0117269.g002" target="_blank">Fig. 2-A, 2-B, 2-C, 2-D, 2-E and 2-F</a> refer to plots for total serum IgY level, H/L ratio, number of Heterophils, number of Lymphocytes, SRBC antibody titer and AI antibody titer, respectively.</p

Haplotype networks of five genes across each population. (A) <i>COX2</i>, (B) <i>COX3</i>, (C) <i>HBA1</i>, (D) <i>HBA2</i>, and (E) <i>HBB</i>.

<p>Haplotype networks of five genes across each population. (A) <i>COX2</i>, (B) <i>COX3</i>, (C) <i>HBA1</i>, (D) <i>HBA2</i>, and (E) <i>HBB</i>.</p

Primers used for the RT-qPCR.

<p>Primers used for the RT-qPCR.</p

Distribution of SNPs on each chromosome after quality control.

<p>^a Two linkage groups.</p><p>^b These SNPs are not mapped to any chromosome.</p><p>^c The physical length of the chromosome was based on the genome build Gallus_gallus-2.1(May, 2006).</p><p>Distribution of SNPs on each chromosome after quality control.</p