20 research outputs found
Manhattan plots of genome-wide association studies for EBVs of commercially important traits in pigs.
<p>The red lines indicate the significance threshold for moderately significant associations (pâ=â5Ă10<sup>â5</sup>). âChromosome 0â harbors SNP markers that have not yet been mapped to the pig reference genome. The inserted quantile-quantile (QQ) plots show the observed versus expected log p-values. The straight line in the QQ plots indicates the distribution of SNP markers under the null hypothesis and the skew at the right edge indicate that these markers are stronger associated with the traits than it would be expected by chance. Please note that in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055951#pone-0055951-g001" target="_blank">Figure 1A</a> there are appear to be associated SNPs on SSC 3, 11, and 14. The two associated SNPs on SSC 3 and 11 mapped to these chromosomes in the Sscrofa 9.2 assembly, but are no longer placed on any chromosome in the Sscrofa 10.2 assembly.</p
Top allelic association hits in the GWAS for QTL affecting commercially important traits.
a<p>p-values were calculated using Ï2 tests in an allelic association study.</p>b<p>The positions of the associated SNPs on the latest version of the pig reference genome were determined by BLAST searches with the flanking sequences of the SNPs as provided by illumina with respect to the Sscrofa 10.2 assembly. Some of the flanking sequences did not give a significant BLAST hit with respect to this genome reference sequence.</p
Genotype-phenotype correlations.
<p>The animals were grouped according to genotype at the best associated SNPs of each of the four detected QTL. Animal numbers are indicated at the bottom. The call rates for these SNPs were >98.9%. For each of the four QTL the homozygous alternative genotype classes have different phenotypic distributions (p<0.05, Welch's t-test). (A) EBV pH1 distributions with respect to genotype at SNP ASGA0061594 on SSC 14. (B) EBV carcass length in boars with respect to genotype at SNP ASGA0010032 on SSC 2. (C) EBV rear view hind legs distributions in Swiss Large White boars with respect to genotype at SNP ALGA0058443 on SSC 10. (D) EBV rear view hind legs distributions in Swiss Large White boars with respect to genotype at SNP H3GA0045902 on SSC 16.</p
Fertinatural Ltda.
Fertinatural Ltda. es una empresa que incursiona en el mercado nacional empezando por el Valle del Cauca y sus alrededores, a travĂ©s de un fertilizante hecho a base de ĂĄcido hĂșmico el cual genera mayores beneficios para las cosechas, a diferencia de los fertilizantes quĂmicos generalmente utilizados por los agricultore
Additional file 3: of A GJA9 frameshift variant is associated with polyneuropathy in Leonberger dogs
Haplotype reconstruction for the centromeric region of acrocentric CFA15 of 314 dogs. (XLSX 3145 kb
Genotype, sex, and age-of-onset distribution for well-phenotyped case and control Leonbergers.
<p>Top: CFA16 <i>ARHGEF10</i> deletion genotyping of the original GWAS cohort, the larger, independent validation group, and all dogs combined. <i>D/D</i>â=âhomozygous for the <i>ARHGEF10</i> deletion. <i>D/N</i>â=âheterozygous for the <i>ARHGEF10</i> deletion. <i>N/N</i>â=âhomozygous normal. Each genotype group is further broken into sex and age-of-onset of clinical signs (either before or during the dog's third year, or after the dog's third year). Chi-square test of homogeneity p-values are reported for both genotypic and allelic frequencies (although these were calculated without using the sex or age-of-onset splits). Bottom: CFA7 TIGRP2P93473_rs9189862 SNP (located at Mb position 25,888,992) genotyping of the original GWAS cohort, and a combined cohort of all cases and controls meeting the inclusion criteria (GWAS dogs are included here). CFA: <i>Canis lupus familiaris</i> chromosome; GWAS: genome-wide association study.</p><p>Genotype, sex, and age-of-onset distribution for well-phenotyped case and control Leonbergers.</p
Genome-wide association mapping of Leonberger PN.
<p>(A) Manhattan plot of GWAS for PN with 93 (52 cases, 41 controls) Leonbergers. X-axisâ=âchromosome, Y-axisâ=ânegative decadic logarithms of permutation-corrected P-values. (B) Manhattan plot of GWAS for PN with 93 Leonbergers. X-axisâ=âchromosome, Y-axisâ=ânegative decadic logarithms of permutation-corrected P-values, after correction for population stratification and cryptic relatedness using a mixed model approach and genomic control. (C) The quantile-quantile (QQ) plot corresponding to (B).</p
SNP haplotypes and genes from the GWAS identified CFA16 region associated with Leonberger PN.
<p>A representative sample of the observed CFA16 haplotypes is demonstrated using eleven Leonbergers, with both haplotypes shown for each dog as green or yellow bars. LEO 1-4 and LEO 9 - 11 are cases (indicated in red), while LEO 5-8 are controls (indicated in blue). The most significantly associated SNP (BICF2G630820235) is highlighted in orange. Green bars represent the most significantly associated haplotype, which, in some cases extended the entire 1.5 Mb region. However, a minimum associated haplotype of approximately 250 kb (enclosed in the dark outlined box) was observed. An alternate haplotype, demonstrated by the yellow bars, was present in many of the controls and some of the cases. Some PN cases (LEO 9-11) are either heterozygous or devoid of the âgreenâ case-associated haplotype and a phenotypically normal dog (LEO 8) is heterozygous for the associated haplotype. CFA16 (Mb, CanFam2) ENSEMBL-annotated genes in the region are shown at the bottom of the figure.</p
Age-of-onset based on <i>ARHGEF10</i> genotype.
<p>Age-of-onset of clinical signs for all well-phenotyped cases (where age-of-onset was reported) is shown for all cases from the original GWAS and the independent, validation group, by <i>ARHGEF10</i> genotype. Not all 206 dogs are shown due to the fact that, while we sometimes knew the dog had clinical signs by a certain age, the exact onset of those signs before that age was unknown.</p
<i>ARHGEF10</i> mutation analysis.
<p>(A) Genomic DNA. Electropherograms of the <i>ARHGEF10</i> c.1955_1958+6delCACGGTGAGC mutation. Representative sequence traces of PCR products amplified from genomic DNA of 3 dogs with the different genotypes are shown. (B) Transcript. Electropherograms of RT-PCR using primers in exon 17 and 19. Representative sequence traces of RT-PCR products amplified from cDNA of 3 dogs with the different genotypes are shown. Note the underrepresentation of the mutant transcript in the heterozygous dog, which is probably due to nonsense mediated decay (NMD). Both the normal and the new splice site created by the deletion are underlined (Panel A); the cryptic splice site in the deletion allele creates a cDNA missing only four base pairs, which creates a frame shift and predicts a premature stop codon within seven amino acid residues (Panel B).</p