MOESM1 of Insights into the genetic variation of maternal behavior and suckling performance of continental beef cows

Additional file 1. Description of the recorded traits. Description: Description of the way the three traits were recorded on a station

Additional file 1: of Detection of quantitative trait loci for maternal traits using high-density genotypes of Blonde d’Aquitaine beef cattle

Number of genotyped animals in Blonde d’Aquitaine breed according to the chip density. (PNG 601 kb

Additional file 2: of Detection of quantitative trait loci for maternal traits using high-density genotypes of Blonde d’Aquitaine beef cattle

Strong evidence QTL for CS, PO, CSm, MY, S and WWm. (PDF 1422 kb

Supplementary material for <b>Genetic parameters, GWAS and selection perspective on gestation length in 16 French cattle breeds </b><i>by Jourdain et al., 2024</i>

The file contents all the supplementary materials mentionned in the article Genetic parameters, GWAS and selection perspective on gestation length in 16 French cattle breeds by Jourdain et al., 2024.Page 1 & 2 are presented Supplementary tables 1 & 2Page 3 to 34 are presented Supplementary figures 1 to 16, including the descriptive data of gestation length for each of the breeds used in the paper </p

MOESM1 of A missense variant in the coil1A domain of the keratin 25 gene is associated with the dominant curly hair coat trait (Crd) in horse

Additional file 1: Table S1. List of animals included in the study. This table provides detailed information about identification, pedigree, phenotypes and genotypes of animals included in the study. The full pedigree is also provided. Table S2a. Details on markers and haplotypes in the mapped region. This table provides markers and their position, including the KRT25 variant along ECA11. Colors are used to depict haplotypes, assuming 18 founder haplotypes (12 “non-curly” haplotypes carried by crossbreed animals as well as the six most frequent other haplotypes, including one “curly” haplotype). Haplotypes are given for each animal, according to pedigree data. Table S2b. Delineation of the critical mapping region by haplotype analysis. Haplotypes were sorted out according to their sequence and the associated coat phenotype. Critical recombination events are easily detected by color changes and help identify the upper and lower bounds of the mapping interval. Table S3. PCR primers used to genotype candidate genes. This table provides detailed information about chromosome positions, alleles, gene names, ID, primer sequences, fragment lengths and Tm. Table S4. Statistics on genome-wide detection of functional variants. Table S4 provides statistics on variant detection based on NGS sequencing, with numbers of new and known variants (whole genome and genes) according to their consequence as predicted by VEP. Positional candidate variants are also reported. Table S5. List of gene variants predicted to impact protein functionality. Table S5 includes chromosome positions, alleles, gene ID and functional annotations. The last column (Existing variation) indicates variants; which were already known in dbSNP. Table S6. Concordant variants identified in the critical mapping interval. Table S6 includes chromosome positions, alleles, functional annotations and gene ID for concordant variants. Table S7. Horses genotyped by PCR and Sanger sequencing. Horse names, phenotype and genotype for the KRT24:g.21932167G>T, Top2A:g.22186465C>T and Top2A: g.22191762G>T variants are presented. Table S8. Pedigree information for the progeny of Walker’s Prince T and Dravkvallons Ite O Maguzu. Table S8 provides pedigree and phenotype data obtained from breeders and the Curly horse pedigree database ( http://www.curlyhorses.info/mainsearch.asp ). Table S9. Comparison of NCBI and Ensembl annotations within the keratin cluster on ECA11. Annotation features are listed along ECA11, from position 2,136,900 to 2,197,100 pb; some discrepancy is observed upstream of the critical mapping interval

Identification of a variant in <i>KIF1C</i> gene in bovine animals affected by progressive ataxia.

<p>(A) Sanger sequence electropherogram traces for the causal mutation in the bovine <i>KIF1C</i> gene done on a wild type (WT), a heterozygous carrier and an affected animal. The G>A substitution affects the last nucleotide of bovine exon 5. Translated amino acids are presented below the genomic sequence. (B) Schematic diagram of coding exons from <i>KIF1C</i> gene in cattle (protein with 1104 amino acids) with the predicted functional domains of the protein, with the position of the mutation indicated (<i>arrow</i>). (C) Based on protein alignment, the affected amino acid is highly conserved in vertebrates and located in a conserved region of the protein. MACMU, <i>Macaca mulatta</i>; FELCA, <i>Felis catus</i>; BOVIN, bovine (<i>Bos taurus</i>); CANLF, <i>Canis lupus familiaris</i>; XENTR, <i>Xenopus tropicalis</i>; DANRE, <i>Danio rerio</i>.</p

Variants detected by whole-genome sequencing of 3 animals, including 2 with progressive ataxia.

<p>Variants detected by whole-genome sequencing of 3 animals, including 2 with progressive ataxia.</p

The participating cells in lesions.

<p>(A) Prominent astrocytic reaction as evidenced by anti-GFAP antibody (GFAP, green; Dapi, blue). Astrocytic reaction, engulfing the lesion; a few astrocytic feet penetrated the lesion (<i>white asterisk</i>). (B) Microglial activation, immunolabelled by anti Iba1, reproduced similar topography as the astrocytic reaction by surrounding the lesion, and few microglial cell processes infiltrated the lesion (<i>white asterisk</i>) (Iba1, green; Dapi, blue). Concurrently, astrocytic and microglial cell activations are present not only around the lesions but also elsewhere. (C) Immunostaining of anti-oligodendrocyte specific protein (anti-OSP), a cell membrane oligodendrocyte marker (OSP, green; Dapi, blue. Big or confluent lesions (<i>white arrows</i>), where the centre is occupied by many OSP-positive and intricate processes of different shapes and sizes, which presumably depend on the plane section. (D) Double immunostaining showed that the two markers–cytoplasmic (MBP) (red) and membrane (OSP) (green)–of oligodendrocytes were present together in the demyelinating lesions and the centre of the plaque was double-immunostained (<i>white arrows</i>). (E) Anti-actin immunostaining (red), Dapi (blue), actin protein aggregates were also accumulated in the centre (<i>arrow</i>) of the plaque and in the cytoplasm of some surrounding cells (<i>white arrows</i>). (F) Double immunostaining of actin (red) and MBP (green) Dapi (blue). Within the core of the plaque with actin immunostaining, note the presence of oligodendrocyte processes (<i>white arrows</i>). Scale bar: (A) and (B) 30 μm, (C) 20 μm, (D) 50 μm, (E) and (F) 20 μm.</p

Association between the ataxia variant and morphology traits in animals of the Charolais breed.

<p>Association between the ataxia variant and morphology traits in animals of the Charolais breed.</p

<i>KIF1C</i> variant affects mRNA expression and leads to a functional knock-out.

<p>(A) Schematic diagram of the <i>KIF1C</i> gene in bovine sequence, located on chromosome 19, with the mutation indicated by an arrow. Primer pairs p1 and p2 (respectively amplifying <i>KIF1C</i> exons 1 to 11 and exons 13 to 20) are shown downstream of the diagram. RT-PCR from WT and affected bovine brains with p1 and p2 primer pairs demonstrated that <i>KIF1C</i> expression is modified in affected animals both in quantity–with mRNA decay–and quality (several transcripts in affected animals). <i>RPL13</i> (ribosomal protein L13) was used as a housekeeping gene. (B) Schematic diagram of <i>KIF1C</i> transcripts in affected bovine. The normal transcript bears the G>A mutation and leads to a mutated protein; the alternative transcript results from defective splicing and leads to exon 5 skipping. (C) Proteins were extracted from brains of WT and affected bovines, and from HeLa cells. Samples were analysed by immunoblotting with antibody against KIF1C proteins. No KIF1C protein was found in affected animals. WT, wild type; Aff, affected.</p