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An F2 population (695 individuals) was established from broiler chickens divergently selected for either high (HG) or low (LG) growth, and used to localize QTL for developmental changes in body weight (BW), shank length (SL9) and shank diameter (SD9) at 9 weeks. QTL mapping revealed three genome-wide QTL on chromosomes (GGA) 2, 4 and 26 and three suggestive QTL on GGA 1, 3 and 5. Most of the BW QTL individually explained 2–5% of the phenotypic variance. The BW QTL on GGA2 explained about 7% of BW from 3 to 7 weeks of age, while that on GGA4 explained 15% of BW from 5 to 9 weeks. The BW QTL on GGA2 and GGA4 could be associated with early and late growth respectively. The GGA4 QTL also had the largest effect on SL9 and SD9 and explained 7% and 10% of their phenotypic variances respectively. However, when SL9 and SD9 were corrected with BW9, a shank length percent QTL was identified on GGA2. We identified novel QTL and also confirmed previously identified loci in other chicken populations. As the foundation population was established from commercial broiler strains, it is possible that QTL identified in this study could still be segregating in commercial strains. [ABSTRACT FROM AUTHOR]

Quantitative trait loci (QTL) influencing the weight of abdominal fat (AF) and of breast muscle (BM) were detected on chicken chromosome 5 (GGA5) using two successive F2 crosses between two divergently selected ‘Fat’ and ‘Lean’ INRA broiler lines. Based on these results, the aim of the present study was to identify the number, location and effects of these putative QTL by performing multitrait and multi-QTL analyses of the whole available data set. Data concerned 1186 F2 offspring produced by 10 F1 sires and 85 F1 dams. AF and BM traits were measured on F2 animals at slaughter, at 8 (first cross) or 9 (second cross) weeks of age. The F0, F1 and F2 birds were genotyped for 11 microsatellite markers evenly spaced along GGA5. Before QTL detection, phenotypes were adjusted for the fixed effects of sex, F2 design, hatching group within the design, and for body weight as a covariable. Univariate analyses confirmed the QTL segregation for AF and BM on GGA5 in male offspring, but not in female offspring. Analyses of male offspring data using multitrait and linked-QTL models led us to conclude the presence of two QTL on the distal part of GGA5, each controlling one trait. Linked QTL models were applied after correction of phenotypic values for the effects of these distal QTL. Several QTL for AF and BM were then discovered in the central region of GGA5, splitting one large QTL region for AF into several distinct QTL. Neither the ‘Fat’ nor the ‘Lean’ line appeared to be fixed for any QTL genotype. These results have important implications for prospective fine mapping studies and for the identification of underlying genes and causal mutations. [ABSTRACT FROM AUTHOR]

The satiety hormone leptin has a key role in the control of energy homeostasis in mammals. Leptin is produced almost exclusively by the adipose tissue and signals the amount of fat stores primarily to the hypothalamus, but also to peripheral tissues. Recently, we identified the long sought leptin (SEROUSSI et al., 2016), in the "dark side of the chicken genome", meaning extremely GC-rich regions that have been difficult to sequence and assemble. Expression profiling of the avian leptins showed a different pattern compared to mammals, surprisingly with no expression in the adipose tissue. Nevertheless, we found that leptin and leptin receptor (LEPR) genes are expressed in tissues that are implicated in the response to leptin signalling in mammals, and their expression pointed to an autocrine/paracrine instead of endocrine mode of action. Therefore, the role of avian leptins may be relevant to the control of reproduction, stress response and metabolism, but in a different way than in mammals, as it is not the signal of the adipose tissue. Following the success of the identification of chicken leptin and realizing its presence in RNA-seq data rather than genomic assemblies, we asked if other missing genes in chicken could be identified using the RNA-seq approach. Extensive RNA-seq analysis of visceral fat, hypothalamus and pituitary, followed by transcript assembly and bioinformatic analysis led to the identification of 191 novel genes in chickens (BORNELOV et al., 2017), all with very high GC content (~70%). These included the tumour necrosis factor (TNF, also known as TNF-alpha) and nephrin (NPHS1), which were long sought after in the chicken genome. Interestingly, 25 of our novel genes were mapped to the chicken genome in the most recent genome assembly Galgal5. This mapping showed that about 70% of the genes were mapped to chicken microchromosomes, which are known to be GC-rich. The same proportion of genes were mapped in gene blocks demonstrating that the indication that missing genes arranged in gene clusters in other vertebrates cannot be taken as an indication for their evolutionary loss. Altogether, these findings suggest that other missing genes in chickens may be positioned in GC-rich gene clusters in the chicken genome. Among our novel chicken genes, we found five genes belonging to the leptin synteny group in vertebrates: RBM28, SND1, LRRC4, and FLNC. We used this identification to map the chicken leptin gene and its syntenic genes to chicken chromosome 1p (SEROUSSI et al., 2017), thus providing the final proof for the correct identification of the chicken leptin gene. [ABSTRACT FROM AUTHOR]

Abstract We investigated the joint evolution of neutral and selected genomic regions in three chicken lines selected for immune response and in one control line. We compared the evolution of polymorphism of 21 supposedly neutral microsatellite markers versus 30 microsatellite markers located in seven quantitative trait loci (QTL) regions. Divergence of lines was observed by factor analysis. Five supposedly neutral markers and 12 markers in theQTL regions showed Fst values greater than 0.15. However, the non-significant difference (P > 0.05) between matrices of genetic distances based on genotypes at supposedly neutral markers on the one hand, and at markers in QTL regions, on the other hand, showed that none of the markers in the QTL regions were influenced by selection. A supposedly neutral marker and a marker located in the QTL region on chromosome 14 showed temporal variations in allele frequencies that could not be explained by drift only. Finally, to confirm thatmarkers located inQTL regions on chromosomes 1, 7 and 14were under the influence of selection, simulations were performed using haplotype dropping along the existing pedigree. In the zone located on chromosome 14, the simulation results confirmed that selection had an effect on the evolution of polymorphism of markers within the zone.

Abstract Quantitative trait loci (QTL) for abdominal fatness and breast muscle weight were investigated in a three-generation design performed by inter-crossing two experimental meat-type chicken lines that were divergently selected on abdominal fatness. A total of 585 F2 male offspring from 5 F1 sires and 38 F1 dams were recorded at 8 weeks of age for live body, abdominal fat and breast muscle weights. One hundred-twenty nine microsatellite markers, evenly located throughout the genome and heterozygous for most of the F1 sires, were used for genotyping the F2 birds. In each sire family, those offspring exhibiting the most extreme values for each trait were genotyped. Multipoint QTL analyses using maximum likelihood methods were performed for abdominal fat and breast muscle weights, which were corrected for the effects of 8-week body weight, dam and hatching group. Isolated markers were assessed by analyses of variance. Two significant QTL were identified on chromosomes 1 and 5 with effects of about one within-family residual standard deviation. One breast muscle QTL was identified on GGA1 with an effect of 2.0 within-family residual standard deviation.

Abstract We present a gene-based RH map of the chicken microchromosome GGA14, known to have synteny conservations with human chromosomal regions HSA16p13.3 and HSA17p11.2. Microsatellite markers from the genetic map were used to check the validity of the RH map and additional markers were developed from chicken EST data to yield comparative mapping data. A high rate of intra-chromosomal rearrangements was detected by comparison to the assembled human sequence. Finally, the alignment of the RH map to the assembled chicken sequence showed a small number of discordances, most of which involved the same region of the chromosome spanning between 40.5 and 75.9 cR6000 on the RH map.

Abstract As a first step towards the development of radiation hybrid maps, we have produced a radiation hybrid panel in the chicken by fusing female embryonic diploid fibroblasts irradiated at 6 000 rads with HPRT-deficient hamster Wg3hCl2 cells. Due to the low retention frequency of the chicken fragments, a high number of clones was produced from which the best ones were selected. Thus, 452 fusion clones were tested for retention frequencies with a panel of 46 markers. Based on these results, 103 clones with a mean marker retention of 23.8% were selected for large scale culture to produce DNA in sufficient quantities for the genotyping of numerous markers. Retention frequency was tested again with the same 46 markers and the 90 best clones, with a final mean retention frequency of 21.9%, were selected for the final panel. This panel will be a valuable resource for fine mapping of markers and genes in the chicken, and will also help in building BAC contigs.

Abstract The bulked segregant analysis methodology has been used to map, with microsatellite markers, two morphological mutations in the chicken: polydactyly (PO) and naked neck (NA). These autosomal mutations show partial dominance for NA, and dominance with incomplete penetrance for PO. They were mapped previously to different linkage groups of the classical map, PO to the linkage group IV and NA being linked to the erythrocyte antigen CPPP. An informative family of 70 offspring was produced by mating a sire, heterozygous for each of the mutations, to 7 dams homozygous recessive for each locus. Three DNA pools were prepared, pool PO included 20 chicks exhibiting at least one extra-toe, pool NA included 20 non-polydactyly chicks showing the typical phenotype associated with heterozygosity for the naked neck mutation, and pool NP included 20 chicks exhibiting neither of the mutant phenotypes. Typings were done on an ABI-373 automatic sequencer with 147 microsatellite markers covering most of the genome. An unbalanced distribution of sire marker alleles were detected between pool PO, and pools NA and NP, for two markers of chromosome 2p, MCW0082 and MCW0247. A linkage analysis taking into account the incomplete penetrance of polydactyly (80%) was performed with additional markers of this region and showed that the closest marker to the PO locus was MCW0071 (5 cM, lod score = 9). MCW0071 lies within the engrailed gene EN2 in the chicken. In the mouse, the homologous gene maps on chromosome 5, close to the hemimelic extra-toes mutation Hx. In the case of the NA locus, markers of chromosome 3 were selected because CPPP was mapped on this chromosome. Analysis of individual typings showed a linkage of 5.7 cM (lod score = 13) between the NA locus and ADL0237 in the distal region of chromosome 3q. These results contribute to connecting the former classical map to the molecular genetic map of the chicken, and open the way to the identification of the molecular nature of two developmental mutations of the chicken that are known to occur in many breeds of chickens.