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Search Results: 1 - 10 of 15857 matches for " Tixier-Boichard Michèle "
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Estimation of genetic variability and selection response for clutch length in dwarf brown-egg layers carrying or not the naked neck gene
Chih-Feng Chen, Michèle Tixier-Boichard
Genetics Selection Evolution , 2003, DOI: 10.1186/1297-9686-35-2-219
Abstract: (To access the full article, please see PDF)
Genotype by environment interactions in relation to growth traits in slow growing chickens
N'Dri Aya,Sellier Nadine,Tixier-Boichard Michèle,Beaumont Catherine
Genetics Selection Evolution , 2007, DOI: 10.1186/1297-9686-39-5-513
Abstract: Since feed conversion ratio (FCR) is higher in slow-growing "Label Rouge" chickens than in broiler chickens, it is important to work on its improvement in this breed. However, this involves rearing animals in cages (C), an environment very different from that used for selection (in floor pens, S) and production (outdoor, E). The aim of this study was to evaluate the importance of genotype by environment (G × E) interactions between S, C, and E environments, to find the best way to select for FCR, using 2002 related animals. Growth curve parameters were estimated and body composition measured. Individual feed conversion ratios (FCR) were recorded between 8 and 10 weeks in C. The presence of G × E interactions was assessed by the genetic correlations between the same trait recorded in different environments. Moderate but significant G × E interactions were detected for carcass traits, a significant one was observed between E and S or C for growth curve parameters but none between C and S. If G × E interactions are set aside, i.e. selecting on traits recorded in C, abdominal fatness is the best indirect selection criterion for FCR but if they are taken in account then leg yield or growth curve parameters in S and growth curve parameters in E are better.
A single point-mutation within the melanophilin gene causes the lavender plumage colour dilution phenotype in the chicken
Mohsen Vaez, Sarah A Follett, Bertrand Bed'hom, David Gourichon, Michèle Tixier-Boichard, Terry Burke
BMC Genetics , 2008, DOI: 10.1186/1471-2156-9-7
Abstract: We have used a candidate-gene approach based on an expectation of homology with mammals to isolate a gene involved in pigmentation in chicken. Comparative sequence analysis of candidate genes in the chicken identified a strong association between a mutation in the MLPH gene and the diluted pigmentation phenotype. This mutation results in the amino acid change R35W, at a site also associated with similar phenotypes in mice, humans and cats.This is the first time that an avian species with a mutation in the MLPH gene has been reported.Lavender (LAV*L) is an autosomal recessive mutation of the chicken (Gallus gallus) affecting the neural crest derived melanocytes [1]. It causes the dilution of both eumelanin and phaeomelanin to a light grey or buff, respectively (Figure 1). Light and electron microscope studies have revealed that, although lavender melanocytes possess relatively normal dendrite morphology, there is defective peripheral accumulation of melanosomes to the dendrites [2]. This results in the patchy transfer of melanosomes into the keratinocytes of the growing feather. The dilution effect is essentially the result of a mixture of pigmented and unpigmented regions within the feather barbs. Although lavender melanocytes are defective in melanosomal translocation, they show no apparent ultrastructural defect in the microfilament system [2].Similar dilution effects can be seen in the mouse mutants dilute, ashen and leaden. The melanocytes of these mutants each display a similarly defective melanosomal transport system to that seen in lavender chickens, resulting in the patchy transfer of pigment to the keratinocytes of the hair. Dilute, ashen and leaden have been extensively studied and the process of peripheral accumulation of melanosomes has been shown to be controlled by an unconventional myosin, MYOVa [3], the ras-related GTPase RAB27a [4] and the Rab effector melanophilin (MLPH, also known as Slac-2) [5]. In humans, mutations in these genes have been ident
Complete association between a retroviral insertion in the tyrosinase gene and the recessive white mutation in chickens
Chung-Ming Chang, Jean-Luc Coville, Gérard Coquerelle, David Gourichon, Ahmad Oulmouden, Michèle Tixier-Boichard
BMC Genomics , 2006, DOI: 10.1186/1471-2164-7-19
Abstract: Molecular analysis of the chicken TYR gene has revealed a major structural difference (Restriction Fragment Length Polymorphism, RFLP) in the genomic DNA of the recessive white chicken. A major size difference of 7.7 kb was found in intron 4 of the TYR gene by long-range PCR. Molecular cloning and sequencing results showed the insertion of a complete avian retroviral sequence of the Avian Leukosis Virus (ALV) family. Several aberrant transcripts of the tyrosinase gene were found in 10 week old recessive white chickens but not in the homozygous wild type colored chicken. We established a rapid genotyping diagnostic test based on the discovery of this retroviral insertion. It shows that all homozygous carriers of this insertion had a white plumage in various chicken strains. Furthermore, it was possible to distinguish heterozygous carriers from homozygous normal chickens in a segregating line.In this study, we conclude that the insertion of a complete avian retroviral sequence in intron 4 of the tyrosinase gene is diagnostic of the recessive white mutation in chickens. This insertion causes aberrant transcripts lacking exon 5, and we propose that this insertion is the causal mutation for the recessive white allele in the chicken.In birds and mammals, pigmentation of the feather and fur is determined mainly by the distribution of two melanin pigments, eumelanin (black-brown pigment) and phaeomelanin (yellow-red pigment). The synthesis of both pigments depends on tyrosinase, the key enzyme in melanin biogenesis in pigment cells, which catalyzes tyrosine in the first two biochemical steps resulting in the production of dihydroxyphenylalanine (DOPA) and dopaquinone [1]. Tyrosinase also catalyses the subsequent step in the formation of eumelanin [2] with the dehydrogenation of 5,6-dihydroxyindole-2-carbonic acid (DHICA). Without a proper enzymatic function of tyrosinase, the melanin synthesis pathway is blocked or incomplete; the animals exhibit an albino phenotype. In hum
Performance comparison of dwarf laying hens segregating for the naked neck gene in temperate and subtropical environments
Chih-Feng Chen, David Gourichon, Nein-Zu Huang, Yen-Pai Lee, André Bordas, Michèle Tixier-Boichard
Genetics Selection Evolution , 2009, DOI: 10.1186/1297-9686-41-13
Abstract: In poultry selection programmes, birds are generally raised in a uniform environment to record the selected traits and evaluate genetic values. Thus, most commercial populations are obtained from breeding farms with a controlled environment and are delivered to production farms with variable environments across the world. As a consequence, genotype × environment (GxE) interactions may occur. Under subtropical environments, growth rate as well as egg production are generally depressed by high ambient temperature [1,2]. Introduction of some major genes, such as the naked neck (NA) gene, in chicken lines can be used to alleviate heat stress, as discussed in several studies carried out at high ambient temperatures [1,3-5]. Heat tolerance of laying hens is an important issue for the impact of G × E on egg production because the productive period is long and the impact of heat stress increases with the hens' age [6].At INRA, a selection experiment was undertaken to improve egg production of brown-egg layers by increasing clutch length, in the presence of two major genes known to improve heat tolerance, the naked neck gene [7] and the sex-linked dwarf gene [8]. After 16 generations, significant genetic progress on egg production was observed in two dwarf lines, one carrying the NA gene and one not carrying it [9-11]. The reduction of feather mass due to the NA gene is lower in heterozygous birds than in homozygous birds, i.e. 27% and 22% respectively for heterozygous females and males, and 41% and 33% respectively for homozygous females and males [12]. Heat tolerance is significantly improved by the presence of the NA gene and significant genotype by temperature interactions were observed for egg production, egg mass and feed intake under a 32°C constant temperature environment, which represents a severe temperature stress [3]. The purpose of this paper was to study the laying performance in real subtropical conditions of the genotypes obtained from the selection experimen
Mapping the Naked Neck (NA) and Polydactyly (PO) mutants of the chicken with microsatellite molecular markers
Frédérique Pitel, Régis Bergé, Gérard Coquerelle, Richard PMA Crooijmans, Martien AM Groenen, Alain Vignal, Michèle Tixier-Boichard
Genetics Selection Evolution , 2000, DOI: 10.1186/1297-9686-32-1-73
Abstract: (To access the full article, please see PDF)
Endogenous Retrovirus EAV-HP Linked to Blue Egg Phenotype in Mapuche Fowl
David Wragg, Joram M. Mwacharo, José A. Alcalde, Chen Wang, Jian-Lin Han, Jaime Gongora, David Gourichon, Michèle Tixier-Boichard, Olivier Hanotte
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071393
Abstract: Oocyan or blue/green eggshell colour is an autosomal dominant trait found in native chickens (Mapuche fowl) of Chile and in some of their descendants in European and North American modern breeds. We report here the identification of an endogenous avian retroviral (EAV-HP) insertion in oocyan Mapuche fowl and European breeds. Sequencing data reveals 100% retroviral identity between the Mapuche and European insertions. Quantitative real-time PCR analysis of European oocyan chicken indicates over-expression of the SLCO1B3 gene (P<0.05) in the shell gland and oviduct. Predicted transcription factor binding sites in the long terminal repeats (LTR) indicate AhR/Ar, a modulator of oestrogen, as a possible promoter/enhancer leading to reproductive tissue-specific over-expression of the SLCO1B3 gene. Analysis of all jungle fowl species Gallus sp. supports the retroviral insertion to be a post-domestication event, while identical LTR sequences within domestic chickens are in agreement with a recent de novo mutation.
Copy Number Variation in Intron 1 of SOX5 Causes the Pea-comb Phenotype in Chickens
Dominic Wright,Henrik Boije,Jennifer R. S. Meadows,Bertrand Bed'hom,David Gourichon,Agathe Vieaud,Michèle Tixier-Boichard,Carl-Johan Rubin,Freyja Imsland,Finn Hallb??k,Leif Andersson
PLOS Genetics , 2009, DOI: 10.1371/journal.pgen.1000512
Abstract: Pea-comb is a dominant mutation in chickens that drastically reduces the size of the comb and wattles. It is an adaptive trait in cold climates as it reduces heat loss and makes the chicken less susceptible to frost lesions. Here we report that Pea-comb is caused by a massive amplification of a duplicated sequence located near evolutionary conserved non-coding sequences in intron 1 of the gene encoding the SOX5 transcription factor. This must be the causative mutation since all other polymorphisms associated with the Pea-comb allele were excluded by genetic analysis. SOX5 controls cell fate and differentiation and is essential for skeletal development, chondrocyte differentiation, and extracellular matrix production. Immunostaining in early embryos demonstrated that Pea-comb is associated with ectopic expression of SOX5 in mesenchymal cells located just beneath the surface ectoderm where the comb and wattles will subsequently develop. The results imply that the duplication expansion interferes with the regulation of SOX5 expression during the differentiation of cells crucial for the development of comb and wattles. The study provides novel insight into the nature of mutations that contribute to phenotypic evolution and is the first description of a spontaneous and fully viable mutation in this developmentally important gene.
Epilepsy Caused by an Abnormal Alternative Splicing with Dosage Effect of the SV2A Gene in a Chicken Model
Marine Douaud, Katia Feve, Fabienne Pituello, David Gourichon, Simon Boitard, Eric Leguern, Gérard Coquerelle, Agathe Vieaud, Cesira Batini, Robert Naquet, Alain Vignal, Michèle Tixier-Boichard, Frédérique Pitel
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026932
Abstract: Photosensitive reflex epilepsy is caused by the combination of an individual's enhanced sensitivity with relevant light stimuli, such as stroboscopic lights or video games. This is the most common reflex epilepsy in humans; it is characterized by the photoparoxysmal response, which is an abnormal electroencephalographic reaction, and seizures triggered by intermittent light stimulation. Here, by using genetic mapping, sequencing and functional analyses, we report that a mutation in the acceptor site of the second intron of SV2A (the gene encoding synaptic vesicle glycoprotein 2A) is causing photosensitive reflex epilepsy in a unique vertebrate model, the Fepi chicken strain, a spontaneous model where the neurological disorder is inherited as an autosomal recessive mutation. This mutation causes an aberrant splicing event and significantly reduces the level of SV2A mRNA in homozygous carriers. Levetiracetam, a second generation antiepileptic drug, is known to bind SV2A, and SV2A knock-out mice develop seizures soon after birth and usually die within three weeks. The Fepi chicken survives to adulthood and responds to levetiracetam, suggesting that the low-level expression of SV2A in these animals is sufficient to allow survival, but does not protect against seizures. Thus, the Fepi chicken model shows that the role of the SV2A pathway in the brain is conserved between birds and mammals, in spite of a large phylogenetic distance. The Fepi model appears particularly useful for further studies of physiopathology of reflex epilepsy, in comparison with induced models of epilepsy in rodents. Consequently, SV2A is a very attractive candidate gene for analysis in the context of both mono- and polygenic generalized epilepsies in humans.
The Crest Phenotype in Chicken Is Associated with Ectopic Expression of HOXC8 in Cranial Skin
Yanqiang Wang, Yu Gao, Freyja Imsland, Xiaorong Gu, Chungang Feng, Ranran Liu, Chi Song, Michèle Tixier-Boichard, David Gourichon, Qingyuan Li, Kuanwei Chen, Huifang Li, Leif Andersson, Xiaoxiang Hu, Ning Li
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034012
Abstract: The Crest phenotype is characterised by a tuft of elongated feathers atop the head. A similar phenotype is also seen in several wild bird species. Crest shows an autosomal incompletely dominant mode of inheritance and is associated with cerebral hernia. Here we show, using linkage analysis and genome-wide association, that Crest is located on the E22C19W28 linkage group and that it shows complete association to the HOXC-cluster on this chromosome. Expression analysis of tissues from Crested and non-crested chickens, representing 26 different breeds, revealed that HOXC8, but not HOXC12 or HOXC13, showed ectopic expression in cranial skin during embryonic development. We propose that Crest is caused by a cis-acting regulatory mutation underlying the ectopic expression of HOXC8. However, the identification of the causative mutation(s) has to await until a method becomes available for assembling this chromosomal region. Crest is unfortunately located in a genomic region that has so far defied all attempts to establish a contiguous sequence.
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