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1.
Poult Sci ; 93(5): 1067-75, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24795298

RESUMEN

The improved genetic potential of contemporary commercial broilers cannot be fully expressed under hot conditions that depress growth rate, decrease breast meat yield, and reduce meat quality. The negative heat effects are attributed to the insulating feather coverage, which, under high ambient temperatures (AT), hinders dissipation of the excessive internally produced heat. Accordingly, featherless broilers (sc/sc), their feathered sibs (+/sc), and contemporary broilers (+/+) were subjected to control AT (26°C) and hot AT (32°C) to test the hypothesis that lack of feathers contributes to higher breast muscle yield and better meat quality, especially under hot conditions, and that differences related to lack of feathers are related to cardiovascular capacity. In 2 similar trials, the superior genetic background of the contemporary broilers was manifested under control conditions; their mean BW was about 15% higher than the means of the featherless broilers and their feathered sibs. The hot conditions depressed BW of the 2 feathered groups by approximately 25%, with hardly any effect on featherless broiler BW. Breast meat yield (% of BW) in the featherless broilers was higher than in those with feathers, especially under the hot AT. Furthermore, the featherless broilers were characterized by superior meat quality as indicated by lower drip loss, lower lightness, and higher redness. The superior meat quality of the featherless broilers could be explained by their larger hearts and higher hematocrit values, suggesting superior cardiovascular capacity to supply oxygen and nutrients to the breast muscles. On the practical side, the results clearly indicate that modern featherless broilers can reach normal BW, as well as yield and quality of breast meat, under hot conditions as well. It appears that broiler meat production in hot regions and climates can be substantially improved by introducing the featherless gene into contemporary commercial broiler stocks. This has become more feasible since the recent development of a simple DNA test to identify carriers of the recessive sc mutation.


Asunto(s)
Crianza de Animales Domésticos/métodos , Pollos/fisiología , Plumas/fisiología , Carne/análisis , Músculos Pectorales/fisiología , Animales , Fenómenos Fisiológicos Cardiovasculares , Pollos/crecimiento & desarrollo , Femenino , Calor , Masculino , Carne/normas , Músculos Pectorales/crecimiento & desarrollo , Distribución Aleatoria
2.
Poult Sci ; 93(5): 1076-88, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24795299

RESUMEN

Breast meat yield (% of BW) of featherless broilers (sc/sc) is higher than that of their feathered sibs (+/sc) and contemporary broilers (+/+) under hot temperature (32°C) conditions. This study tested the hypothesis that the advantage to the featherless broiler condition with respect to breast meat yield and quality is due to differences in muscle development during pre- and posthatch periods. Broilers from the 3 genetic groups were reared under normal (26°C) and hot (32°C) conditions and slaughtered on d 29 and 47. Evaluation of myofiber diameter (mean and distribution) and blood-vessel density in breast muscle sections sampled on these days revealed that the fluctuations in breast muscle yields of the different genetic groups under different temperature conditions and the better muscle growth of the featherless broilers are due to changes in muscle hypertrophy and vascularization. In addition, the featherless broilers presented continuous satellite cell proliferation and a slower rate of differentiation compared with the feathered broilers on immediate posthatch period, suggesting a higher reserve of myogenic progeny cells that will contribute to later muscle hypertrophy. In the embryos, breast muscle yield was higher for the featherless versus feathered counterparts between embryonic day (E) 15 and E20. This was manifested in a shift toward higher myofiber diameters in the featherless embryos on E18, and a higher number of myoblasts, which could be explained by higher insulin-like growth factor-I levels in the muscle tissue and lower triiodothyronine levels in the plasma on E17. Together, the data show the advantage of being featherless under hot conditions with regard to breast muscle growth and hypertrophy, and overall performance. Moreover, featherless embryos had increased breast muscle weight compared with their feathered counterparts, likely due to a higher proliferation rate of myoblasts and higher muscle hypertrophy.


Asunto(s)
Crianza de Animales Domésticos/métodos , Pollos/crecimiento & desarrollo , Plumas/fisiología , Fibras Musculares Esqueléticas/citología , Fibras Musculares Esqueléticas/fisiología , Músculos Pectorales/crecimiento & desarrollo , Animales , Proliferación Celular , Embrión de Pollo/citología , Embrión de Pollo/crecimiento & desarrollo , Pollos/anatomía & histología , Femenino , Calor , Masculino
3.
BMC Genomics ; 13: 257, 2012 Jun 19.
Artículo en Inglés | MEDLINE | ID: mdl-22712610

RESUMEN

BACKGROUND: Scaleless (sc/sc) chickens carry a single recessive mutation that causes a lack of almost all body feathers, as well as foot scales and spurs, due to a failure of skin patterning during embryogenesis. This spontaneous mutant line, first described in the 1950s, has been used extensively to explore the tissue interactions involved in ectodermal appendage formation in embryonic skin. Moreover, the trait is potentially useful in tropical agriculture due to the ability of featherless chickens to tolerate heat, which is at present a major constraint to efficient poultry meat production in hot climates. In the interests of enhancing our understanding of feather placode development, and to provide the poultry industry with a strategy to breed heat-tolerant meat-type chickens (broilers), we mapped and identified the sc mutation. RESULTS: Through a cost-effective and labour-efficient SNP array mapping approach using DNA from sc/sc and sc/+ blood sample pools, we map the sc trait to chromosome 4 and show that a nonsense mutation in FGF20 is completely associated with the sc/sc phenotype. This mutation, common to all sc/sc individuals and absent from wild type, is predicted to lead to loss of a highly conserved region of the FGF20 protein important for FGF signalling. In situ hybridisation and quantitative RT-PCR studies reveal that FGF20 is epidermally expressed during the early stages of feather placode patterning. In addition, we describe a dCAPS genotyping assay based on the mutation, developed to facilitate discrimination between wild type and sc alleles. CONCLUSIONS: This work represents the first loss of function genetic evidence supporting a role for FGF ligand signalling in feather development, and suggests FGF20 as a novel central player in the development of vertebrate skin appendages, including hair follicles and exocrine glands. In addition, this is to our knowledge the first report describing the use of the chicken SNP array to map genes based on genotyping of DNA samples from pooled whole blood. The identification of the sc mutation has important implications for the future breeding of this potentially useful trait for the poultry industry, and our genotyping assay can facilitate its rapid introgression into production lines.


Asunto(s)
Pollos/genética , Codón sin Sentido/genética , ADN/genética , Plumas/crecimiento & desarrollo , Factores de Crecimiento de Fibroblastos/genética , Genoma/genética , Polimorfismo de Nucleótido Simple/genética , Secuencia de Aminoácidos , Animales , Secuencia de Bases , Cruzamiento , Pollos/crecimiento & desarrollo , Mapeo Cromosómico , Análisis Mutacional de ADN , Factores de Crecimiento de Fibroblastos/química , Genotipo , Datos de Secuencia Molecular , Fenotipo
4.
Am J Hum Genet ; 86(2): 273-8, 2010 Feb 12.
Artículo en Inglés | MEDLINE | ID: mdl-20137772

RESUMEN

Human disorders of phosphate (Pi) handling and hypophosphatemic rickets have been shown to result from mutations in PHEX, FGF23, and DMP1, presenting as X-linked recessive, autosomal-dominant, and autosomal-recessive patterns, respectively. We present the identification of an inactivating mutation in the ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) gene causing autosomal-recessive hypophosphatemic rickets (ARHR) with phosphaturia by positional cloning. ENPP1 generates inorganic pyrophosphate (PPi), an essential physiologic inhibitor of calcification, and previously described inactivating mutations in this gene were shown to cause aberrant ectopic calcification disorders, whereas no aberrant calcifications were present in our patients. Our surprising result suggests a different pathway involved in the generation of ARHR and possible additional functions for ENPP1.


Asunto(s)
Raquitismo Hipofosfatémico Familiar/enzimología , Raquitismo Hipofosfatémico Familiar/genética , Silenciador del Gen , Genes Recesivos/genética , Enfermedades Genéticas Ligadas al Cromosoma X , Predisposición Genética a la Enfermedad , Mutación/genética , Hidrolasas Diéster Fosfóricas/genética , Pirofosfatasas/genética , Adolescente , Adulto , Secuencia de Aminoácidos , Secuencia de Bases , Secuencia Conservada , Factor-23 de Crecimiento de Fibroblastos , Humanos , Datos de Secuencia Molecular , Hidrolasas Diéster Fosfóricas/química , Polimorfismo de Nucleótido Simple/genética , Pirofosfatasas/química , Adulto Joven
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