RESUMEN
Excessive adiposity has become a major drawback in meat-type chicken production. However, few studies were conducted to analyze the liver expression of genes involved in pathways and mechanisms leading to adiposity. A previous study performed by differential display on RNAs extracted from chicken livers from lean and fat lines allowed us to isolate cDNA products of genes with putative differential expression. In this study, a cDNA microarray resource was developed from these products together with cDNAs from genes involved in or related to lipid metabolism. This resource was used to analyze gene expression in the liver from lean and fat chickens. Some genes were found with a difference in expression between lean and fat animals and/or correlated to adipose tissue weight. Cytochrome P450 2C45, thought to play a role in biotransformation of steroids and poly-unsaturated fatty acids, was more expressed in lean chickens whereas fatty acid synthase, stearoyl-CoA desaturase, sterol response element binding factor 1 and hepatocyte nuclear factor 4, respectively involved in lipogenesis and its regulation, were more expressed in fat chickens. These results indicate that mechanisms involved in the expression and regulation of lipogenic genes could play a key role in fatness ontogenesis in chickens from lean and fat lines.
Asunto(s)
Adiposidad/genética , Pollos/genética , Perfilación de la Expresión Génica , Hígado/metabolismo , Análisis de Secuencia por Matrices de Oligonucleótidos , Delgadez/genética , Animales , Regulación hacia Abajo/genética , Masculino , ARN Mensajero/genética , ARN Mensajero/metabolismo , Reproducibilidad de los Resultados , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Regulación hacia Arriba/genéticaRESUMEN
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 cR(6000) on the RH map.
Asunto(s)
Pollos/genética , Cromosomas/genética , Mapeo de Híbrido por Radiación , Animales , Secuencia de Bases , Biología Computacional , Cartilla de ADN , Etiquetas de Secuencia Expresada , Orden Génico , Marcadores Genéticos/genética , Humanos , Repeticiones de Microsatélite/genética , Datos de Secuencia Molecular , Alineación de Secuencia , Análisis de Secuencia de ADNRESUMEN
To identify the genes directly responsible, through DNA polymorphism, for the difference in fatness observed between a lean and a fat chicken line, we studied five genes (ACL, ACC, FAS, ME, SCD1) encoding key enzymes involved in liver fatty acid synthesis and secretion. Genetic linkage was tested between polymorphic sites in the genes and the fatness trait segregating in an F2 design obtained by inter-crossing the two fat and lean lines. Despite a confirmation of a higher mRNA level in the fat birds, no genetic linkage of the gene alleles with the phenotype could be found. As a test of the implication of upstream regulatory transcription factors, SREPB genes were also studied. The lack of genetic linkage of SREBP genes with fatness shows that these genes are not directly responsible through polymorphism for fatness variability in our model. Moreover, the similar SREBP mRNA levels observed between the two lines led us to exclude also transcriptional factors regulating the two SREBP genes as being directly responsible for fatness variability. However, the genes involved in post-translational modifications of SREBPs remain candidates to investigate. These results emphasised the interest to perform expression and genetic linkage studies jointly, to progress in identifying the genetic origin of variability of a quantitative trait.
