Hepatic lipogenesis gene expression in two experimental egg-laying lines divergently selected on residual food consumption

Two Rhode Island Red egg-laying lines have been divergently selected on residual food intake (low intake R- line, high intake R+ line) for 19 generations. In addition to direct response, correlated responses have altered several other traits such as carcass adiposity and lipid contents of several tissues, the R+ animals being leaner than the R- ones. In a search for the biological origin of the differences observed in fat deposit, the hepatic mRNA amounts of genes involved in lipid metabolism were investigated. No difference was found between lines for mRNA levels of ATP citrate-lyase, acetyl-CoA carboxylase, fatty acid synthase, malic enzyme and CCAAT/enhancer binding protein α, a transcription factor acting on several lipogenesis genes. The genes coding for stearoyl-CoA desaturase and apolipoprotein A1 displayed significantly lower mRNA levels in the R+ cockerels compared to the R-. All together these mRNA levels explained 40% of the overall variability of abdominal adipose tissue weight, suggesting an important role of both genes in the fatness variability

Messenger RNA levels and transcription rates of hepatic lipogenesis genes in genetically lean and fat chickens

Levels of body fat content in commercial meat chickens have prompted research in order to control the development of this trait. Based on experimentally selected divergent lean and fat lines, many studies have shown that liver metabolism has a major role in the fatness variability. In order to identify which genes are involved in this variability, we investigated the expression of several genes implicated in the hepatic lipid metabolism. The studied genes code for enzymes of fatty acid synthesis [ATP citrate-lyase (ACL), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), malic enzyme (ME), stearoyl-CoA desaturase (SCD1)], for an apolipoprotein [apolipoprotein A1 (APOA1)], and for the CCAAT/enhancer binding protein α (C/EBPα), which is a transcription factor implied in the regulation of several genes of lipid metabolism. The results show that the fat-line chickens display significantly higher hepatic transcription rates and mRNA levels than the lean-line chickens for the ACL, ME and APOA1 genes. This suggests that these genes could be responsible for the phenotypic fatness variability

Using transcriptome profiling to characterize QTL regions on chicken chromosome 5

<p>Abstract</p> <p>Background</p> <p>Although many QTL for various traits have been mapped in livestock, location confidence intervals remain wide that makes difficult the identification of causative mutations. The aim of this study was to test the contribution of microarray data to QTL detection in livestock species. Three different but complementary approaches are proposed to improve characterization of a chicken QTL region for abdominal fatness (AF) previously detected on chromosome 5 (GGA5).</p> <p>Results</p> <p>Hepatic transcriptome profiles for 45 offspring of a sire known to be heterozygous for the distal GGA5 AF QTL were obtained using a 20 K chicken oligochip. mRNA levels of 660 genes were correlated with the AF trait. The first approach was to dissect the AF phenotype by identifying animal subgroups according to their 660 transcript profiles. Linkage analysis using some of these subgroups revealed another QTL in the middle of GGA5 and increased the significance of the distal GGA5 AF QTL, thereby refining its localization. The second approach targeted the genes correlated with the AF trait and regulated by the GGA5 AF QTL region. Five of the 660 genes were considered as being controlled either by the AF QTL mutation itself or by a mutation close to it; one having a function related to lipid metabolism (HMGCS1). In addition, a QTL analysis with a multiple trait model combining this 5 gene-set and AF allowed us to refine the QTL region. The third approach was to use these 5 transcriptome profiles to predict the paternal Q versus q AF QTL mutation for each recombinant offspring and then refine the localization of the QTL from 31 cM (100 genes) at a most probable location confidence interval of 7 cM (12 genes) after determining the recombination breakpoints, an interval consistent with the reductions obtained by the two other approaches.</p> <p>Conclusion</p> <p>The results showed the feasibility and efficacy of the three strategies used, the first revealing a QTL undetected using the whole population, the second providing functional information about a QTL region through genes related to the trait and controlled by this region (HMGCS1), the third could drastically refine a QTL region.</p

A high-resolution radiation hybrid map of chicken chromosome 5 and comparison with human chromosomes

BACKGROUND: The resolution of radiation hybrid (RH) maps is intermediate between that of the genetic and BAC (Bacterial Artificial Chromosome) contig maps. Moreover, once framework RH maps of a genome have been constructed, a quick location of markers by simple PCR on the RH panel is possible. The chicken ChickRH6 panel recently produced was used here to construct a high resolution RH map of chicken GGA5. To confirm the validity of the map and to provide valuable comparative mapping information, both markers from the genetic map and a high number of ESTs (Expressed Sequence Tags) were used. Finally, this RH map was used for testing the accuracy of the chicken genome assembly for chromosome 5. RESULTS: A total of 169 markers (21 microsatellites and 148 ESTs) were typed on the ChickRH6 RH panel, of which 134 were assigned to GGA5. The final map is composed of 73 framework markers extending over a 1315.6 cR distance. The remaining 61 markers were placed alongside the framework markers within confidence intervals. CONCLUSION: The high resolution framework map obtained in this study has markers covering the entire chicken chromosome 5 and reveals the existence of a high number of rearrangements when compared to the human genome. Only two discrepancies were observed in relation to the sequence assembly recently reported for this chromosome

Transcriptome profiling of the feeding-to-fasting transition in chicken liver

<p>Abstract</p> <p>Background</p> <p>Starvation triggers a complex array of adaptative metabolic responses including energy-metabolic responses, a process which must imply tissue specific alterations in gene expression and in which the liver plays a central role. The present study aimed to describe the evolution of global gene expression profiles in liver of 4-week-old male chickens during a 48 h fasting period using a chicken 20 K oligoarray.</p> <p>Results</p> <p>A large number of genes were modulated by fasting (3532 genes with a pvalue corrected by Benjamini-Hochberg < 0.01); 2062 showed an amplitude of variation higher than +/- 40% among those, 1162 presented an human ortholog, allowing to collect functional information. Notably more genes were down-regulated than up-regulated, whatever the duration of fasting (16 h or 48 h). The number of genes differentially expressed after 48 h of fasting was 3.5-fold higher than after 16 h of fasting. Four clusters of co-expressed genes were identified by a hierarchical cluster analysis. Gene Ontology, KEGG and Ingenuity databases were then used to identify the metabolic processes associated to each cluster. After 16 h of fasting, genes involved in ketogenesis, gluconeogenesis and mitochondrial or peroxisomal fatty acid beta-oxidation, were up-regulated (cluster-1) whereas genes involved in fatty acid and cholesterol synthesis were down-regulated (cluster-2). For all genes tested, the microarray data was confirmed by quantitative RT-PCR. Most genes were altered by fasting as already reported in mammals. A notable exception was the <it>HMG-CoA synthase 1 </it>gene, which was up-regulated following 16 and 48 h of fasting while the other genes involved in cholesterol metabolism were down-regulated as reported in mammalian studies. We further focused on genes not represented on the microarray and candidates for the regulation of the target genes belonging to cluster-1 and -2 and involved in lipid metabolism. Data are provided concerning PPARa, SREBP1, SREBP2, NR1H3 transcription factors and two desaturases (FADS1, FADS2).</p> <p>Conclusion</p> <p>This study evidences numerous genes altered by starvation in chickens and suggests a global repression of cellular activity in response to this stressor. The central role of lipid and acetyl-CoA metabolisms and its regulation at transcriptional level are confirmed in chicken liver in response to short-term fasting. Interesting expression modulations were observed for <it>NR1H3, FADS1 </it>and <it>FADS2 </it>genes. Further studies are needed to precise their role in the complex regulatory network controlling lipid metabolism.</p