Project description:A deletion mutation in the growth hormone receptor (GHR) gene results in the inhibition of skeletal muscle growth and fat deposition in dwarf chickens. In this study, microarray techniques were used to detect the miRNA and mRNA expression profiles of 14-day-old embryo and 7-week-old chicken skeletal muscle of deletion-type dwarf chickens and normal-type chickens. Skeletal muscle tissues of Dwarf recessive White Rock chickens and normal recessive White Rock chickens were used to make the microarray assay. Results show the expression of miR-1623 and miR-181b in 14-day-old embryos and of let-7b and miR-128 in 7-week-old chickens. let-7b was the only miRNA found to be completely complementary to its target in the 3'UTR of GHR and inhibited GHR gene expression. KEGG (Kyoto Encyclopaedia of Genes and Genomes) pathway analysis and RT-PCR verified that there were three main signalling pathways regulating the skeletal muscle growth and fat deposition of chickens influenced by the let-7b-regulated GHR gene. The suppression of the cytokine signalling 3 (SOCS3) gene was found to be involved in the signalling pathway of adipocytokines. We found that let-7b is the critical miRNA involved in the regulation of the GHR gene. SOCS3 plays a critical role in the network regulating skeletal muscle growth and fat deposition via let-7b-mediated GHR gene expression. Two groups were analyzed in the array assay: one group consisted of normal recessive White Rock 14-day-old embryo leg muscle tissues, and the other group consisted of dwarf recessive White Rock 14-day-old embryo leg muscle tissues. The control samples were labeled as A1, A2, A3, and the dwarf chicken samples were labeled as B1, B2, and B3. 9 total embryos per breed, 3 embryos used per breed for each sample. 523 mature miRNA sequences were assembled and integrated into the LC miRNA microarray design, and different expression miRNAs were measured on the 7000HT Fast Real-Time PCR system. This submission represents the miRNA profiling component of the study.
Project description:A deletion mutation in the growth hormone receptor (GHR) gene results in the inhibition of skeletal muscle growth and fat deposition in dwarf chickens. In this study, microarray techniques were used to detect the miRNA and mRNA expression profiles of 14-day-old embryo and 7-week-old chicken skeletal muscle of deletion-type dwarf chickens and normal-type chickens. Skeletal muscle tissues of Dwarf recessive White Rock chickens and normal recessive White Rock chickens were used to make the microarray assay. Results show the expression of miR-1623 and miR-181b in 14-day-old embryos and of let-7b and miR-128 in 7-week-old chickens. let-7b was the only miRNA found to be completely complementary to its target in the 3'UTR of GHR and inhibited GHR gene expression. KEGG (Kyoto Encyclopaedia of Genes and Genomes) pathway analysis and RT-PCR verified that there were three main signalling pathways regulating the skeletal muscle growth and fat deposition of chickens influenced by the let-7b-regulated GHR gene. The suppression of the cytokine signalling 3 (SOCS3) gene was found to be involved in the signalling pathway of adipocytokines. We found that let-7b is the critical miRNA involved in the regulation of the GHR gene. SOCS3 plays a critical role in the network regulating skeletal muscle growth and fat deposition via let-7b-mediated GHR gene expression. Two groups were analyzed in the array assay: one group consisted of normal recessive White Rock 7-week-old chicken leg muscle tissues, and the other group consisted of dwarf recessive White Rock 7-week-old chicken leg muscle tissues. The control samples were labeled as A1b, A2b, A3b, and the dwarf chicken samples were labeled as B1b, B2b, and B3b. 9 total chickens per breed, 3 chickens used per breed for each sample. 523 mature miRNA sequences were assembled and integrated into the LC miRNA microarray design, and different expression miRNAs were measured on the 7000HT Fast Real-Time PCR system. REPLACE This submission represents the miRNA profiling component of the study.
Project description:The aim of this study was to identify genes involved in the variation of the muscle glycogen content at death (estimated through the glycolytic potential, GP), a determining factor of meat quality in chicken. Gene expression profiles of Pectoralis major muscle were established using microarrays. We compared Fat and Lean chickens issued from two lines divergently selected for abdominal fatness and also differed for muscle GP. A total of 197 genes were differentially expressed between Fat and Lean pure chickens. Several of these genes were validated by qRT-PCR. For the genes with human orthologs, annotation analyses were performed and mainly revealed pathways involved carbohydrate, fatty-acid, and protein metabolism. The relationship between gene expression and meat quality has to now be validated by further e-QTL studies on the F2 population. 8 samples from Fat chickens were compared to 8 samples from Lean chickens, 4 of these were dye-swapped.
Project description:To better understand the hepatic metabolic response to intermittent fasting in chickens, Red Junglefowl chickens were raised on ad libitum (AL) feed until 14 days of age and then kept on AL feeding, switched to chronic feed restriction (CR) to around 70% or switched to an intermittent fasting (IF) regimen consisting of two fed days (150% of age-matched weight-specific AL intake offered daily) followed by a non-fed day. AL and CR were culled at 36 days of age, and IF birds either at 40 days of age (second consecutive feeding day) or 41 days of age (fasting day).
Project description:To generate epi-lines, two third-generation msh1 T-DNA mutant (SAIL_877_F01) plants were used to pollinate Col-0 to generate two independent F1 populations. Derived F1 progenies were self-pollinated to generate F2 populations that were genotyped for the msh1 T-DNA mutation. MSH1 F2 plants were self-pollinated to produce F3 families that were used in the study.
Project description:To generate epi-lines, two third-generation msh1 T-DNA mutant (SAIL_877_F01) plants were used to pollinate Col-0 to generate two independent F1 populations. Derived F1 progenies were self-pollinated to generate F2 populations that were genotyped for the msh1 T-DNA mutation. MSH1 F2 plants were self-pollinated to produce F3 families that were used in the study.
Project description:A deletion mutation in the growth hormone receptor (GHR) gene results in the inhibition of skeletal muscle growth and fat deposition in dwarf chickens. In this study, microarray techniques were used to detect the miRNA and mRNA expression profiles of 14-day-old embryo and 7-week-old chicken skeletal muscle of deletion-type dwarf chickens and normal-type chickens. Skeletal muscle tissues of Dwarf recessive White Rock chickens and normal recessive White Rock chickens were used to make the microarray assay. Results show the expression of miR-1623 and miR-181b in 14-day-old embryos and of let-7b and miR-128 in 7-week-old chickens. let-7b was the only miRNA found to be completely complementary to its target in the 3'UTR of GHR and inhibited GHR gene expression. KEGG (Kyoto Encyclopaedia of Genes and Genomes) pathway analysis and RT-PCR verified that there were three main signalling pathways regulating the skeletal muscle growth and fat deposition of chickens influenced by the let-7b-regulated GHR gene. The suppression of the cytokine signalling 3 (SOCS3) gene was found to be involved in the signalling pathway of adipocytokines. We found that let-7b is the critical miRNA involved in the regulation of the GHR gene. SOCS3 plays a critical role in the network regulating skeletal muscle growth and fat deposition via let-7b-mediated GHR gene expression.