Bos taurus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA95961 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Myostatin is a highly conserved Transforming Growth Factor beta family member which negatively regulates muscle development. Double-muscled (DM) cattle have a loss-of-function mutation in their myostatin gene responsible for a hypermuscular phenotype mainly due to hyperplasia. Thus these animals represent a good model for understanding the mechanisms at the origin of muscular hypertrophy. In order to identify individual genes or networks that may be myostatin targets, we looked for genes differentially expressed between DM and normal (NM) animals (n=3 per group) in the semitendinosus muscle (a hypertrophied muscle in DM animals) at 260 days of fetal development (intensive muscle biochemical differentiation). The experiment was carried out using muscle-dedicated high density oligonucleotide arrays of around 6,000 muscle specific genes. A great number of genes was found to be differentially expressed according to the genetic type (some with a change higher than 5-fold), and according to the zygosity of the myostatin mutation. They belonged to various functional categories. The genes down-regulated in DM fetuses corresponded mainly to genes encoding extracellular matrix proteins, slow contractile proteins and ribosomal proteins. On the other hand, the genes up-regulated in DM fetuses were involved mainly in the regulation of transcription, cell cycle/apoptosis, translation, or DNA metabolism. These data singled out features indicating that DM muscle had shifted towards a more glycolytic metabolism, had an altered extracellular matrix composition (e.g. down-regulation of COL1A1, COL1A2, and up-regulation of collagen IV) and a decreased adipocyte differentiation (down-regulation of C1QTNF3). Altered gene expression in the three major muscle compartments (e.g. fibers, connective tissue and intramuscular adipose tissue) is in agreement with the well known characteristics of DM cattle. In addition, novel potential targets of the myostatin gene were identifed. Thus, the myostatin loss-of-function mutation affected several physiological processes involved in the development and the determinism of the functional characteristics of the muscle tissue. Keywords: Double-muscled, myostatin loss-of-function, bovine fetuses
2007-07-17 | GSE5456 | GEO
Project description:Myostatin is a highly conserved Transforming Growth Factor beta family member which negatively regulates muscle development. Double-muscled (DM) cattle have a loss-of-function mutation in their myostatin gene responsible for a hypermuscular phenotype mainly due to hyperplasia. Thus these animals represent a good model for understanding the mechanisms at the origin of muscular hypertrophy. In order to identify individual genes or networks that may be myostatin targets, we looked for genes differentially expressed between DM and normal (NM) animals (n=3 per group) in the semitendinosus muscle (a hypertrophied muscle in DM animals) at 260 days of fetal development (intensive muscle biochemical differentiation). The experiment was carried out using muscle-dedicated high density oligonucleotide arrays of around 6,000 muscle specific genes. A great number of genes was found to be differentially expressed according to the genetic type (some with a change higher than 5-fold), and according to the zygosity of the myostatin mutation. They belonged to various functional categories. The genes down-regulated in DM fetuses corresponded mainly to genes encoding extracellular matrix proteins, slow contractile proteins and ribosomal proteins. On the other hand, the genes up-regulated in DM fetuses were involved mainly in the regulation of transcription, cell cycle/apoptosis, translation, or DNA metabolism. These data singled out features indicating that DM muscle had shifted towards a more glycolytic metabolism, had an altered extracellular matrix composition (e.g. down-regulation of COL1A1, COL1A2, and up-regulation of collagen IV) and a decreased adipocyte differentiation (down-regulation of C1QTNF3). Altered gene expression in the three major muscle compartments (e.g. fibers, connective tissue and intramuscular adipose tissue) is in agreement with the well known characteristics of DM cattle. In addition, novel potential targets of the myostatin gene were identifed. Thus, the myostatin loss-of-function mutation affected several physiological processes involved in the development and the determinism of the functional characteristics of the muscle tissue. Transcriptomic profiling of Semitendinosus (ST) muscle of three double-muscled fetuses were analyzed relative to three conventional fetuses. Each individual sample was compared to a reference pool. Four chips were hybridized per sample comparison.
2010-07-01 | E-GEOD-5456 | biostudies-arrayexpress
Project description:With regulatory roles in development, cell proliferation and disease, micro-RNA (miRNA) biology is of great importance and a potential key to novel RNA-based therapeutic regimens. Biochemically based sequencing approaches have provided robust means of uncovering miRNA binding landscapes on transcriptomes of various species. However, a current limitation to the therapeutic potential of miRNA biology in cattle is the lack of validated miRNAs targets. Here, we use cross-linking immunoprecipitation (CLIP) of the Argonaute (AGO) proteins and unambiguous miRNA-target identification through RNA chimeras to define a regulatory map of miRNA interactions in the cow (Bos taurus). The resulting interactome is the deepest reported to date for any species, demonstrating that comprehensive maps can be empirically obtained. We observe that bovine miRNA targeting principles are consistent with those observed in other mammals. Motif and structural analyses define expanded pairing rules with most interactions combining seed-based pairing with distinct, miRNA-specific patterns of auxiliary pairing. Further, miRNA-target chimeras had predictive value in evaluating true regulatory sites of the miR-17 family. Finally, we define miRNA-specific targeting for >5000 mRNAs and determine gene ontologies (GO) for these targets. This confirmed repression of genes important for embryonic development and cell cycle progress by the let-7 family, and repression of those involved in cell cycle arrest by the miR-17 family, but it also suggested a number of unappreciated miRNA functions. Our results provide a significant resource for transcriptomic understanding of bovine miRNA regulation, and demonstrate the power of experimental methods for establishing comprehensive interaction maps.
2017-07-11 | GSE90089 | GEO
Project description:The Transcriptional Landscape of Bovine Skeletal Muscle
| PRJNA134273 | ENA
Project description:Comparison of gene expression profile of bovine muscle samples
| PRJNA136767 | ENA
Project description:Comparison of transcriptome of in vitro and in vivo-produced bovine fetuses specifically in liver and placental tissues.
| PRJNA140705 | ENA
Project description:Inhibition of myostatin signaling induces strong skeletal muscle growth making it an attractive target to treat muscle wasting and sarcopenia. However, the biological function of myostatin in the heart is barely understood. We demonstrate that conditional inactivation of myostatin in the adult murine heart leads to cardiac hypertrophy, heart failure and increased lethality. To induce cardiomyocyte specific loss of myostatin a conditionally active Mstn^fl/fl allele was generated by insertion of loxP elements upstream and downstream of exons 1 and 2 of the mouse myostatin gene. The selection cassette was removed in vivo by flp-recombination. To inactivate myostatin, mice were mated to alphaMyHC-MCM mice (Sohal, DS, et al. (2001) Circulation Research 89, 20-25). Cre-recombination was achieved by intraperitoneal administration of Tamoxifen (40 mg/kg) for 5 consecutive days. The respective control alphaMyHC-MCM animals were equally treated.
2014-05-16 | E-MEXP-3744 | biostudies-arrayexpress
Project description:Genome-Wide Landscapes of DNA Methylomes in Bovine Muscle Tissue
| PRJNA200698 | ENA