Dataset Information

Target genes of myostatin loss-of-function in muscles of late bovine fetuses.

ABSTRACT: BACKGROUND: Myostatin, a muscle-specific member of the Transforming Growth Factor beta family, negatively regulates muscle development. Double-muscled (DM) cattle have a loss-of-function mutation in their myostatin gene responsible for the hypermuscular phenotype. Thus, these animals are a good model for understanding the mechanisms underpinning muscular hypertrophy. In order to identify individual genes or networks that may be myostatin targets, we looked for genes that were differentially expressed between DM and normal (NM) animals (n = 3 per group) in the semitendinosus muscle (hypertrophied in DM animals) at 260 days of fetal development (when the biochemical differentiation of muscle is intensive). A heterologous microarray (human and murine oligonucleotide sequences) of around 6,000 genes expressed in muscle was used. RESULTS: Many genes were found to be differentially expressed according to genetic type (some with a more than 5-fold change), and according to the presence of one or two functional myostatin allele(s). They belonged to various functional categories. The genes down-regulated in DM fetuses were mainly those encoding extracellular matrix proteins, slow contractile proteins and ribosomal proteins. The genes up-regulated in DM fetuses were mainly involved in the regulation of transcription, cell cycle/apoptosis, translation or DNA metabolism. These data highlight features indicating that DM muscle is shifted towards a more glycolytic metabolism, and has an altered extracellular matrix composition (e.g. down-regulation of COL1A1 and COL1A2, and up-regulation of COL4A2) and decreased adipocyte differentiation (down-regulation of C1QTNF3). The altered gene expression in the three major muscle compartments (fibers, connective tissue and intramuscular adipose tissue) is consistent with the well-known characteristics of DM cattle. In addition, novel potential targets of the myostatin gene were identified (MB, PLN, troponins, ZFHX1B). CONCLUSION: Thus, the myostatin loss-of-function mutation affected several physiological processes involved in the development and determination of the functional characteristics of muscle tissue.

SUBMITTER: Cassar-Malek I

PROVIDER: S-EPMC1831773 | biostudies-literature | 2007

REPOSITORIES: biostudies-literature

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Target genes of myostatin loss-of-function in muscles of late bovine fetuses.

Cassar-Malek Isabelle I Passelaigue Florent F Bernard Carine C Léger Jean J Hocquette Jean-François JF

BMC genomics 20070301

<h4>Background</h4>Myostatin, a muscle-specific member of the Transforming Growth Factor beta family, negatively regulates muscle development. Double-muscled (DM) cattle have a loss-of-function mutation in their myostatin gene responsible for the hypermuscular phenotype. Thus, these animals are a good model for understanding the mechanisms underpinning muscular hypertrophy. In order to identify individual genes or networks that may be myostatin targets, we looked for genes that were differential ...[more]

PMID: 17331240

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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.

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

Project description:BackgroundBovine leptospirosis is an important reproductive disease and abortion is a major sign, leading to economic impacts. Due to its multifactorial etiology, the proper diagnosis of the cause of the abortion is crucial. Necropsy of the fetuses followed by molecular analysis is recommended for diagnosis, and the investigation mainly occurs in the kidneys and liver. This study aimed to analyze unconventional sites for the presence of leptospiral DNA in bovine anicteric aborted fetuses.MethodsFive fetuses of the same herd were received for necropsy and diagnosis. Conventional lipL32-PCR was performed in the fetuses' kidneys, livers, lungs, hearts, spleens, subcapsular kidney content, abomasal fluid, and in the cavity's hemorrhagic contents. To complete the investigation, the sera of 30 cows of the herd were collected to perform the serologic screening by Microscopic Agglutination Test. In addition, six subfertile non-pregnant cows from the same herd were selected due to their low reproductive performance, and genital samples (uterine fragment and cervicovaginal mucus) and urine were collected for lipL32-PCR. PCR-positive samples were submitted to a nested PCR of the secY gene and intended for sequencing.ResultsThe herd presented seroreactive animals (11/30, 36.6%), all against the Sejroe serogroup, with titers between 200 and 1600. In necropsy, four fetuses showed hemorrhagic and anicteric lesions, while one fetus had no macroscopic lesions. Regarding molecular analysis, all the fetuses were positive in lipL32-PCR and the positive sites were the heart, lungs, subcapsular kidney content, thymus, kidneys, liver, and abomasal fluid. Only one fetus presented positive results in the kidney and liver, while three fetuses were positive in the abomasal fluid. Five of six cows were positive for lipL32-PCR, all being positive only in genital samples. Of the fetuses and the cows, seven sequences were obtained and all were identified as Leptospira interrogans serogroup Sejroe serovar Hardjoprajitno.ConclusionsIn order to improve the diagnosis of leptospirosis in cows, it is recommended to perform a comprehensive analysis of the samples, beyond the kidneys and liver. Thus, we highly encourage testing multiple organs by PCR to investigate abortions suspected of bovine leptospirosis, particularly in anicteric fetuses.

Dataset Information

Target genes of myostatin loss-of-function in muscles of late bovine fetuses.

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Target genes of myostatin loss-of-function in muscles of late bovine fetuses.

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