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Gene expression analysis in skeletal muscle and heart of 11 days-old TK2 knockout mice

ABSTRACT: TK2 deficiency causes severe mtDNA depeltion in several tissues, including skeletal muscle and heart. TK2 knockout mice grow slower and their skeletal muscles appeared significantly underdeveloped, whereas heart was close to normal size. We used microarrays in order to compare the transcriptomes in skeletal muscle and heart tissue of 11 days-old TK2 knockout pups with the sames tissues of wild-type pups at the same age. We collected skeletal muscle from the hind limb and hearts of three 11 days-old TK2 knockout and three wild-type pups and extracted total RNA. These RNA samples were used for hybridization in Affymetrix arrays.

ORGANISM(S): Mus musculus

SUBMITTER: João Paredes

PROVIDER: E-GEOD-38449 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression analysis in skeletal muscle and heart of 11 days-old TK2 knockout mice

Project description:TK2 deficiency causes severe mtDNA depeltion in several tissues, including skeletal muscle and heart. TK2 knockout mice grow slower and their skeletal muscles appeared significantly underdeveloped, whereas heart was close to normal size. We used microarrays in order to compare the transcriptomes in skeletal muscle and heart tissue of 11 days-old TK2 knockout pups with the sames tissues of wild-type pups at the same age.

2012-07-31 | GSE38449 | GEO

cDNA microarray expression data of heart, skeletal muscle and liver comparing Irf2bp2-null mice to wild type controls

Project description:Interferon regulatory factor 2 binding protein 2 (Irf2bp2), a co-repressor of Irf2, is required for fetal hepatic erythropoiesis through the expansion of erythromyeloid progenitors. Mice with germline ablation of the entire Irf2bp2 transcript produced no viable Irf2bp2-null (knockout, KO) pups in first litters. In subsequent litters, fewer than 1/3 of the expected KO pups were born and half survived to adulthood. Heart, skeletal muscle and liver tissues (tissues with high Irf2bp2 expression) were acquired from WT and KO mice, followed by RNA extraction using the RNeasy Midi Kit and subsequent gene expression profiling using the Affymetrix Mouse Gene 1.0 ST v1 array. Transcriptome profiles of surviving KO mice were contrasted to WT mice giving insight to modified gene expression in the absence of Irf2bp2 across multiple vital tissues.

2023-02-02 | E-MTAB-11558 | biostudies-arrayexpress

Assessment of the response of aerobic and anaerobic muscle tissues of gilthead sea bream (Sparus aurata L.) to caloric restriction

Project description:Fish were fed from May to August (11 weeks) with a commercial diet (D-2 Excel 1P, Skretting, Stavanger, Norway) twice per day at two different feeding levels: full ration until visual satiety (MAX group), and maintenance ration (30% of the satiation level) (MANT group). The effect of ration size on aerobic (red skeletal muscle, heart) and anaerobic (white skeletal muscle) muscle tissue transcriptome was addressed by means of microarray analysis. The following tissues of animal from the MAX and MANT groups were analyzed: white skeletal muscle, red skeletal muscle and heart.

2014-07-09 | E-GEOD-47859 | biostudies-arrayexpress

Mus musculus

Project description:Gene expression analysis in skeletal muscle and heart of 11 days-old TK2 knockout mice

| PRJNA167961 | ENA

Assessment of the response of aerobic and anaerobic muscle tissues of gilthead sea bream (Sparus aurata L.) to caloric restriction

2014-07-09 | GSE47859 | GEO

Differential Gene Expression and Mitochondrial Dysfunction in Imprinting center deletion (PWS- IC del) Mouse model of Prader-Willi Syndrome

Project description:Prader-Willi syndrome (PWS) is a genetic disorder caused by deficiency of imprinted gene expression from the paternal chromosome 15q11-15q13 and clinically characterized by neonatal hypotonia, short stature, cognitive impairment, hypogonadism, hyperphagia, morbid obesity and diabetes. Previous clinical studies suggest that a defect in energy metabolism may be involved in the pathogenesis of PWS. Assessment of enzyme activities of mitochondrial oxidative phosphorylation (OXPHOS) complexes in the brain, heart, liver and muscle were assessed. We used microarrays to detail the global programme of gene expression underlyingthe PWS and identified distinct classes of disregulated genes during this process. Skeletal (quadriceps) muscle Vastus Lateralis and whole brain samples from the mutant mice and their wild-type age-matched littermates were analyzed by microarray technology using the Mouse Genome 430 2.0 arrays (Affymetrix).

2013-04-19 | E-GEOD-41759 | biostudies-arrayexpress

Effect of Lead on Genome-Wide Expression in Developing Mouse Brain during Synaptogenesis

Project description:Lead exposure causes a variety of health effects, especially in children, that may include cognitive and behavioural problems. This study explores the mechanisms associated with this relationship by assessing alterations in gene expression of C57BL/6J pups treated with 50mg/kg lead compared to controls. In addition this study also analyzed brain gene expression differences in Metallothionein I and II (Mt-I and Mt-II) knockout mice treated with lead. Pups of three genotypes (C57BL/6J, Mt-KO with a C57BL/6J background and Heterozygote Mt-KO) were injected with lead acetate during synaptogenesis and weight-matched controls were injected with saline at the same time points. Whole brains were harvested and RNA extracted and pooled from 5 pups and hybridized to Mouse Genome 430 2.0 Arrays. In total 6 arrays were used, one for each genotype and treatment.

2014-01-20 | E-GEOD-26894 | biostudies-arrayexpress

Muscleblind-like compound knockout models for myotonic dystrophy

Project description:Myotonic dystrophy (DM) is a multi-systemic disease that severely impacts cardiac and skeletal muscle functions as well as the central nervous system. DM is unusual because it is RNA-mediated disease due to the expression of C(C)UG expansion RNAs that inhibit the activities of the muscleblind-like (MBNL) proteins. In mice, studies using Mbnl1 and Mbnl2 single knockouts have revealed that Mbnl1 plays a predominant role in skeletal and heart muscle alternative splicing regulation while Mbnl2 performs an analogous splicing function in the brain. However, Mbnl single knockout models fail to recapitulate the full-range of adult-onset DM muscle symptoms. Here, we report that Mbnl1; Mbnl2 double knockouts are embryonic lethal while Mbnl1-/-; Mbnl2+/- mice, which express no Mbnl1 and reduced levels of Mbnl2, are viable but develop cardinal features of adult-onset DM cardiac and skeletal muscle disease including reduced lifespan, heart conduction block, severe myotonia and progressive skeletal muscle weakness. Mbnl2 protein levels are elevated in both Mbnl1-/- and Mbnl1-/-; Mbnl2+/- knockouts where Mbnl2 targets Mbnl1-regulated exons. These findings support the MBNL loss-of-function model for DM and provide novel Mbnl compound knockout models to investigate the molecular pathways disrupted by RNA-mediated disease. Mbnl2 protein-RNA interactions were assessed in 4-month-old WT and Mbnl1-/- quadriceps muscles in triplicates by HITS-CLIP.

2013-12-01 | E-GEOD-47794 | biostudies-arrayexpress

CRISPR/Cas9-mediated Nexilin deficiency interferes with cardiac contractile function in zebrafish in vivo

Project description:Nexilin (NEXN) plays a crucial role in stabilizing the sarcomeric Z-disk of striated muscle fibers and, when mutated, leads to dilated cardiomyopathy in humans. Due to its early neonatal lethality in mice, the detailed impact of the constitutive homozygous NEXN knockout on heart and skeletal muscle morphology and function is insufficiently investigated. We characterized a constitutive homozygous CRISPR/Cas9-mediated nexn knockout zebrafish model. We found that Nexn deficient embryos developed significantly reduced cardiac contractility and under stressed conditions also impaired skeletal muscle organization whereas skeletal muscle function seemed not to be affected. Remarkably, in contrast to nexn morphants, CRISPR/Cas9 nexn-/- knockout embryos showed a milder phenotype without the development of a pronounced pericardial edema or blood congestion. nexn-specific expression analysis as well as whole transcriptome profiling suggest some degree of compensatory mechanisms. Transcripts of numerous essential sarcomeric proteins were massively induced and may mediate a sarcomere stabilizing function in nexn-/- knockout embryos.

2023-12-20 | GSE239788 | GEO

The role of TEFM in mitochondrial gene expression [TruSeq]

Project description:We investigated the role of TEFM in vivo by creating heart- and skeletal-muscle specific knockout of this gene. We identified that TEFM is required for the processivity of POLRMT and its loss leads to significantly decreased mitochondrial transcription.

2019-04-01 | GSE102254 | GEO

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