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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Skeletal Muscle-Specific Akt Knockout Mice

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Skeletal Muscle-Specific Akt Knockout Mice

PROVIDER: PRJNA818289 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18397813_1.fastq.gz	Fastqsanger.gz
	SRR18397813_2.fastq.gz	Fastqsanger.gz
	SRR18397814_1.fastq.gz	Fastqsanger.gz
	SRR18397814_2.fastq.gz	Fastqsanger.gz
	SRR18397815_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Skeletal Muscle-Specific Akt Knockout Mice

Project description:Impact of knocking out of Akt in fast-twitch muscle on the transcritome was characterized by down-regulation of genes involved in mitochondria and electron transport chain.

2022-06-02 | GSE199074 | GEO

RNAseq analysis of skeletal muscle transcriptomes from wild-type and LONP1 skeletal muscle specific knockout (LONP1-MKO) mice

Project description:Mitochondria serve diverse functions and are essential organelles that require continuous surveillance to maintaintheir integrity and function. LONP1 is an evolutionarily conservedserine peptidase that safeguards mitochondrial protein quality from yeast to human.To investigatethe physiological role of LONP1-mediated mitochondrial quality-control in skeletal musclein vivo, we generated skeletal muscle-specificLonp1-knockout mice (referred to as LONP1 MKO). We performedtranscriptome analysis by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both wild-type (WT) and LONP1-MKO mice. Knockout of LONP1 in skeletal muscle resulted in deregulation of 457 genes in 2-week-old mice and of 1922 genes in 6-week-old mice. Gene ontology analysis revealed that LONP1 deficiency triggers unfolded protein response (UPR) in skeletal muscle.Moreover, GSEA analysis of transcriptomic datain 6-week-old micefurther revealed that genes deregulated by LONP1 deficiency were significantly enriched during aging.Together, the transcriptional profiling results suggest a critical role of LONP1 in regulating skeletal muscle metabolism and health.

2022-01-05 | GSE166071 | GEO

RNAseq analysis of skeletal muscle transcriptomes from wild-type, LONP1 skeletal muscle specific knockout (LONP1 mKO) and LONP1ATF4 skeletal muscle double-knockout (LONP1ATF4 DmKO) mice.

Project description:Studying the molecular basis for the skeletal muscle mitochondrial stress response could potentially be targeted to counteract metabolic disorders such as obesity. We uncovered a crucial role for the mitochondrial protease LONP1 in controlling the muscle mitochondrial proteostasis stress response that governs systemic metabolic homeostasis. Skeletal muscle-specific ablation of LONP1 led to broad genomic reprogramming of muscle and protected the mice from HFD-induced obesity. To thoroughly analyze pathways that are affected by ATF4 deficiency in the context of LONP1 mKO, we performed RNA-Seq transcriptome analysis of skeletal muscles from WT, LONP1 mKO and LONP1ATF4 DmKO mice. We identified a total of 3017 differentially expressed genes with a cutoff of 1.5-fold, and p < 0.05. Surprisingly, we found that ATF4 loss blunted a subset of regulated genes in LONP1 mKO muscles, whereas the majority of differentially regulated genes in LONP1 mKO muscles were not affected by ATF4 ablation. GO analysis of ATF4-dependent genes regulated by LONP1 ablation revealed significant enrichment in amino acid metabolic processes, Interestingly, however, LONP1 deficiency induced activation of muscle UPR and UPR-related RNA processing as well as myokine pathways were not affected by ATF4 ablation. Therefore, our results highlight a ATF4-independent mechanism in mediating the UPRmt in mammals.

2022-07-28 | GSE192990 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of c-myc Over-expression and Acute High-Intensity Contraction on Skeletal Muscle mRNA Transcriptomes

Project description:Purpose of this study was to compare the effect of c-myc over expression and acute high intensity muscle contraction on mRNA transcriptome in skeletal muscle

2022-11-14 | GSE161402 | GEO

Raptor and rapamycin dependent proteomic changes in Akt overexpressing skeletal muscle

Project description:Analysis of proteomic changes upon deletion of Raptor or inhibition by rapamycin in mouse muscles over expressing a constitutively active Akt.

2022-08-08 | PXD028796 | Pride

RNAseq analysis of skeletal muscle transcriptomes from wild-type, FNIP1-knockout (FNIP1-KO) mice, and mice expressing FNIP1 only in skeletal muscle (FNIP1-TgKO).

Project description:This experiment was conducted to identify FNIP1-dependent mRNA transcripts alteration in skeletal muscle. Mouse FNIP1 was specifically overexpressed in skeletal muscle in FNIP1-transgenic (FNIP1-Tg) mice. FNIP1-Tg mice were crossed with FNIP1-knockout (FNIP1-KO) mice to generate FNIP1-TgKO mice expressing FNIP1 only in skeletal muscle but not in other tissues. The muscle glycolytic-to-oxidative transformation is determined, largely in part, at the level of gene expression. To gain insight into the FNIP1-dependent regulation of skeletal muscle energy metabolism, transcriptome analysis was performed by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both FNIP1-KO and FNIP1-TGKO mice. We were particularly interested in the subset of genes that were regulated only in the FNIP1-KO mice but not in FNIP1-TGKO mice. Gene ontology (GO) analysis revealed that the primary FNIP1-regulated genes were mitochondrial metabolic genes. A broad array of genes involved in mitochondria was regulated FNIP1-KO muscle in a FNIP1-dependent manner. Together, the transcriptional profiling results indicate that a significant subset of FNIP1 target genes, were those involved in mitochondrial function.

2021-03-17 | GSE150193 | GEO

Skeletal Muscle Transcriptomics

Project description:Skeletal Muscle Transcriptomics

| PRJNA532382 | ENA

RNAseq analysis of skeletal muscle transcriptomes from wild-type and LONP1 skeletal muscle specific knockout (LONP1-MKO) mice

Project description:RNAseq analysis of skeletal muscle transcriptomes from wild-type and LONP1 skeletal muscle specific knockout (LONP1-MKO) mice

| PRJNA699182 | ENA

Real-time quantitative PCR analysis of WT and NOD1 knockout zebrafish (PI3K-AKT)

Project description:Zebrafish larvae from WT and NOD1-1IS-/- collected at 10 dpf were used for Zebrafish PI3K-AKT Signaling Pathway RT2 Profiler PCR Array.

2017-06-23 | GSE80622 | GEO

Skeletal muscle dysfunction in muscle-specific LKB1 knockout mice.

Project description:Liver kinase B1 (LKB1) is a tumor-suppressing protein that is involved in the regulation of muscle metabolism and growth by phosphorylating and activating AMP-activated protein kinase (AMPK) family members. Here we report the development of a myopathic phenotype in skeletal and cardiac muscle-specific LKB1 knockout (mLKB1-KO) mice. The myopathic phenotype becomes overtly apparent at 30-50 wk of age and is characterized by decreased body weight and a proportional reduction in fast-twitch skeletal muscle weight. The ability to ambulate is compromised with an often complete loss of hindlimb function. Skeletal muscle atrophy is associated with a 50-75% reduction in mammalian target of rapamycin pathway phosphorylation, as well as lower peroxisome proliferator-activated receptor-alpha coactivator-1 content and cAMP response element binding protein phosphorylation (43 and 40% lower in mLKB1-KO mice, respectively). Maximum in situ specific force production is not affected, but fatigue is exaggerated, and relaxation kinetics are slowed in the myopathic mice. The increased fatigue is associated with a 30-78% decrease in mitochondrial protein content, a shift away from type IIA/D toward type IIB muscle fibers, and a tendency (P=0.07) for decreased capillarity in mLKB1-KO muscles. Hearts from myopathic mLKB1-KO mice exhibit grossly dilated atria, suggesting cardiac insufficiency and heart failure, which likely contributes to the phenotype. These findings indicate that LKB1 plays a critical role in the maintenance of both skeletal and cardiac function.

| S-EPMC2886679 | biostudies-literature

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