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

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

PROVIDER: PRJNA699182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13618490_1.fastq.gz	Fastqsanger.gz
	SRR13618490_2.fastq.gz	Fastqsanger.gz
	SRR13618491_1.fastq.gz	Fastqsanger.gz
	SRR13618491_2.fastq.gz	Fastqsanger.gz
	SRR13618492_1.fastq.gz	Fastqsanger.gz

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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.

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Effect of ATF4 gene knockout on skeletal muscle mRNA levels in fasted mice.

Project description:ATF4 is a fasting-induced trascription factor that promotes skeletal muscle atrophy. The goal of these studies was to determine how of loss of ATF4 affects skeletal muscle mRNA expression. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls were fasted for 24 hours and then tibialis anterior muscles were harvested. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

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Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

2015-09-03 | E-GEOD-72658 | biostudies-arrayexpress

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Project description:In the present study we have studied the mechanistic and functional aspects of NCoR1 function in mouse skeletal muscle. NCoR1 muscle-specific knockout mice exhibited an increased oxidative metabolism. Global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha) overexpression on oxidative metabolism in skeletal muscle. The repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1alpha-mediated coactivation of ERRalpha. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases. Gene expression of a total of 20 gastrocnemius samples from control (CON, n = 5), NCoR1 muscle-specific knockout (NCoR1 MKO, n = 5), wild type (WT, n = 5) and PGC-1alpha muscle-specific transgenic (PGC-1alpha mTg, n = 5) adult male mice was analyzed using GeneChipÂ® Gene 1.0 ST Array System (Affymetrix). NCoR1 MKO and PGC-1alpha mTg samples were compared to CON and WT samples, respectively.

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Effect of USP21 deficiency on transcriptomes in skeletal muscle of mice

Project description:Skeletal muscle is the pivotal organ for energy homeostasis, but the regulatory mechanisms are largely unknown. Here, we report that ubiquitin specific protease 21 (USP21) is a regulator of skeletal muscle physiology. To elucidate features important for USP21, we performed RNA-sequencing analysis using the muscle tissue of muscle-specific USP21 knockout (USP21-MKO) mice or wild-type littermates with floxed genotype, screened and analyzed the differentially expressed genes. Transcriptomics assay enabled us to discover major signaling nodes persistently activated by USP21 ablation in close association with the genes linked to fuel oxidation. Consequently, USP21 ablation altered gross metabolic phenotypes.

2022-01-11 | GSE159558 | GEO

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.

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RNAseq analysis of skeletal muscle transcriptomes from wild type and MLL4SET-MKO mice

Project description:This experiment was conducted to identify mRNA transcripts alteration in skeletal muscle of MLL4SET muscle-specific knockout mice. Enhancers play central role in controlling gene expression in time and space. Primed enhancers are marked by histone H3 lysine 4 (H3K4) mono/di-methylation (H3K4me1/2). Mixed-lineage leukemia 4 (MLL4/KMT2D) is an evolutionarily conserved H3K4me1/2 methyltransferase that is required for enhancer activation. Here, we identified the genome-wide MLL4 occupancy in mouse skeletal muscle by ChIP-seq coupled with RNA-seq analysis. Gene ontology analysis revealed that MLL4 controls muscle fiber-type switching. We thus have revealed novel MLL4 targets involved in muscle metabolism.

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Project description:Gadd45a is a stress-induced protein that causes skeletal muscle atrophy. The goal of these studies was to determine the effects of Gadd45a overexpression on mRNA levels in mouse skeletal muscle. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Tibialis anterior (TA) muscles from muscle-specfic ATF4 knockout mice (ATF4 mKO) were transfected with either 20 mg empty plasmid (pcDNA3) (left TA) or 20 mg pCMV-FLAG-Gadd45a (right TA) and harvested 7 days later. mRNA levels in Gadd45a-transfected muscles were normalized to levels in control transfected muscles.

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RNAseq analysis of skeletal muscle transcriptomes from wild type and MLL4SET-MKO mice

Project description:RNAseq analysis of skeletal muscle transcriptomes from wild type and MLL4SET-MKO mice

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