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Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

ABSTRACT: Purpose: To study Nf1 regulated pathways in controlling juvenile satellite cells quiescence induction. Methods: We sequenced total mRNAs isolated from juvenile satellite cells FACS sorted from postnatal day 7 Control (Nf1flox/+ Myf5Cre+) and KO (Nf1flox/flox Myf5Cre+) mouse hindlimb skeletal muscle. Results: Our study suggests that Nf1 is required for maintaining the balance between quiescence induction and amplification / differentiation in the postnatal MP pool. Conclusions: The tumor suppressor Nf1 maintains the myogenic progenitor (MP) pool during postnatal muscle development.

ORGANISM(S): Mus musculus

PROVIDER: GSE159021 | GEO | 2021/09/25

REPOSITORIES: GEO

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Neurofibromin (Nf1) is required for skeletal muscle development

Project description:Neurofibromatosis type 1 (NF1) is a multi-system disease caused by mutations in the NF1 gene encoding a Ras-GAP protein, neurofibromin, which negatively regulates Ras signalling. Besides neuroectodermal malformations and tumours, the skeletal system is often affected (e.g. scoliosis and long bone dysplasia), demonstrating the importance of neurofibromin for development and maintenance of the musculoskeletal system. Here we focus on the role of neurofibromin in skeletal muscle development. Nf1 gene inactivation in the early limb bud mesenchyme using Prx1-cre (Nf1Prx1) resulted in muscle dystrophy characterised by fibrosis, reduced number of muscle fibres, and reduced muscle force. To gain insight into the molecular changes of the observed muscle dystrophy and fibrosis and to compare these with other known muscle dystrophies, we performed transcriptional profiling of the entire triceps muscles of threemonth-old wild type (wt) and mutant animals using Affymetrix high-density microrrays. We analyzed triceps muscles from 4 three-month-old wt controls and 4 three-month-old Nf1Prx1 mice using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by the Affymetrix Exon Array Computational Tool. RNA isolated from each animal was hybridized to a separate microarray.

2011-05-18 | E-GEOD-29343 | biostudies-arrayexpress

Neurofibromin (Nf1) is required for skeletal muscle development

2011-05-18 | GSE29343 | GEO

Cell autonomous requirement of Neurofibrimin (Nf1) for postnatal muscle hypertrophic growth and metabolic homeostasis

Project description:Background Neurofibromatosis type 1 (NF1) is a multi-organ disease caused by mutations in Neurofibromin (NF1). Amongst other features, NF1 patients frequently show reduced muscle mass and strength, impairing patients’ mobility and increasing the risk of fall. The role of Nf1 in muscle and the cause for the NF1-associated myopathy is mostly unknown. Methods To dissect the function of Nf1 in muscle, we created muscle-specific knockout mouse models for Nf1, inactivating Nf1 in the prenatal myogenic lineage either under the Lbx1 promoter or under the Myf5 promoter. Mice were analyzed during pre-and postnatal myogenesis and muscle growth. Results Nf1Lbx1 and Nf1Myf5 animals showed only mild defects in prenatal myogenesis. Nf1Lbx1 animals were perinatally lethal, while Nf1Myf5 animals survived up to approx. 25 weeks. Nf1Myf5 animals showed decreased postnatal growth, reduced muscle size, and fast fiber atrophy. Proteome and transcriptome analysis of muscle tissue indicated decreased protein synthesis and increased proteasomal degradation, and decreased glycolytic and increased oxidative activity in muscle tissue. Real-time respirometry demonstrated enhanced oxidative metabolism in Nf1Myf5 muscles concomitant to a fiber type shift from type 2B to type 2A and type 1. Nf1Myf5 muscles showed hallmarks of mild oxidative stress and increased activation of AMPK indicating an energy deficit, increased expression of atrogenes and decreased activation of mTORC1. Proteome and transcriptome analysis indicated that oxidative fibers mainly relied on fatty acid catabolism. Inline, Nf1Myf5 animals showed a drastic reduction of white, but not brown, adipose tissue. Conclusions Our results demonstrate a cell-autonomous role for Nf1 in myogenic cells during postnatal muscle growth required for metabolic and proteostatic homeostasis. Furthermore, Nf1 deficiency in muscle leads to cross-tissue communication and mobilization of lipid reserves.

2020-10-26 | PXD017958 | Pride

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors

| PRJNA667433 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [ChIP-seq]

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [ChIP-seq]

| PRJNA667437 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [RNA-seq]

| PRJNA667436 | ENA

Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [MeDIP-Seq]

Project description:Neurofibromin (Nf1) controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors [MeDIP-Seq]

| PRJNA667435 | ENA

Cell autonomous requirement of Neurofibrimin (Nf1) for postnatal muscle hypertrophic growth and metabolic homeostasis

Project description:Our results demonstrate a cell-autonomous role for Nf1 in myogenic cells during postnatal muscle growth required for metabolic and proteostatic homeostasis.

2021-01-04 | GSE147605 | GEO

Early postnatal expression data from mouse skeletal muscle stem cells

Project description:Satellite cells are the primary source of stem cells for skeletal muscle growth and regeneration. Since adult stem cell maintenance involves a fine balance between intrinsic and extrinsic mechanisms, we performed genome-wide chronological expression profiling to identify the transcriptomic changes involved during early postnatal growth till acquisition of satellite cell quiescence. Muscle samples were isolated from the trunk of Pax3GFP/+ mice. After digestion, GFP cells were purified via FACS and process for RNA extraction and hybridization on Affymetrix microarrays (Affymetrix Mouse Genome 430 2.0 Arrays). The different ages selected for sample isolation were P1-P12-P28 (P, postnatal days), covering proliferant and quiescent satellite cells. The three stages were done in triplicate for P28 and 4 times for P1-P12, so 11 samples included in the microarray.

2015-04-21 | E-GEOD-65927 | biostudies-arrayexpress

Expression data of three sets of cells: (1) Schwann cells and macrophages from 1m-old WT DRG, (2) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 1m-old neurofibroma, (3) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 7m-old neurofibroma

Project description:Schwann cells and macrophages were dissociated from normal DRGs and 1- and 7-month-old neurofibroma. Schwann cells from neurofibroma have Nf1-/- phenotypes. All macrophages have Nf1+/+ phenotypes. We used microarrays (Affymetrix MoGene 2.0 ST GeneChip) to detect transcriptomal changes between 7-month-old neurofibroma Schwann cells (or macrophages) versus 1-month-old wild-type (or neurofibroma) Schwann cells (or macrophages). Expression data of three sets of cells: (1)Schwann cells and macrophages from 1-month-old wild-type mouse dorsal root ganglia, (2) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 1-month-old neurofibroma, (3) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 7-month-old neurofibroma We chopped mouse DRG/neurofibromas into 1-3 mm^3 pieces and plated them in dissociation medium containing 20mL L-15 (Mediatech), 0.5 mg/mL collagenase type 1 (Worthington; Lakewood, NJ), and 2.5 mg/mL dispase protease type II (Cambrex; East Rutherford, NJ) at 37Â°C for 4-6 hours with shaking. The dissociation reaction was stopped by adding DMEM +10%FBS. Undigested DRG/tumors were excluded by 100ÂµM cell strainer. Cells were collected by centrifugation. For each microarrays (Schwann cell, macrophage), Affymetrix GeneChip Command Console (v4.0.0) was used to create .chp files. All the probe sets on Affymetrix Mouse Gene 2.0 ST array (Mogene-2_0-st-v1.na33.2.mm10) were summarized by Affymetix Expression Console program using robust multi-chip average (RMA) method . After preprocessing steps, data from two batches were combined and their batch effects were corrected using ComBat method Please note that [1] all MP samples are Nf1+/+ (no mutation on Nf1 gene) and the only difference is their ages (1month, 7month) and [2] the 'nf1' in sample title reperesents "neurofibroma type1 disease", not "Nf1 gene".

2017-05-01 | E-GEOD-78901 | biostudies-arrayexpress

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