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RNA sequencing of TA muscle in miR-501KO mice and control littermates at day 6 of CTX-induced muscle regeneration

ABSTRACT: Adult muscle stem cells show a high transcriptional and clonal heterogeneity during ageing. Whether microRNAs contribute to this diversity is not known. Here we use global and tissue-specific genetic deletion of microRNA (miR)-501 that is highly enriched in activated myogenic progenitor cells 3 to address this question. Deletion of miR-501 reduced myofiber size and resilience of muscle fibers to injury and exercise in adult skeletal muscle. miR-501 elicits this effect by changing sarcomeric gene expression in newly built myofibers in vivo.

ORGANISM(S): Mus musculus

PROVIDER: GSE199111 | GEO | 2023/03/16

REPOSITORIES: GEO

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A myogenin+/CD74+ adult muscle stem cell population during regeneration of skeletal muscle lacking miR-501

Project description:Adult muscle stem cells show a high transcriptional and clonal heterogeneity during ageing. Whether microRNAs contribute to this diversity is not known. Here we use tissue-specific genetic deletion of microRNA (miR)-501 that is highly enriched in activated myogenic progenitor cells to address this question. Single-cell sequencing revealed a novel subpopulation of committed myogenic progenitor cells in miR-501 knockout mice that express high levels of terminal differentiation markers and inflammatory genes such as CD74. Our data show that stem cell heterogeneity in skeletal muscle during ageing is under miRNA control.

2023-03-21 | GSE200501 | GEO

The RNA binding protein Arrest (Aret) regulates myofibril maturation in Drosophila flight muscle

Project description:In Drosophila, fibrillar flight muscles (IFMs) enable flight, while tubular muscles mediate other body movements. Here, we use RNA-sequencing and isoform-specific reporters to show that spalt major (salm) determines fibrillar muscle physiology by regulating transcription and alternative splicing of a large set of sarcomeric proteins. We identify the RNA binding protein Arrest (Aret, Bruno) as downstream of salm. Aret shuttles between cytoplasm and nuclei, and is essential for myofibril maturation and sarcomere growth of IFMs. Molecularly, Aret regulates IFM-specific transcription and splicing of various sarcomeric targets, including Stretchin and wupA (TnI), and thus maintains muscle fiber integrity. As Aret and its sarcomeric targets are evolutionarily conserved, similar principles may regulate mammalian muscle morphogenesis. 9 samples from Drosophila melanogaster were analyzed in duplicate: control dissected wildtype flight muscle at 30h APF, 72h APF and 0 day adult, jump muscle and whole leg from 1d adult and RNAi/mutant conditions for salm (1d flight muscle) and aret (30h, 72h and 1d flight muscle)

2014-12-23 | E-GEOD-63707 | biostudies-arrayexpress

Functional TDP-43 amyloids bind sarcomeric mRNA to direct skeletal muscle formation

Project description:Cytoplasmic aggregates of TDP-43 are found in neuronal and skeletal muscle diseases yet it is not understood how these protein aggregates relate to the biological function of TDP-43. By examining normal skeletal muscle formation, we discovered TDP-43 redistributes from the nucleus into the cytoplasm and forms higher-ordered aggregates. These skeletal muscle TDP-43 aggregates adopt an amyloid-like structure capable of binding RNA. In skeletal muscle, TDP-43 binds UG-rich, sarcomeric mRNAs and oligomerizes on these long mRNA transcripts facilitating amyloid formation. Tissue specific genetic deletion of TDP-43 in skeletal muscle disrupts the formation and maintenance of the sarcomere and mislocalizes sarcomeric mRNAs. Thus, cytoplasmic, amyloid-like TDP-43 aggregates that traffic mRNAs could serve as a precursor to pathological TDP-43 aggregates common in degenerative neuromuscular disease.

2018-09-05 | GSE104796 | GEO

mir-1 coordinately regulates lysosomal v-ATPase and biogenesis to affect muscle contractility upon proteotoxic challenge during ageing

Project description:Muscle function relies on the precise architecture of dynamic contractile elements, which must be fine-tuned to maintain motility throughout life. Muscle is also highly plastic, and remodeled in response to stress, growth, neural and metabolic inputs. The evolutionarily conserved muscle microRNA, mir1, regulates distinct aspects of muscle biology during development, but whether it plays a role during ageing is unknown. Here we investigated the role of C. elegans mir-1 in muscle function in response to proteostatic stress during adulthood. mir-1 deletion results in improved mid-life muscle motility, pharyngeal pumping, and organismal longevity under conditions of polyglutamine repeat proteotoxic challenge. We identified multiple vacuolar ATPase subunits as subject to mir-1 control, and the regulatory subunit vha-13/ATP6VIA as a direct target downregulated via its 3’UTR to mediate mir-1 physiology. mir-1 further regulates nuclear localization of lysosomal biogenesis factor HLH-30/TFEB and lysosomal acidification. Our studies reveal that mir-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact muscle function and health during ageing.

2021-07-14 | PXD023544 | Pride

USP18-dependent muscle proteome

Project description:USP18 is an interferon type 1 (IFN-1) induced gene that negatively regulates the IFN-1 signalling pathway, which plays a role in many immune related pathologies. Dermatomyositis (DM) is characterised by excessive IFN-1 immune response and muscle degeneration. We found USP18 to be expressed in DM myofibers suggesting a role in muscle cell biology. USP18 depletion induced muscle cell differentiation under nutrient-rich conditions independent of IFN-1 signalling. Downregulation of cell cycle gene network and sarcomeric protein networks, and dysregulation of myogenic (co-)transcription regulators were found in USP18-depleted differentiated cells. Sarcomeric integrity of USP18-depleted cells deteriorated during muscle cell maturation. Our results revealed USP18 as a critical regulator at the intersection between proliferation and differentiation as well as during the maturation of muscle cells. We suggest that a USP18 IFN-1-independent pathway may contribute to muscle regeneration in muscle pathologies.

2023-05-10 | PXD032406 | Pride

The Skeletal Muscle Molecular Clock Regulates Sarcomere Length Through Titin Splicing [1]

Project description:Circadian rhythms have been implicated in regulating skeletal muscle structure and function, but no mechanisms have connected the molecular clock to sarcomeric proteins. We identified an isoform shift in the sarcomeric ruler, titin, and showed that the skeletal muscle molecular clock regulates titin isoform and subsequently sarcomere length through RBM20, an RNA binding protein that controls titin splicing.

2022-09-07 | GSE172067 | GEO

The Skeletal Muscle Molecular Clock Regulates Sarcomere Length Through Titin Splicing [2]

2022-09-07 | GSE189863 | GEO

An FGF-2 signaling pathway that is activated in aged skeletal muscle promotes intramuscular adipogenesis

Project description:Aged skeletal muscle is markedly affected by fatty muscle infiltration and strategies to reduce the occurrence of adipocytes within skeletal muscle, the intramuscular adipose tissue (IMAT), are urgently needed. Fibroblast growth factor-2 (FGF-2) is a critical growth factor for muscle tissue. Here, we show that FGF-2 not only stimulates muscle growth, but also promotes intramuscular adipogenesis. Using multiple screening assays for upstream and downstream signaling of microRNA (miR)-29a we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle from aged mice. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1 which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and AAV-mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular fat formation in vivo. Thus, our data highlight an ambivalent role of FGF-2 for adult skeletal muscle and reveal a novel pathway to combat fat accumulation in aged skeletal muscle.

2021-08-23 | PXD020575 | Pride

The RNA binding protein Arrest (Aret) regulates myofibril maturation in Drosophila flight muscle

2014-12-23 | GSE63707 | GEO

Mechanisms underlying the sparing of masticatory muscle function relative to biceps femoris muscle in an experimental critical illness model

Project description:Background: The aim of this study is to improve our understanding of the mechanisms underlying the sparing of masticatory muscles relative to limb muscles in ICU patients with acute quadriplegic myopathy (AQM) by using a unique porcine ICU model, i.e., 5-day longitudinal experiments where animals are sedated, mechanically ventilated and exposed to factors triggering AQM, such as muscle unloading, endotoxin-induced sepsis, and systemic exposure to CS and NMBA. Results: An altered expression was notably observed in heat-shock proteins genes, sarcomeric proteins and myostatin genes were noticed. Hence, modifications in heat-shock proteins, sarcomeric proteins and myostatin genes are in sharp contrast to alterations in the limb muscles and it is postulated that elevated heat-shock proteins and decreased sarcomeric protein and myostatin genes play a protective role in the masticatory muscle relative to limb muscle in ICU patients with AQM. Conclusions: This intervention had no significant effect on masseter muscle fiber size or force-generation capacity. This is in sharp contrast to the dramatic decrease observed in specific force in limb muscle fibers from the same animals. However, significant differences were observed between the craniofacial and the limb muscle with a masseter muscle specific regulation of i) transcriptional and growth factors like RUNX1, FOXO1A, TBX1, PGC1-β and myostatin, ii) several heat shock protein genes like HSP 90, HSP 105/110 and αB-crystallin, iii) a matrix metalloproteinase inhibitor (TIMP2) and iv) oxidative stress responsive elements such as SRXN1 and SOD2. These muscle-type specific differences, the alterations in heat shock protein, sarcomeric protein and myostatin genes are forwarded as important factors underlying the sparing of masticatory muscles compared with limb muscles in critically ill ICU patients with Acute Quadriplegic Myopathy. Keywords: Treatment, immobilization, muscle function.

2010-09-21 | GSE24239 | GEO

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