Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA329009 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3902240_1.fastq.gz | Fastqsanger.gz | |||
| SRR3902240_2.fastq.gz | Fastqsanger.gz | |||
| SRR3902241_1.fastq.gz | Fastqsanger.gz | |||
| SRR3902241_2.fastq.gz | Fastqsanger.gz | |||
| SRR3902242_1.fastq.gz | Fastqsanger.gz |
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Project description:A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle [Tw2 vs Pax7]
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Project description:A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle [Tw2 vs Pax7 fresh sort]
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Project description:A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle
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Project description:Skeletal muscle possesses remarkable regenerative potential due to satellite cells, a stem cell population located beneath the muscle basal lamina. By lineage tracing of progenitor cells expressing the Twist2 (Tw2) transcription factor in mice, we discovered a unique myogenic lineage that resides outside the basal lamina of adult muscle and contributes specifically to type IIb/x myofibers during adulthood and muscle regeneration. Tw2+ progenitors are molecularly and anatomically distinct from satellite cells, are highly myogenic in vitro and can fuse with satellite cells. Transplantation of Tw2+ progenitors into adult mice is sufficient to reconstitute new myofibers, and genetic ablation of endogenous Tw2+ progenitors causes wasting of type IIb myofibers. We show that Tw2 expression maintains progenitor cells in an undifferentiated state that is poised to initiate myogenesis in response to appropriate cues that suppress Tw2 expression. Tw2-expressing progenitors represent a previously unrecognized, fiber-type specific progenitor cell involved in muscle growth and regeneration.
2017-01-13 | GSE84379 | GEO
Project description:Skeletal muscle possesses remarkable regenerative potential due to satellite cells, a stem cell population located beneath the muscle basal lamina. By lineage tracing of progenitor cells expressing the Twist2 (Tw2) transcription factor in mice, we discovered a unique myogenic lineage that resides outside the basal lamina of adult muscle and contributes specifically to type IIb/x myofibers during adulthood and muscle regeneration. Tw2+ progenitors are molecularly and anatomically distinct from satellite cells, are highly myogenic in vitro and can fuse with satellite cells. Transplantation of Tw2+ progenitors into adult mice is sufficient to reconstitute new myofibers, and genetic ablation of endogenous Tw2+ progenitors causes wasting of type IIb myofibers. We show that Tw2 expression maintains progenitor cells in an undifferentiated state that is poised to initiate myogenesis in response to appropriate cues that suppress Tw2 expression. Tw2-expressing progenitors represent a previously unrecognized, fiber-type specific progenitor cell involved in muscle growth and regeneration.
2017-01-13 | GSE84378 | GEO
Project description:Skeletal muscle possesses remarkable regenerative potential due to satellite cells, a stem cell population located beneath the muscle basal lamina. By lineage tracing of progenitor cells expressing the Twist2 (Tw2) transcription factor in mice, we discovered a unique myogenic lineage that resides outside the basal lamina of adult muscle and contributes specifically to type IIb/x myofibers during adulthood and muscle regeneration. Tw2+ progenitors are molecularly and anatomically distinct from satellite cells, are highly myogenic in vitro and can fuse with satellite cells. Transplantation of Tw2+ progenitors into adult mice is sufficient to reconstitute new myofibers, and genetic ablation of endogenous Tw2+ progenitors causes wasting of type IIb myofibers. We show that Tw2 expression maintains progenitor cells in an undifferentiated state that is poised to initiate myogenesis in response to appropriate cues that suppress Tw2 expression. Tw2-expressing progenitors represent a previously unrecognized, fiber-type specific progenitor cell involved in muscle growth and regeneration.
2017-01-13 | GSE84377 | GEO
Project description:Twist transcription factors function as ancestral regulators of mesodermal cell fates in organisms ranging from Drosophlia to mammals. Through lineage tracing of Twist2 (Tw2) expressing cells with tamoxifen-inducible Tw2-CreERT2 and tdTomato reporter mice, we discovered a unique cell population that progressively contributes to multiple cell types in the adult heart, including cardiomyocytes, endothelial cells and fibroblasts. Clonal analysis confirmed the ability of Tw2-derived tdTO+ (Tw2-tdTO+) cells to form CMs in vitro. Within the adult heart, Tw2-tdTO+ cardiomyocytes accounted for ~13% of total cardiomyocytes, the majority of which resulted from fusion of Tw2-tdTO+ cells with existing cardiomyocytes. Tw2-tdTO+ cells also contribute to cardiac remodeling after injury. We conclude that a Tw2-tdTO+ cells participate in lifelong maintenance of cardiac function, at least in part through de novo formation of cardiomyocytes and fusion with preexisting cardiomyocytes, as well as in the genesis of other cellular components of the adult heart.
2020-01-08 | GSE97160 | GEO
Project description:Twist transcription factors function as ancestral regulators of mesodermal cell fates in organisms ranging from Drosophlia to mammals. Through lineage tracing of Twist2 (Tw2) expressing cells with tamoxifen-inducible Tw2-CreERT2 and tdTomato reporter mice, we discovered a unique cell population that progressively contributes to multiple cell types in the adult heart, including cardiomyocytes, endothelial cells and fibroblasts. Clonal analysis confirmed the ability of Tw2-derived tdTO+ (Tw2-tdTO+) cells to form CMs in vitro. Within the adult heart, Tw2-tdTO+ cardiomyocytes accounted for ~13% of total cardiomyocytes, the majority of which resulted from fusion of Tw2-tdTO+ cells with existing cardiomyocytes. Tw2-tdTO+ cells also contribute to cardiac remodeling after injury. We conclude that a Tw2-tdTO+ cells participate in lifelong maintenance of cardiac function, at least in part through de novo formation of cardiomyocytes and fusion with preexisting cardiomyocytes, as well as in the genesis of other cellular components of the adult heart.
2020-01-08 | GSE118410 | GEO
Project description:Muscle atrophy contributes to the poor prognosis of many physiopathological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca2+] which control aerobic metabolism, cell death and survival pathways. We have investigated in vivo the effects of mitochondrial Ca2+ homeostasis in skeletal muscle function and trophism, by overexpressing or silencing the Mitochondrial Calcium Uniporter (MCU). The results coherently demonstrate that both in developing and in adult muscles MCU-dependent mitochondrial Ca2+ uptake has a marked trophic effect that does not depend on autophagy or aerobic control, but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1M-NM-14 and Igf1-Akt/PKB. In adult mice, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca2+-dependent organelle-to-nucleus signaling route, which links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in sarcopenia. Experiments were performed on biological replicates of single skeletal muscle fibres. Seven fibres were chosen for their Mutochondrial Calcium Uniporter (MCU) overexpression and other seven fibres because MCU was silenced. Overexpression and silencing were performed injecting skeletal muscle with AAV containing MCU gene or short interfering oligos specific for MCU. As control was profiled eigth fibres transfected with AAV and eigth wild type fibres. Analyses were performed 7 days and 14 days after the AAV injection (3 fibers after 7 days and 4 fibers after 14 days for MCU overexpression and silencing, four fibres after 7 days and four after 14 days for control).
2015-03-05 | E-GEOD-60931 | biostudies-arrayexpress
Project description:Muscle atrophy contributes to the poor prognosis of many physiopathological conditions, but pharmacological therapies are still limited. Muscle activity leads to major swings in mitochondrial [Ca2+] which control aerobic metabolism, cell death and survival pathways. We have investigated in vivo the effects of mitochondrial Ca2+ homeostasis in skeletal muscle function and trophism, by overexpressing or silencing the Mitochondrial Calcium Uniporter (MCU). The results coherently demonstrate that both in developing and in adult muscles MCU-dependent mitochondrial Ca2+ uptake has a marked trophic effect that does not depend on autophagy or aerobic control, but impinges on two major hypertrophic pathways of skeletal muscle, PGC-1α4 and Igf1-Akt/PKB. In adult mice, MCU overexpression protects from denervation-induced atrophy. These data reveal a novel Ca2+-dependent organelle-to-nucleus signaling route, which links mitochondrial function to the control of muscle mass and may represent a possible pharmacological target in sarcopenia.
2015-03-05 | GSE60931 | GEO