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Notch signaling/MyoD double deficient embryonic muscle progenitors

ABSTRACT: Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite deregulate the expression of basal lamina components and adhesion molecules like integrin a7, collagen XVIIIa1, Megf10 and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers.

ORGANISM(S): Mus musculus

PROVIDER: GSE39379 | GEO | 2012/12/31

SECONDARY ACCESSION(S): PRJNA170741

REPOSITORIES: GEO

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Notch signaling/MyoD double deficient embryonic muscle progenitors

Project description:Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite deregulate the expression of basal lamina components and adhesion molecules like integrin a7, collagen XVIIIa1, Megf10 and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers. Gene expression analysis using total RNA from FACS-isolated Vcam-1+/CD31-/CD45-/Sca1- embryonic muscle progenitor cells from E17.5 back muscle tissue of MyoD-/-, Pax3cre/+;Rbpjflox/flox;MyoD-/- and Pax3cre/+;DnMamlflox/flox;MyoD-/- mice.

2012-12-31 | E-GEOD-39379 | biostudies-arrayexpress

A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle [Tw2 vs Pax7 fresh sort]

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

A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle [Tw2 vs Pax7]

2017-01-13 | GSE84378 | GEO

A Unique Twist-Dependent Progenitor Cell Contributes to Adult Skeletal Muscle [Tw2 overexpression]

2017-01-13 | GSE84377 | GEO

Sex hormones establish a reserve pool of adult muscle stem cells at puberty

Project description:Quiescent satellite cells, also known as adult muscle stem cells, possess a remarkable ability to regenerate skeletal muscle upon injury throughout life. Although they mainly originate from multipotent stem/progenitors of the somite, the mechanism underlying the establishment of quiescent satellite cell populations is unknown. Here, we show that sex hormones induce Mind bomb-1 (Mib1) expression in myofibers at puberty, which activates Notch signaling in cycling juvenile satellite cells and causes them to be converted into quiescent adult satellite cells. Myofibers lacking Mib1 failed to send Notch signals to juvenile satellite cells, leading to impaired cell cycle exit and depletion. Genetic and inhibitor studies revealed that the hypothalamic-pituitary-gonadal axis drives Mib1 expression in the myofiber niche. Our data show how sex hormones establish quiescent adult satellite cell populations by regulating the myofiber niche at puberty. Microarray analysis of Veh or DHT-injected 10-day-old mice s.c. injected with Veh or DHT. TA muscles were isolated 24 h after the injection.

2015-09-01 | E-GEOD-64454 | biostudies-arrayexpress

Transcription profiling of mouse satellite cells isolated from skeletal muscle

Project description:(Abstract of publication submitted currently) To clarify molecular regulation of satellite cells, we performed genome-wide gene expression analysis of quiescent satellite cells isolated from mouse skeletal muscle by flow cytometry. We identified 53 novel quiescent satellite cell-specific genes whose expressions are sharply down-regulated upon activation. The gene list contains a number of cell surface molecules, transcriptional factors, and cytokines and other signal transduction molecules. We further confirmed that Odz4 and calcitonin receptor proteins were expressed by quiescent but not by activated satellite cells in vivo. Importantly, we found that Pax7+/calcitonin receptor+ satellite cells reappear in close association with regenerating myofibers 7 days after muscle damage, often outside the basal lamina. Moreover, an agonist of calcitonin receptor suppressed the activation of quiescent satellite cells on myofibers in in vitro culture, suggesting that calcitonin receptor signaling plays an important role in renewal and maintenance of satellite cells. Our results show the gene expression profile of quiescent satellite cells for the first time and reveal the temporal and spatial reappearance of a satellite cell pool. Experiment Overall Design: Satellite cells and non-satellite cells were examined. Totally three types of cells (groups), the satellite cells in quiescent and activated states and the non-satellite cells, were compared. Each has 4 replicates.

2008-06-12 | E-GEOD-3483 | biostudies-arrayexpress

Satellite cell – specific deletion of CIPC alleviates myopathy in mdx mice.

Project description:The regeneration of skeletal muscle relies on satellite cells which can proliferate, differentiate and form new myofibers upon injury. Emerging evidence suggests that misregulations of satellite cell fate and function influence the severity of Duchenne Muscular Dystrophy (DMD). The myogenic identity and maintenance of the pool of satellite cells is determined by the transcription factor PAX7. Satellite cell proliferation and self-renewal is regulated by the circadian clock. Here, we show that the CLOCK-interacting protein, Circadian (CIPC), a negative-feedback regulator of the circadian clock, is up-regulated during myoblast differentiation. Specific deletion of CIPC in satellite cells alleviated myopathy, improved muscle function and reduced fibrosis in mdx mice. CIPC deficiency led to activation of the ERK1/2 and JNK1/2 signaling pathways, which in turn activated the transcription factor SP1 to trigger the transcription of PAX7. Therefore, CIPC is a negative regulator of satellite cell function and loss of CIPC in satellite cells promotes muscle regeneration.

2022-01-27 | GSE195468 | GEO

Single Cell sequencing of mononuclear cells from regenerating skeletal muscle

Project description:Skeletal muscle stem cells, or satellite cells (SCs), are essential to regenerate and maintain muscle. Quiescent SCs reside in an asymmetric niche between the basal lamina and myofiber membrane. To repair muscle, SCs activate, proliferate, and differentiate, fusing to repair myofibers or reacquiring quiescence to replenish the SC niche. Little is known about when SCs reacquire quiescence during regeneration or the cellular processes that direct SC fate decisions and progression through myogenesis. Single cell sequencing of myogenic cells in regenerating muscle identifies SCs reacquiring quiescence and reveals that non-cell autonomous signaling networks influence SC fate decisions during regeneration. Single cell RNA-sequencing of regenerating skeletal muscle reveals that RBP expression, including numerous neuromuscular disease-associated RBPs, is temporally regulated in skeletal muscle stem cells and correlates to stages of myogenic differentiation. By combining machine learning with RBP engagement scoring, we discover that the neuromuscular disease associated RBP Hnrnpa2b1 is a differentiation-specifying regulator of myogenesis controlling myogenic cell fate transitions during terminal differentiation.

2022-06-11 | GSE205690 | GEO

Sex hormones establish a reserve pool of adult muscle stem cells at puberty

2015-09-01 | GSE64454 | GEO

miR-206 modulates the pathogenesis of muscular dystrophy of mdx mice

Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.

2012-04-30 | E-GEOD-36077 | biostudies-arrayexpress

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