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Transcription profiling of mouse neuronal differentiation of primary myoblast sphere cultures

ABSTRACT: Adult mouse muscle was enzymatically dissociated. Muscle derived stem cells proliferate unattached, in spheres, in the proliferation medium. Cells from spheres were also incubated in a differentiation medium. They differentiated into neurons after 7 days in culture. Experiment Overall Design: this experiment include 2 samples and 12 replicates

ORGANISM(S): Mus musculus

SUBMITTER: OGIC Info Ontario Genomics Innovation Centre (OGIC)

PROVIDER: E-GEOD-4088 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Neuronal Differentiation of Primary Myoblast Sphere Cultures

Project description:Adult mouse muscle was enzymatically dissociated. Muscle derived stem cells proliferate unattached, in spheres, in the proliferation medium. Cells from spheres were also incubated in a differentiation medium. They differentiated into neurons after 7 days in culture. Keywords: neuronal differentiation

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Transcriptome analysis of control and SKOV3 floating sphere cells and sphere differentiated cells

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Transcription profiling of mouse FM95-14 fetal myoblast differentiation - time series

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The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression

Project description:Myoblast fusion (MF) is a complex process required for muscle formation. During development, post-natal muscle growth and adult muscle regeneration, myoblasts proliferate and fuse to generate multinucleated fibers. MF defects have been described in an increasing number of muscle diseases. Moreover, MF plays also a relevant role in the delivery of therapeutics to muscle fibers. Hence, the identification of novel MF activators bears strong therapeutic relevance. Despite the central role of MF, the mechanisms governing this process are incompletely understood, and no epigenetic regulator has ever been described. Ash1L is a histone methyltransferase responsible for H3K36me2 and a member of the Trithorax group of epigenetic activators. It is involved in several diseases, including FSHD muscular dystrophy, autism and cancer. Nevertheless, its physiological role in skeletal muscle is unknown. For the first time, we found that Ash1L expression is regulated during skeletal muscle development, positively correlated with that of key MF genes and reduced in Duchenne muscular dystrophy. During physiological muscle differentiation or muscle regeneration, Ash1L shows a peak of expression coincident with the activation of MF. Loss-of-function experiments support a selective and evolutionary conserved requirement for Ash1L in MF. Accordingly, Ash1L KO mice display small and underdeveloped skeletal muscles due to a MF defect. By combining RNA- and ChIP-sequencing, we identified direct Ash1L targets in muscle. Intriguingly, nearly all of them are known Polycomb target genes suggesting that Ash1L is required to counteract Polycomb repressive activity to allow activation of key myogenesis genes. In particular, we found that Ash1L drives MF by directly activating the expression of the key MF gene Cdon. Our results promote Ash1L as the first epigenetic regulator of MF and suggest that its activity could be targeted to improve cell therapy for muscle diseases.

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Mouse myoblast fusion - Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190

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Determination of Lsd1 function in C2C12 myoblast cells by global transcriptome analysis

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