Gene Regulatory Networks and Transcriptional Mechanisms that Control Myogenesis

Buckingham, Margaret; Rigby, Peter

doi:10.1016/j.devcel.2013.12.020

Cited by 543 publications

(512 citation statements)

References 93 publications

(106 reference statements)

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“…We next asked whether miRNAs participate in the quiescence of adult MuSCs. There is evidence that non-coding RNAs, including miRNAs, are involved in the regulation of skeletal muscle cells during development [18][19][20][21][22] and of quiescent of MuSCs in the adult 10,[22][23][24] . To examine the impact of miRNAs on the growth and differentiation of MuSCs, Dicer was deleted in Pax3/Pax7-expressing adult GFP þ cells of 12 weeks old Pax3 GFP/ þ ; Pax7 CreER/ þ ; Dcr f/f mice produced from Pax7 CreER/ þ ; Dcr f/f female mice crossed with Pax3 GFP/ þ ; Dcr f/f male mice, which did not reveal a haploinsufficient phenotype, by administration of 4-hydroxytamoxifen five times for a week ( Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

2014

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Skeletal muscle stem cells (MuSCs), the major source for skeletal muscle regeneration in vertebrates, are in a state of cell cycle arrest in adult skeletal muscles. Prior evidence suggests that embryonic muscle progenitors proliferate and differentiate to form myofibres and also self-renew, implying that MuSCs, derived from these cells, acquire quiescence later during development. Depletion of Dicer in adult MuSCs promoted their exit from quiescence, suggesting microRNAs are involved in the maintenance of quiescence. Here we identified miR-195 and miR-497 that induce cell cycle arrest by targeting cell cycle genes, Cdc25 and Ccnd. Reduced expression of MyoD in juvenile MuSCs, as a result of overexpressed miR-195/ 497 or attenuated Cdc25/Ccnd, revealed an intimate link between quiescence and suppression of myogenesis in MuSCs. Transplantation of cultured MuSCs treated with miR-195/497 contributed more efficiently to regenerating muscles of dystrophin-deficient mice, indicating the potential utility of miR-195/497 for stem cell therapies.

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Section: Resultsmentioning

confidence: 99%

miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

2014

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“…In Pax3 −/− ;Myf5 −/− double mutants most skeletal muscles are lost. However, muscles in the cranial part of the embryo are not affected in these mutant mice (3), showing that myogenesis in head skeletal muscles is controlled by a different upstream genetic network (2). Indeed, head muscles are formed from cranial mesoderm, derived from Pax3 − ;Mesp1 + (mesoderm posterior homolog transcription factor 1) cells (4,5).…”

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confidence: 99%

“…However, upstream regulators of the myogenic program differ in different parts of the body. Skeletal muscles of the trunk and limbs derive from the somites and thus are descendants of progenitors expressing Pax3, a paired box transcription factor that plays a major role in the control of myogenesis (1,2). In Pax3 −/− ;Myf5 −/− double mutants most skeletal muscles are lost.…”

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confidence: 99%

Clonal analysis reveals a common origin between nonsomite-derived neck muscles and heart myocardium

Lescroart

Hamou

Francou

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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108

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Neck muscles constitute a transition zone between somite-derived skeletal muscles of the trunk and limbs, and muscles of the head, which derive from cranial mesoderm. The trapezius and sternocleidomastoid neck muscles are formed from progenitor cells that have expressed markers of cranial pharyngeal mesoderm, whereas other muscles in the neck arise from Pax3-expressing cells in the somites. Mef2c-AHF-Cre genetic tracing experiments and Tbx1 mutant analysis show that nonsomitic neck muscles share a gene regulatory network with cardiac progenitor cells in pharyngeal mesoderm of the second heart field (SHF) and branchial arch-derived head muscles. Retrospective clonal analysis shows that this group of neck muscles includes laryngeal muscles and a component of the splenius muscle, of mixed somitic and nonsomitic origin. We demonstrate that the trapezius muscle group is clonally related to myocardium at the venous pole of the heart, which derives from the posterior SHF. The left clonal sublineage includes myocardium of the pulmonary trunk at the arterial pole of the heart. Although muscles derived from the first and second branchial arches also share a clonal relationship with different SHF-derived parts of the heart, neck muscles are clonally distinct from these muscles and define a third clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal mesoderm. By linking neck muscle and heart development, our findings highlight the importance of cardiopharyngeal mesoderm in the evolution of the vertebrate heart and neck and in the pathophysiology of human congenital disease.neck muscles | myocardium | retrospective clonal analysis | mouse embryo | Tbx1

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“…Formation of multinucleated, contractile skeletal myotubes from muscle precursor cells involves precise integration of numerous muscle gene programs that are regulated by the cooperative activity of muscle-specific and broadly expressed transcription factors (1,2). The gene regulatory network that drives skeletal muscle formation in Drosophila is centered on MEF2, 2 the exclusive member of this evolutionarily conserved transcription factor in these animals, whose activity is essential for muscle differentiation and the control of a spectrum of genes throughout all stages of muscle development (3)(4)(5).…”

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confidence: 99%

MEF2 Transcription Factors Regulate Distinct Gene Programs in Mammalian Skeletal Muscle Differentiation

Estrella

Desjardins

Nocco

et al. 2015

Journal of Biological Chemistry

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Background: Myocyte enhancer factor 2 (MEF2) proteins are essential for skeletal muscle development and regeneration, but their diverse roles in differentiation have not been defined. Results: Individual MEF2 proteins regulate distinct gene programs in skeletal muscle. Conclusion: Certain genes are preferentially sensitive to a specific MEF2 isoform. Significance: These findings provide opportunities to modulate MEF2 isoform-sensitive genes in skeletal muscle health and disease.

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Gene Regulatory Networks and Transcriptional Mechanisms that Control Myogenesis

Cited by 543 publications

References 93 publications

miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

Clonal analysis reveals a common origin between nonsomite-derived neck muscles and heart myocardium

MEF2 Transcription Factors Regulate Distinct Gene Programs in Mammalian Skeletal Muscle Differentiation

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