MyoD or Myf-5 is required for the formation of skeletal muscle

Rudnicki, Michael A.; Schnegelsberg, Patrick N.J.; Stead, R. H.; Braun, Thomas; Arnold, Hans-Henning; Jaenisch, Rudolf

doi:10.1016/0092-8674(93)90621-v

Cited by 1,524 publications

(1,050 citation statements)

References 26 publications

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“…The MyoD mutant mice do exhibit an increase in the level of Myf-5 expression, which may help to compensate for the loss of MyoD . However, mice mutant for both these genes fail to establish any muscle lineage (Rudnicki et al, 1993). We have not investigated the expression of MyoD in the newt.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of myogenic regulatory genes and Msx‐1 during dedifferentiation and redifferentiation of regenerating amphibian limbs

Simon

Nelson

Goff

et al. 1995

Developmental Dynamics

108

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An amputated limb of an adult urodele amphibian is capable of undergoing regeneration. The new structures form from an undifferentiated mass of cells called the regenerative blastema. The cells of the blastema are believed to derive from differentiated tissues of the adult limb. However, the exact source of these cells and the process by which they undergo dedifferentiation are poorly understood. In order to elucidate the molecular and cellular basis for dedifferentiation we isolated a number of genes which are potential regulators of the process. These include Msx‐1, which is believed to support the undifferentiated and proliferative state of cells in the embryonic limb bud; and two members of the myogenic regulatory gene family, MRF‐4 and Myf‐5, which are expressed in differentiated muscle and regulate muscle‐specific gene activity. As anticipated, we find that Msx‐1 is strongly up‐regulated during the initiation of regeneration. It remains expressed throughout regeneration but is not found in the fully regenerated limb. The myogenic gene MRF‐4 has the reverse expression pattern. It is expressed in adult limb muscle, is rapidly shut off in early regenerative blastemas, and is only reexpressed at the completion of regeneration. These kinetics are paralleled by those of a musclespecific Myosin gene. In contrast Myf‐5, a second member of the myogenic gene family, continues to be expressed throughout the regenerative process. Thus, MRF‐4 and Myf‐5 are likely to play distinct roles during regeneration. MRF‐4 may directly regulate muscle phenotype and as such its repression may be a key event in dedifferentiation. Myf‐5 may play a role in maintaining a distinct myogenic lineage during regeneration. © 1995 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Differential expression of myogenic regulatory genes and Msx‐1 during dedifferentiation and redifferentiation of regenerating amphibian limbs

Simon

Nelson

Goff

et al. 1995

Developmental Dynamics

108

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“…Our understanding of skeletal muscle development has been substantially enhanced by the creation and analysis of mice carrying null mutations in one or more of these myogenic regulators (reviewed by Weintraub, 1993;Arnold and Braun, 1996). For example, it is now clear that in mice MyoD and Myf-5 share redundant functions for generating myoblasts, but expression of either one or the other is essential for skeletal muscle development (Rudnicki et al, 1993). In contrast, mice with null mutations in myogenin make myoblasts, but they fail to di erentiate (Hasty et al, 1993;Nabeshima et al, 1993).…”

Section: Lessons From Skeletal Muscle Developmentmentioning

confidence: 99%

Rhabdomyosarcoma – working out the pathways

1999

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Rhabdomyosarcomas constitute a collection of childhood malignancies thought to arise as a consequence of regulatory disruption of skeletal muscle progenitor cell growth and di erentiation. Our understanding of the pathogenesis of this neoplasm has recently bene®ted from the study of normal and malignant myogenic cells in vitro, facilitating the identi®cation of diagnostic cytogenetic markers and the elucidation of mechanisms by which myogenesis is regulated. It is now appreciated that the delicate balance between proliferation and di erentiation, mutually exclusive yet intimately associated processes, is normally controlled in large part through the action of a multitude of growth factors, whose signals are interpreted by members of the MyoD family of helix ± loop ± helix proteins, and key regulatory cell cycle factors. The latter have proven to be frequent targets of mutational events that subvert myogenesis and promote the development of rhabdomyosarcoma. Although signi®cant progress has been made in the treatment of rhabdomyosarcoma, patients presenting with metastatic disease or certain high risk features are still faced with a dismal prognosis. Only now are genetically engineered mouse models becoming available that are certain to provide fresh insights into the molecular/genetic pathways by which rhabdomyosarcomas arise and progress, and to suggest novel avenues of therapeutic opportunity.

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“…At the embryonic stage, PAX7 is first expressed in the central dermomyotome and then colocalized with PAX3 in the myotome (Relaix, Rocancourt, Mansouri & Buckingham, 2005). The PAX3 + /PAX7 + cells then become embryonic muscle progenitor cells, which enter into the myogenic process and are differentiated into myoblasts with the expression of MYF5 and MYOD (Bober et al., 1991; Rudnicki et al., 1993; Sassoon et al., 1989). At the postnatal stage, satellite cells originate from PAX3 + /PAX7 + cells.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effects of TGFβ2, WNT9a, and FGFR4 signals attenuate satellite cell differentiation during skeletal muscle development

Zhang

et al. 2018

Aging Cell

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SummarySatellite cells play a key role in the aging, generation, and damage repair of skeletal muscle. The molecular mechanism of satellite cells in these processes remains largely unknown. This study systematically investigated for the first time the characteristics of mouse satellite cells at ten different ages. Results indicated that the number and differentiation capacity of satellite cells decreased with age during skeletal muscle development. Transcriptome analysis revealed that 2,907 genes were differentially expressed at six time points at postnatal stage. WGCNA and GO analysis indicated that 1,739 of the 2,907 DEGs were mainly involved in skeletal muscle development processes. Moreover, the results of WGCNA and protein interaction analysis demonstrated that Tgfβ2, Wnt9a, and Fgfr4 were the key genes responsible for the differentiation of satellite cells. Functional analysis showed that TGFβ2 and WNT9a inhibited, whereas FGFR4 promoted the differentiation of satellite cells. Furthermore, each two of them had a regulatory relationship at the protein level. In vivo study also confirmed that TGFβ2 could regulate the regeneration of skeletal muscle, as well as the expression of WNT9a and FGFR4. Therefore, we concluded that the synergistic effects of TGFβ2, WNT9a, and FGFR4 were responsible for attenuating of the differentiation of aging satellite cells during skeletal muscle development. This study provided new insights into the molecular mechanism of satellite cell development. The target genes and signaling pathways investigated in this study would be useful for improving the muscle growth of livestock or treating muscle diseases in clinical settings.

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MyoD or Myf-5 is required for the formation of skeletal muscle

Cited by 1,524 publications

References 26 publications

Differential expression of myogenic regulatory genes and Msx‐1 during dedifferentiation and redifferentiation of regenerating amphibian limbs

Differential expression of myogenic regulatory genes and Msx‐1 during dedifferentiation and redifferentiation of regenerating amphibian limbs

Rhabdomyosarcoma – working out the pathways

Synergistic effects of TGFβ2, WNT9a, and FGFR4 signals attenuate satellite cell differentiation during skeletal muscle development

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