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Differential requirements for Myocyte Enhancer Factor-2 during adult myogenesis in Drosophila.

Anton L Bryantsev | Phillip W Baker | TyAnna L Lovato | MaryAnn S Jaramillo | Richard M Cripps
Developmental biology | 2012

Identifying the genetic program that leads to formation of functionally and morphologically distinct muscle fibers is one of the major challenges in developmental biology. In Drosophila, the Myocyte Enhancer Factor-2 (MEF2) transcription factor is important for all types of embryonic muscle differentiation. In this study we investigated the role of MEF2 at different stages of adult skeletal muscle formation, where a diverse group of specialized muscles arises. Through stage- and tissue-specific expression of Mef2 RNAi constructs, we demonstrate that MEF2 is critical at the early stages of adult myoblast fusion: mutant myoblasts are attracted normally to their founder cell targets, but are unable to fuse to form myotubes. Interestingly, ablation of Mef2 expression at later stages of development showed MEF2 to be more dispensable for structural gene expression: after myoblast fusion, Mef2 knockdown did not interrupt expression of major structural gene transcripts, and myofibrils were formed. However, the MEF2-depleted fibers showed impaired integrity and a lack of fibrillar organization. When Mef2 RNAi was induced in muscles following eclosion, we found no adverse effects of attenuating Mef2 function. We conclude that in the context of adult myogenesis, MEF2 remains an essential factor, participating in control of myoblast fusion, and myofibrillogenesis in developing myotubes. However, MEF2 does not show a major requirement in the maintenance of muscle structural gene expression. Our findings point to the importance of a diversity of regulatory factors that are required for the formation and function of the distinct muscle fibers found in animals.

Pubmed ID: 22008792

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Associated grants

  • Agency: NIGMS NIH HHS, United States
    Id: R25 GM060201-11
  • Agency: NIGMS NIH HHS, United States
    Id: R25 GM060201
  • Agency: NCRR NIH HHS, United States
    Id: 1P20RR18754
  • Agency: NCRR NIH HHS, United States
    Id: P20 RR018754
  • Agency: NIGMS NIH HHS, United States
    Id: R01 GM061738
  • Agency: NIGMS NIH HHS, United States
    Id: GM061738
  • Agency: NIGMS NIH HHS, United States
    Id: R01 GM061738-10A1

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