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Differential physiological roles for BIN1 isoforms in skeletal muscle development, function and regeneration.

Ivana Prokic1,2,3,4, Belinda S Cowling1,2,3,4, Candice Kutchukian5

  • 1Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Department of Translational Medicine, 67404 Illkirch, France.

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|September 30, 2020
PubMed
Summary

Amphiphysin 2 (BIN1) is crucial for skeletal muscle development and intracellular organization. Its specific isoforms fine-tune regeneration, explaining congenital versus adult centronuclear myopathies (CNM).

Keywords:
Animal modelBAR domainCentronuclear myopathyDynaminMyoblast fusionMyotonic dystrophyMyotubular myopathySH3 domainTriadXLMTM

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Area of Science:

  • Muscle biology
  • Cellular organization
  • Membrane dynamics

Background:

  • Skeletal muscle development and regeneration are complex processes.
  • Intracellular organization of muscle fibers during these stages is not fully understood.
  • Amphiphysin 2 (BIN1), a membrane remodeling protein, is implicated in centronuclear myopathies (CNM) and has muscle-specific isoforms.

Purpose of the Study:

  • To investigate the cellular and physiological roles of BIN1 in skeletal muscle.
  • To elucidate the function of BIN1's ubiquitous and muscle-specific isoforms in muscle development and regeneration.

Main Methods:

  • Creation and characterization of constitutive and inducible muscle-specific and ubiquitous *Bin1* knockout mouse models.
  • Analysis of skeletal muscle defects, T-tubule organization, and regeneration capacity in knockout mice.

Main Results:

  • Constitutive *Bin1*-deficient mice exhibited perinatal lethality with severe skeletal muscle defects, including misplaced T-tubules and organelles.
  • Deletion of muscle-specific BIN1 isoforms in adult mice did not affect unchallenged muscle but delayed regeneration when ubiquitous isoforms were forced.
  • Ubiquitous BIN1 function is essential for muscle development and function.

Conclusions:

  • BIN1 plays a critical role in early skeletal muscle development and intracellular organization.
  • Muscle-specific BIN1 isoforms are important for efficient muscle regeneration in adulthood.
  • Congenital CNM may result from developmental defects, while later-onset CNM could stem from regeneration impairments related to BIN1 function.