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Proteins targeted to the nucleus carry short stretches of amino acid sequences called the nuclear localization signal or NLS. Classical nuclear localization signals are of two types: monopartite and bipartite NLS. Monopartite classical NLS (cNLS) consists of a single cluster of 4-8 amino acids. Bipartite cNLS consists of two clusters of  2-3 amino acids and a 9-12 residue long proline-rich linker bridging the two clusters. Signal clusters are rich in positively charged amino acids such as...
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De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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Nuclear protein sorting is the selective trafficking of histones, polymerases, gene regulatory proteins into the nucleus and exporting RNAs and ribosomes to the cytosol. It is a tightly controlled process that regulates gene expression within a cell.
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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
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Nuclear positioning in muscle development and disease.

Eric S Folker1, Mary K Baylies2

  • 1Department of Biology, Boston College Chestnut Hill, MA, USA.

Frontiers in Physiology
|December 31, 2013
PubMed
Summary

Mispositioned myonuclei in muscle cells, often seen as a sign of repair, may actually cause muscle weakness. This review explores nuclear positioning mechanisms and their link to muscular dystrophy.

Keywords:
Nuclear movementcytoskeletonmuscle diseasenucleoskeleton

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Area of Science:

  • Cell Biology
  • Muscle Physiology
  • Molecular Biology

Background:

  • Muscle diseases share symptoms like weakness and loss of function.
  • A common cellular hallmark is the mispositioning of myonuclei, shifting from peripheral to central locations.
  • This nuclear mispositioning is often viewed as a repair indicator rather than a cause of weakness.

Purpose of the Study:

  • To review evidence suggesting myonuclear mispositioning contributes to muscle disease.
  • To explore models of myonuclear movement from nuclear and cytoskeletal perspectives.
  • To compare muscle nuclear movement with that in other cell types and identify disease-related factors.

Main Methods:

  • Literature review of cellular pathologies in muscle disorders.
  • Analysis of working models for myonuclear transport and positioning.
  • Comparison of nuclear movement mechanisms across different cell types.
  • Investigation of genetic factors linked to myonuclear positioning and muscular dystrophy.

Main Results:

  • Myonuclei mispositioning is presented not just as a symptom but potentially as a cause of muscle weakness.
  • Mechanisms of nuclear movement are discussed from both nuclear and cytoskeletal viewpoints.
  • Genes regulating myonuclear positioning are implicated in muscular dystrophy, though causality is under investigation.

Conclusions:

  • Myonuclear position is a critical factor in muscle function and disease, not just a diagnostic marker.
  • Understanding nuclear movement mechanisms is key to deciphering muscle pathologies.
  • Further research into the role of myonuclear positioning in muscular dystrophy is warranted.