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Elimination by necrosis, not apoptosis, of embryonic extraocular muscles in the muscular dysgenesis mutant of the mouse

Abstract

Muscular dysgenesis (mdg) in the mouse is a loss-of-function mutation of the skeletal muscle isoform of the voltage-sensor Ca2+ channel of skeletal muscle (DHP receptor alpha1 subunit, Cchl1a3, Chr1), which is essential for excitation-contraction coupling. Affected individuals (genotype mdg/mdg, phenotype MDG) are unable to breathe and die perinatally. We introduce here extraocular muscles in the study of MDG myopathy and show that, despite their developmental origin from head placodes, they are affected like trunk and limb muscles. MDG myotubes in situ are eliminated by necrosis, not apoptosis.

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Acknowledgements

We thank Sandra Heising for excellent technical help.

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Correspondence to Harald Jockusch.

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The study was supported by the Deutsche Forschungsgemeinschaft, SFB 223 C03, E02

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Heimann, P., Kuschel, T. & Jockusch, H. Elimination by necrosis, not apoptosis, of embryonic extraocular muscles in the muscular dysgenesis mutant of the mouse. Cell Tissue Res 315, 243–247 (2004). https://doi.org/10.1007/s00441-003-0831-0

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  • DOI: https://doi.org/10.1007/s00441-003-0831-0

Keywords

  • Necrosis/apoptosis
  • Calcium channel
  • Slow T-tubular
  • Muscular dysgenesis
  • Extraocular muscles
  • Mouse (mdg/mdg)