title: 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.
authors: Developmental Biology and Molecular Pathology, W7, Bielefeld University, 33501 Bielefeld, Germany.
authors: Peter
authors: P
authors: Heimann
authors: Thilo
authors: T
authors: Kuschel
authors: Harald
authors: H
authors: Jockusch
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015220:Calcium Channels / Q000235:genetics*; D004622:Embryo, Mammalian / Q000503:physiopathology; D051379:Mice; D008817:Mice, Mutant Strains; D017348:Microscopy, Electron, Scanning Transmission; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000166:cytology*; D018482:Muscle, Skeletal / Q000196:embryology / Q000503:physiopathology*; D009135:Muscular Diseases / Q000503:physiopathology*; D009154:Mutation / Q000235:genetics; D009336:Necrosis
chemical_list: D015220:Calcium Channels