PubMed 14618389
Referenced in: none
Automatically associated channels: Cav1.1
Title: Elimination by necrosis, not apoptosis, of embryonic extraocular muscles in the muscular dysgenesis mutant of the mouse.
Authors: Peter Heimann, Thilo Kuschel, Harald Jockusch
Journal, date & volume: Cell Tissue Res., 2004 Feb , 315, 243-7
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/14618389
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.