Absence of a Major Role for the Snai1 and Snai3 Genes in Regulating Skeletal Muscle Regeneration in Mice

Discussion Our results demonstrate effective skeletal muscle regeneration after cardiotoxin-mediated injury in Snai3 homozygous mutant (Snai3null/Snai3null or Snai3-EYFP/Snai3-EYFP) mice. We further show that mice with skeletal muscle-specific deletion of the Snai1 gene on a Snai3 null genetic background exhibit the same general level of skeletal muscle regeneration as the Snai3 mutant homozygotes. While our histopathological analyses cannot exclude minor regeneration defects in the Snai3 single or Snai1/Snai3 double mutants, it is clear that substantial muscle regeneration occurs after cardiotoxin-mediated injury in these mice. A recent study utilized ChIP-Seq and gene expression analyses to demonstrate that a Snai1-HDAC1/2 repressive complex bound and excluded the myogenic transcription factor MyoD from its targets 14. These authors further showed that a regulatory network involving myogenic regulatory factors, Snai1/Snai2, and the microRNAs miR-30a and miR-206 acted as a molecular switch controlling entry into myogenic differentiation. It is possible that we did not observe a substantial effect on skeletal muscle development or regeneration in our experiments because our mice were wildtype at the Snai2 locus. In 2002, we participated in a study demonstrating that Snai2 gene expression is induced during muscle regeneration, and that Snai2-lacZ homozygous null mice exhibit impaired hindlimb skeletal muscle regeneration 13. At the time of those studies, our Snai2-lacZ mice we...
Source: PLOS Currents Muscular Dystrophy - Category: Neurology Authors: Source Type: research