Mouse dystrophin enhancer preferentially targets lacZ expression in skeletal and cardiac muscle

Dev Dyn. 2002 May;224(1):30-8. doi: 10.1002/dvdy.10080.

Abstract

Duchenne muscular dystrophy is a muscle wasting disease that results from a dystrophin deficiency in skeletal and cardiac muscle. Studies concerning the regulatory elements that govern dystrophin gene expression in skeletal and/or cardiac muscle in both mouse and human have identified a promoter and an enhancer located in intron 1. In transgenic mice, the muscle promoter alone targets the expression of a lacZ reporter gene only to the right ventricle of the heart, suggesting the need for other regulatory elements to target skeletal muscle and the rest of the heart. Here we report that the mouse dystrophin enhancer from intron 1 can target the expression of a lacZ reporter gene in skeletal muscle as well as in other heart compartments of transgenic mice. Our results also suggest that sequences surrounding the mouse dystrophin enhancer may affect its function throughout mouse development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Dystrophin / genetics*
  • Dystrophin / metabolism
  • Embryo, Mammalian / metabolism
  • Embryonic and Fetal Development
  • Enhancer Elements, Genetic / genetics*
  • Female
  • Gene Expression Regulation*
  • Genes, Reporter
  • Humans
  • Lac Operon
  • Male
  • Mice
  • Mice, Inbred Strains
  • Mice, Transgenic
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / metabolism*
  • Muscular Dystrophy, Duchenne / genetics
  • Muscular Dystrophy, Duchenne / metabolism
  • Myocardium / cytology
  • Myocardium / metabolism*
  • Promoter Regions, Genetic

Substances

  • Dystrophin