Deletion of the LMNA initiator codon leading to a neurogenic variant of autosomal dominant Emery-Dreifuss muscular dystrophy

Neuromuscul Disord. 2005 Jan;15(1):40-4. doi: 10.1016/j.nmd.2004.09.007.

Abstract

Mutations in the LMNA gene encoding the nuclear envelope protein, lamins A and C, have been associated with at least nine distinct disorders now called laminopathies, including Emery-Dreifuss muscular dystrophy and Charcot-Marie-Tooth type 2 disease. We identified a novel mutation in the 5' region of the LMNA gene -3del15, resulting in the loss of 15 nucleotides from -3 to +12, including the translation ATG initiator codon. The mutation segregates in a previously described family with a clinical phenotype that shared features of both Emery-Dreifuss muscular dystrophy and Charcot-Marie-Tooth type 2. Thus, the mutation with this unique phenotypical expression represents the first example for a link between the neurogenic and myogenic phenotypes and extends the clinical variability of laminopathies.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Codon, Initiator / genetics*
  • DNA Mutational Analysis / methods
  • Family Health
  • Female
  • Gene Deletion*
  • Humans
  • Lamin Type A / genetics*
  • Male
  • Middle Aged
  • Muscle, Skeletal / pathology
  • Muscular Dystrophy, Emery-Dreifuss / genetics*
  • Muscular Dystrophy, Emery-Dreifuss / pathology

Substances

  • Codon, Initiator
  • Lamin Type A