Three new PLP1 splicing mutations demonstrate pathogenic and phenotypic diversity of Pelizaeus-Merzbacher disease

J Child Neurol. 2014 Jul;29(7):924-31. doi: 10.1177/0883073813492387. Epub 2013 Jun 14.

Abstract

Pelizaeus-Merzbacher disease is a severe X-linked disorder of central myelination caused by mutations affecting the proteolipid protein gene. We describe 3 new PLP1 splicing mutations, their effect on splicing and associated phenotypes. Mutation c.453_453+6del7insA affects the exon 3B donor splice site and disrupts the PLP1-transcript without affecting the DM20, was found in a patient with severe Pelizaeus-Merzbacher disease and in his female cousin with early-onset spastic paraparesis. Mutation c.191+1G>A causes exon 2 skipping with a frame shift, is expected to result in a functionally null allele, and was found in a patient with mild Pelizaeus-Merzbacher disease and in his aunt with late-onset spastic paraparesis. Mutation c.696+1G>A utilizes a cryptic splice site in exon 5, causes partial exon 5 skipping and in-frame deletion, and was found in an isolated patient with a severe classical Pelizaeus-Merzbacher. PLP1 splice-site mutations express a variety of disease phenotypes mediated by different molecular pathogenic mechanisms.

Keywords: PLP1; Pelizaeus-Merzbacher disease; splice-site mutations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autopsy
  • Child
  • Child, Preschool
  • DNA Mutational Analysis
  • Family Health
  • Female
  • Humans
  • Male
  • Middle Aged
  • Mutation / genetics*
  • Myelin Proteolipid Protein / genetics*
  • Neural Conduction / genetics
  • Pelizaeus-Merzbacher Disease* / genetics
  • Pelizaeus-Merzbacher Disease* / pathology
  • Pelizaeus-Merzbacher Disease* / physiopathology
  • Phenotype
  • RNA Splice Sites / genetics*

Substances

  • Myelin Proteolipid Protein
  • PLP1 protein, human
  • RNA Splice Sites