Exome sequencing of two patients in a family with atypical X-linked leukodystrophy

Clin Genet. 2011 Aug;80(2):161-6. doi: 10.1111/j.1399-0004.2011.01721.x. Epub 2011 Jun 21.

Abstract

We encountered a family with two boys similarly showing brain atrophy with reduced white matter, hypoplasia of the brain stem and corpus callosum, spastic paralysis, and severe growth and mental retardation without speaking a word. The phenotype of these patients was not compatible with any known type of syndromic leukodystrophy. Presuming an X-linked disorder, we performed next-generation sequencing (NGS) of the transcripts of the entire X chromosome. A single lane of exome NGS in each patient was sufficient. Six potential mutations were found in both affected boys. Two missense mutations, including c.92T>C (p.V31A) in L1CAM, were potentially pathogenic, but this remained inconclusive. The other four could be excluded. Because the patients did not show adducted thumbs or hydrocephalus, the L1CAM change in this family can be interpreted as different scenarios. Personal genome analysis using NGS is certainly powerful, but interpretation of the data can be a substantial challenge requiring a lot of tasks.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abnormalities, Multiple / genetics
  • Agenesis of Corpus Callosum*
  • Base Sequence
  • Brain Stem / abnormalities*
  • Exons
  • Family
  • Genes, X-Linked
  • Genetic Diseases, X-Linked / diagnosis
  • Genetic Diseases, X-Linked / genetics*
  • Genome, Human
  • High-Throughput Nucleotide Sequencing
  • Humans
  • Hydrocephalus / genetics
  • Intellectual Disability / genetics
  • Leukoencephalopathies / diagnosis
  • Leukoencephalopathies / genetics*
  • Male
  • Mutation*
  • Mutation, Missense
  • Neural Cell Adhesion Molecule L1 / genetics
  • Pedigree

Substances

  • Neural Cell Adhesion Molecule L1