Alu-specific microhomology-mediated deletions in CDKL5 in females with early-onset seizure disorder

Neurogenetics. 2009 Oct;10(4):363-9. doi: 10.1007/s10048-009-0195-z. Epub 2009 May 27.

Abstract

Mutations in the cyclin-dependent kinase-like 5 (CDKL5) gene in Xp22.13 have been associated with infantile spasms, early-onset intractable epilepsy, and a Rett syndrome (RTT)-like phenotype. Using array comparative genomic hybridization, we identified variable-sized microdeletions involving exons 1-4 of the CDKL5 gene in three females with early-onset seizures. Two of these deletions were flanked by Alu repetitive elements and may have resulted from either non-allelic homologous recombination or the microhomology-mediated Fork Stalling and Template Switching/Microhomology-Mediated Break-Induced Replication mechanism. Our findings demonstrate the first instance of genomic deletion as the molecular basis of CDKL5 deficiency in females and highlight the importance of exon targeted array-CGH analysis for this gene in females with drug-resistant early-onset seizures.

Publication types

  • Case Reports
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abnormalities, Multiple / genetics
  • Age of Onset
  • Amino Acid Sequence
  • Base Sequence
  • Child, Preschool
  • Comparative Genomic Hybridization
  • DNA Mutational Analysis
  • Female
  • Humans
  • In Situ Hybridization, Fluorescence
  • Infant
  • Male
  • Molecular Sequence Data
  • Phenotype
  • Protein Serine-Threonine Kinases / genetics*
  • Rett Syndrome / genetics
  • Rett Syndrome / physiopathology
  • Seizures* / genetics
  • Seizures* / physiopathology
  • Sequence Deletion*
  • X Chromosome Inactivation
  • Young Adult

Substances

  • Protein Serine-Threonine Kinases
  • CDKL5 protein, human