AKAP2 identified as a novel gene mutated in a Chinese family with adolescent idiopathic scoliosis

J Med Genet. 2016 Jul;53(7):488-93. doi: 10.1136/jmedgenet-2015-103684. Epub 2016 Mar 17.

Abstract

Background: Adolescent idiopathic scoliosis exhibits high heritability and is one of the most common spinal deformities found in adolescent populations. However, little is known about the disease-causing genes in families with adolescent idiopathic scoliosis exhibiting Mendelian inheritance.

Objective: The aim of this study was to identify the causative gene in a family with adolescent idiopathic scoliosis.

Methods: Whole-exome sequencing was performed on this family to identify the candidate gene. Sanger sequencing was conducted to validate the candidate mutations and familial segregation. Real-time QPCR was used to measure the expression level of the possible causative gene.

Results: We identified the mutation c.2645A>C (p.E882A) within the AKAP2 gene, which cosegregated with the adolescent idiopathic scoliosis phenotypes. AKAP2 is located in a previously reported linkage locus (IS4) on chromosome 9q31.2-q34.2 and has been implicated in skeletal development. The mutation was absent in dbSNP144, ESP6500 and 503 ethnicity-matched controls. Real-time QPCR revealed that the mRNA expression level in the patients was increased significantly compared with the family controls (p<0.0001).

Conclusions: AKAP2 was therefore implicated as a novel gene mutated in a Chinese family with adolescent idiopathic scoliosis. Further studies should be conducted to validate the results from the perspective of both the genetics and pathogenesis of this disease.

Keywords: AKAP2; adolescent idiopathic scoliosis; whole-exome sequencing.

MeSH terms

  • A Kinase Anchor Proteins / genetics*
  • Adolescent
  • Asian People / genetics*
  • Chromosome Mapping
  • Exome / genetics
  • Female
  • Genetic Linkage / genetics
  • Humans
  • Male
  • Membrane Proteins / genetics*
  • Mendelian Randomization Analysis / methods
  • Mutation / genetics*
  • Phenotype
  • Polymorphism, Single Nucleotide / genetics
  • Scoliosis / genetics*

Substances

  • A Kinase Anchor Proteins
  • AKAP2 protein, human
  • Membrane Proteins