[Copy-number variations of SHANK3 and related clinical phenotypes in children with autism]

Zhonghua Er Ke Za Zhi. 2011 Aug;49(8):607-11.
[Article in Chinese]

Abstract

Objective: To explore possible relationship between copy-number variations (CNVs) in 15q11-13, 16p11 and SHANK3 gene by using multiplex ligation-dependent probe amplification (MLPA) and the phenotypes in children with autism and to further explore the clinical application of MLPA to make an etiological diagnosis of Autism.

Methods: The diagnosed of autism was made according to the criteria of the ICD-10 and DSM-IV, with typical cluster of symptoms comprise social disability, communication impairments and repetitious behaviors. MLPA KIT P343-C1 AUTISM-1 was used to detect and describe the incidence of CNVs in these three domains.

Results: Among 109 cases collected from 102 autistic pedigrees, 2 individuals had SHANK3 microdeletion, accounting for approximately 2% (2/109) of cases, suggesting the proportion of SHANK3 microdeletion might contribute to typical autism. The phenotypic traits of patients with SHANK3 microdeletions showed homogenicity in severe core symptoms and mental retardation.

Conclusions: SHANK3 microdeletion is an important genetics component for autism, which may explain 2% typical autism cases. SHANK3 microdeletion might explain autistic core symptoms and mental retardation. MLPA is a sensitive and a high throughput technique to detect CNVs in specific DNA segments, which is beneficial for further investigation of etiology of autism.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autistic Disorder / genetics*
  • Carrier Proteins / genetics*
  • Child
  • Child, Preschool
  • DNA Copy Number Variations*
  • Female
  • Gene Deletion
  • Humans
  • Male
  • Nerve Tissue Proteins
  • Phenotype*

Substances

  • Carrier Proteins
  • Nerve Tissue Proteins
  • SHANK3 protein, human