Copy number variations in a Brazilian cohort with autism spectrum disorders highlight the contribution of cell adhesion genes

Clin Genet. 2022 Jan;101(1):134-141. doi: 10.1111/cge.14072. Epub 2021 Nov 15.

Abstract

Prediction of pathogenicity of rare copy number variations (CNVs), a genomic alteration known to contribute to the etiology of autism spectrum disorder (ASD), represents a serious limitation to interpreting genetic tests, particularly for genetic counseling purposes. Chromosomal microarray analysis (CMA) was conducted in a unique collection of 144 Brazilian individuals with ASD of strong European and African ancestries. Rare CNVs were detected in 39 patients: 41 of unknown significance (VUS), four pathogenic and one likely pathogenic CNVs (clinical yield of 4.1%; 5/122). Based on gene content and recurrence in three large cohorts [a Brazilian neurodevelopmental disorder cohort, the autism MSSNG cohort, and the Canadian-based Centre for Applied Genomics microarray database], this work strengthened the pathogenicity of 14 genes (FAT1, CAMK4, BIRC6, DPP6, CSMD1, CTNNA3, CDH8/CDH11, CDH13, OR1C1, CNTN6, CNTNAP4, FGF2 and PTPRN2) within 14 CNVs. Notably, enrichment of cell adhesion proteins to ASD etiology was identified (p < 0.05), highlighting the importance of these gene families in the etiology of ASD.

Keywords: FGF2; PTPRN2; autism spectrum disorders; cell adhesion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Alleles*
  • Autism Spectrum Disorder / diagnosis*
  • Autism Spectrum Disorder / genetics*
  • Brazil
  • Cell Adhesion / genetics*
  • Child
  • Child, Preschool
  • Chromosome Mapping
  • Comparative Genomic Hybridization
  • DNA Copy Number Variations*
  • Female
  • Genetic Association Studies
  • Genetic Predisposition to Disease*
  • Humans
  • Infant
  • Male
  • Phenotype
  • Young Adult