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Molecular Autism
Published in: Molecular Autism 1/2015

Open Access 01-12-2015 | Research

Integrated analysis of whole-exome sequencing and transcriptome profiling in males with autism spectrum disorders

Authors: Marta Codina-Solà, Benjamín Rodríguez-Santiago, Aïda Homs, Javier Santoyo, Maria Rigau, Gemma Aznar-Laín, Miguel del Campo, Blanca Gener, Elisabeth Gabau, María Pilar Botella, Armand Gutiérrez-Arumí, Guillermo Antiñolo, Luis Alberto Pérez-Jurado, Ivon Cuscó

Published in: Molecular Autism | Issue 1/2015

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Abstract

Background

Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders with high heritability. Recent findings support a highly heterogeneous and complex genetic etiology including rare de novo and inherited mutations or chromosomal rearrangements as well as double or multiple hits.

Methods

We performed whole-exome sequencing (WES) and blood cell transcriptome by RNAseq in a subset of male patients with idiopathic ASD (n = 36) in order to identify causative genes, transcriptomic alterations, and susceptibility variants.

Results

We detected likely monogenic causes in seven cases: five de novo (SCN2A, MED13L, KCNV1, CUL3, and PTEN) and two inherited X-linked variants (MAOA and CDKL5). Transcriptomic analyses allowed the identification of intronic causative mutations missed by the usual filtering of WES and revealed functional consequences of some rare mutations. These included aberrant transcripts (PTEN, POLR3C), deregulated expression in 1.7% of mutated genes (that is, SEMA6B, MECP2, ANK3, CREBBP), allele-specific expression (FUS, MTOR, TAF1C), and non-sense-mediated decay (RIT1, ALG9). The analysis of rare inherited variants showed enrichment in relevant pathways such as the PI3K-Akt signaling and the axon guidance.

Conclusions

Integrative analysis of WES and blood RNAseq data has proven to be an efficient strategy to identify likely monogenic forms of ASD (19% in our cohort), as well as additional rare inherited mutations that can contribute to ASD risk in a multifactorial manner. Blood transcriptomic data, besides validating 88% of expressed variants, allowed the identification of missed intronic mutations and revealed functional correlations of genetic variants, including changes in splicing, expression levels, and allelic expression.
Appendix
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Metadata
Title
Integrated analysis of whole-exome sequencing and transcriptome profiling in males with autism spectrum disorders
Authors
Marta Codina-Solà
Benjamín Rodríguez-Santiago
Aïda Homs
Javier Santoyo
Maria Rigau
Gemma Aznar-Laín
Miguel del Campo
Blanca Gener
Elisabeth Gabau
María Pilar Botella
Armand Gutiérrez-Arumí
Guillermo Antiñolo
Luis Alberto Pérez-Jurado
Ivon Cuscó
Publication date
01-12-2015
Publisher
BioMed Central
Published in
Molecular Autism / Issue 1/2015
Electronic ISSN: 2040-2392
DOI
https://doi.org/10.1186/s13229-015-0017-0

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