Efficient strategy for the molecular diagnosis of intellectual disability using targeted high-throughput sequencing

نویسندگان

  • Claire Redin
  • Bénédicte Gérard
  • Julia Lauer
  • Yvan Herenger
  • Jean Muller
  • Angélique Quartier
  • Alice Masurel-Paulet
  • Marjolaine Willems
  • Gaétan Lesca
  • Salima El-Chehadeh
  • Stéphanie Le Gras
  • Serge Vicaire
  • Muriel Philipps
  • Michaël Dumas
  • Véronique Geoffroy
  • Claire Feger
  • Nicolas Haumesser
  • Yves Alembik
  • Magalie Barth
  • Dominique Bonneau
  • Estelle Colin
  • Hélène Dollfus
  • Bérénice Doray
  • Marie-Ange Delrue
  • Valérie Drouin-Garraud
  • Elisabeth Flori
  • Mélanie Fradin
  • Christine Francannet
  • Alice Goldenberg
  • Serge Lumbroso
  • Michèle Mathieu-Dramard
  • Dominique Martin-Coignard
  • Didier Lacombe
  • Gilles Morin
  • Anne Polge
  • Sylvie Sukno
  • Christel Thauvin-Robinet
  • Julien Thevenon
  • Martine Doco-Fenzy
  • David Genevieve
  • Pierre Sarda
  • Patrick Edery
  • Bertrand Isidor
  • Bernard Jost
  • Laurence Olivier-Faivre
  • Jean-Louis Mandel
  • Amélie Piton
چکیده

BACKGROUND Intellectual disability (ID) is characterised by an extreme genetic heterogeneity. Several hundred genes have been associated to monogenic forms of ID, considerably complicating molecular diagnostics. Trio-exome sequencing was recently proposed as a diagnostic approach, yet remains costly for a general implementation. METHODS We report the alternative strategy of targeted high-throughput sequencing of 217 genes in which mutations had been reported in patients with ID or autism as the major clinical concern. We analysed 106 patients with ID of unknown aetiology following array-CGH analysis and other genetic investigations. Ninety per cent of these patients were males, and 75% sporadic cases. RESULTS We identified 26 causative mutations: 16 in X-linked genes (ATRX, CUL4B, DMD, FMR1, HCFC1, IL1RAPL1, IQSEC2, KDM5C, MAOA, MECP2, SLC9A6, SLC16A2, PHF8) and 10 de novo in autosomal-dominant genes (DYRK1A, GRIN1, MED13L, TCF4, RAI1, SHANK3, SLC2A1, SYNGAP1). We also detected four possibly causative mutations (eg, in NLGN3) requiring further investigations. We present detailed reasoning for assigning causality for each mutation, and associated patients' clinical information. Some genes were hit more than once in our cohort, suggesting they correspond to more frequent ID-associated conditions (KDM5C, MECP2, DYRK1A, TCF4). We highlight some unexpected genotype to phenotype correlations, with causative mutations being identified in genes associated to defined syndromes in patients deviating from the classic phenotype (DMD, TCF4, MECP2). We also bring additional supportive (HCFC1, MED13L) or unsupportive (SHROOM4, SRPX2) evidences for the implication of previous candidate genes or mutations in cognitive disorders. CONCLUSIONS With a diagnostic yield of 25% targeted sequencing appears relevant as a first intention test for the diagnosis of ID, but importantly will also contribute to a better understanding regarding the specific contribution of the many genes implicated in ID and autism.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Mutation in Aminoacyl Trna Synthetase 1 In Autosomal Recessive ‎Intellectual Disability ‎

Background: Intellectual disability (ID) is one of the most common neurodevelopment disorders that caused by both environment and genetic factors. Also genetic defects have involving for approximately 50% of ID etiology, it is demonstrated that genetics play significant role in ID development. The important risk factor in most country in ID is consanguinity marriage. Iran has high frequency of ...

متن کامل

Identification of a novel candidate gene for non-syndromic autosomal recessive intellectual disability: the WASH complex member SWIP.

High-throughput sequencing has greatly facilitated the elucidation of genetic disorders, but compared with X-linked and autosomal dominant diseases, the search for genetic defects underlying autosomal recessive diseases still lags behind. In a large consanguineous family with autosomal recessive intellectual disability (ARID), we have combined homozygosity mapping, targeted exon enrichment and ...

متن کامل

Development of a Targeted Multi-Disorder High-Throughput Sequencing Assay for the Effective Identification of Disease-Causing Variants

BACKGROUND While next generation sequencing (NGS) is a useful tool for the identification of genetic variants to aid diagnosis and support therapy decision, high sequencing costs have limited its application within routine clinical care, especially in economically depressed areas. To investigate the utility of a multi-disease NGS based genetic test, we designed a custom sequencing assay targeti...

متن کامل

Strategies and Clinical Applications of Next Generation Sequencing

Abstract DNA sequencing is one of the great valuable techniques in molecular biology, which can be used to detect the sequence of nucleotides in a DNA fragment. The high-throughput se­quencing known as Next Generation Sequencing (NGS) revolutionized genomic research and molecular biology; therefore, the whole human genome can be sequenced with a low cost in several days. NGS technology is simi...

متن کامل

Identification of genetic causes of congenital neurodevelopmental disorders using genome wide molecular technologies

BACKGROUND Intellectual disability affects about 1-2% of the general population worldwide, and this is the leading socio-economic problem of health care. The evaluation of the genetic causes of intellectual disability is challenging because these conditions are genetically heterogeneous with many different genetic alterations resulting in clinically indistinguishable phenotypes. Genome wide mol...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 51  شماره 

صفحات  -

تاریخ انتشار 2014