Deletions of <i>NRXN1</i> (neurexin‐1) predispose to a wide spectrum of developmental disorders

Michael S. Ching(Boston Children's Hospital), Yiping Shen(Boston Children's Hospital), Wen‐Hann Tan(Boston Children's Hospital), Shafali Jeste(Boston Children's Hospital), Eric M. Morrow(Brown University), Xiaoli Chen(Boston Children's Hospital), Nahit Motavallı Mukaddes(Istanbul University), Seung‐Yun Yoo(Boston Children's Hospital), Ellen Hanson(Boston Children's Hospital), Rachel J. Hundley(Boston Children's Hospital), Christina L. Austin(Boston Children's Hospital), Ronald E. Becker(Boston Children's Hospital), Gerard T. Berry(Boston Children's Hospital), Katherine Driscoll(Boston Children's Hospital), Elizabeth C. Engle(Boston Children's Hospital), Sandra Friedman(Boston Children's Hospital), James F. Gusella(Harvard University), Fuki M. Hisama(Boston Children's Hospital), Mira Irons(Boston Children's Hospital), Tina Lafiosca(Boston Children's Hospital), Elaine LeClair(Boston Children's Hospital), David T. Miller(Boston Children's Hospital), Michael Neessen(Boston Children's Hospital), Jonathan Picker(Boston Children's Hospital), Leonard Rappaport(Boston Children's Hospital), Cynthia M. Rooney(Boston Children's Hospital), Dean Sarco(Boston Children's Hospital), Joan M. Stoler(Boston Children's Hospital), Christopher A. Walsh(Boston Children's Hospital), Robert R. Wolff(Boston Children's Hospital), Ting Zhang(Capital Institute of Pediatrics), Ramzi H. Nasir(Boston Children's Hospital), Bai‐Lin Wu(Boston Children's Hospital)
American Journal of Medical Genetics Part B Neuropsychiatric Genetics
April 7, 2010
Cited by 309Open Access
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Abstract

Research has implicated mutations in the gene for neurexin-1 (NRXN1) in a variety of conditions including autism, schizophrenia, and nicotine dependence. To our knowledge, there have been no published reports describing the breadth of the phenotype associated with mutations in NRXN1. We present a medical record review of subjects with deletions involving exonic sequences of NRXN1. We ascertained cases from 3,540 individuals referred clinically for comparative genomic hybridization testing from March 2007 to January 2009. Twelve subjects were identified with exonic deletions. The phenotype of individuals with NRXN1 deletion is variable and includes autism spectrum disorders, mental retardation, language delays, and hypotonia. There was a statistically significant increase in NRXN1 deletion in our clinical sample compared to control populations described in the literature (P = 8.9 x 10(-7)). Three additional subjects with NRXN1 deletions and autism were identified through the Homozygosity Mapping Collaborative for Autism, and this deletion segregated with the phenotype. Our study indicates that deletions of NRXN1 predispose to a wide spectrum of developmental disorders.


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