De novo genic mutations among a Chinese autism spectrum disorder cohort

Tianyun Wang(Central South University), Hui Guo(Central South University), Bo Xiong(University of Washington), Holly A.F. Stessman(University of Washington), Huidan Wu(Central South University), Bradley P. Coe(University of Washington), Tychele N. Turner(University of Washington), Yanling Liu(Central South University), Wenjing Zhao(Central South University), Kendra Hoekzema(University of Washington), Laura Vives(University of Washington), Lu Xia(Central South University), Meina Tang(Central South University), Jianjun Ou(Central South University), Biyuan Chen(Sun Yat-sen University), Yidong Shen(Central South University), Guanglei Xun(Shandong Mental Health Center), Long Min(Central South University), Janice Lin(University of Washington), Zev Kronenberg(University of Washington), Yu Peng(Central South University), Ting Bai(Central South University), Honghui Li(Liuzhou Maternal and Child Health Hospital), Xiaoyan Ke(Nanjing Brain Hospital), Zhengmao Hu(Central South University), Jingping Zhao(Central South University), Xiaobing Zou(Sun Yat-sen University), Kun Xia(Central South University), Evan E. Eichler(Howard Hughes Medical Institute)
Nature Communications
November 8, 2016
Cited by 391Open Access
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Abstract

Recurrent de novo (DN) and likely gene-disruptive (LGD) mutations contribute significantly to autism spectrum disorders (ASDs) but have been primarily investigated in European cohorts. Here, we sequence 189 risk genes in 1,543 Chinese ASD probands (1,045 from trios). We report an 11-fold increase in the odds of DN LGD mutations compared with expectation under an exome-wide neutral model of mutation. In aggregate, ∼4% of ASD patients carry a DN mutation in one of just 29 autism risk genes. The most prevalent gene for recurrent DN mutations is SCN2A (1.1% of patients) followed by CHD8, DSCAM, MECP2, POGZ, WDFY3 and ASH1L. We identify novel DN LGD recurrences (GIGYF2, MYT1L, CUL3, DOCK8 and ZNF292) and DN mutations in previous ASD candidates (ARHGAP32, NCOR1, PHIP, STXBP1, CDKL5 and SHANK1). Phenotypic follow-up confirms potential subtypes and highlights how large global cohorts might be leveraged to prove the pathogenic significance of individually rare mutations.


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