Singh Tarjinder, Walters James T R, Johnstone Mandy, Curtis David, Suvisaari Jaana, Torniainen Minna, Rees Elliott, Iyegbe Conrad, Blackwood Douglas, McIntosh Andrew M, Kirov Georg, Geschwind Daniel, Murray Robin M, Di Forti Marta, Bramon Elvira, Gandal Michael, Hultman Christina M, Sklar Pamela, Palotie Aarno, Sullivan Patrick F, O'Donovan Michael C, Owen Michael J, Barrett Jeffrey C
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK.
MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.
Nat Genet. 2017 Aug;49(8):1167-1173. doi: 10.1038/ng.3903. Epub 2017 Jun 26.
By performing a meta-analysis of rare coding variants in whole-exome sequences from 4,133 schizophrenia cases and 9,274 controls, de novo mutations in 1,077 family trios, and copy number variants from 6,882 cases and 11,255 controls, we show that individuals with schizophrenia carry a significant burden of rare, damaging variants in 3,488 genes previously identified as having a near-complete depletion of loss-of-function variants. In patients with schizophrenia who also have intellectual disability, this burden is concentrated in risk genes associated with neurodevelopmental disorders. After excluding known risk genes for neurodevelopmental disorders, a significant rare variant burden persists in other genes intolerant of loss-of-function variants; although this effect is notably stronger in patients with both schizophrenia and intellectual disability, it is also seen in patients with schizophrenia who do not have intellectual disability. Together, our results show that rare, damaging variants contribute to the risk of schizophrenia both with and without intellectual disability and support an overlap of genetic risk between schizophrenia and other neurodevelopmental disorders.
通过对4133例精神分裂症患者和9274例对照的全外显子序列中的罕见编码变异、1077个家系三联体中的新生突变以及6882例患者和11255例对照的拷贝数变异进行荟萃分析,我们发现精神分裂症患者在3488个基因中携带大量罕见的有害变异,这些基因先前被确定为功能丧失变异几乎完全缺失。在同时患有智力障碍的精神分裂症患者中,这种负担集中在与神经发育障碍相关的风险基因中。在排除已知的神经发育障碍风险基因后,其他不耐受功能丧失变异的基因中仍存在显著的罕见变异负担;尽管这种效应在同时患有精神分裂症和智力障碍的患者中更为明显,但在没有智力障碍的精神分裂症患者中也可见。总之,我们的结果表明,罕见的有害变异会导致有或没有智力障碍的精神分裂症风险,并支持精神分裂症与其他神经发育障碍之间的遗传风险重叠。