Subaran Ryan L, Odgerel Zagaa, Swaminathan Rajeswari, Glatt Charles E, Weissman Myrna M
Nationwide Children's Hospital, Columbus, Ohio.
New York State Psychiatric Institute, New York, New York.
Am J Med Genet B Neuropsychiatr Genet. 2016 Apr;171B(3):333-41. doi: 10.1002/ajmg.b.32408. Epub 2016 Jan 29.
There are no known genetic variants with large effects on susceptibility to major depressive disorder (MDD). Although one proposed study approach is to increase sensitivity by increasing sample sizes, another is to focus on families with multiple affected individuals to identify genes with rare or novel variants with strong effects. Choosing the family-based approach, we performed whole-exome analysis on affected individuals (n = 12) across five MDD families, each with at least five affected individuals, early onset, and prepubertal diagnoses. We identified 67 genes where novel deleterious variants were shared among affected relatives. Gene ontology analysis shows that of these 67 genes, 18 encode transcriptional regulators, eight of which are expressed in the human brain, including four KRAB-A box-containing Zn(2+) finger repressors. One of these, ZNF34, has been reported as being associated with bipolar disorder and as differentially expressed in bipolar disorder patients compared to healthy controls. We found a novel variant-encoding a non-conservative P17R substitution in the conserved repressor domain of ZNF34 protein-segregating completely with MDD in all available individuals in the family in which it was discovered. Further analysis showed a common ZNF34 coding indel segregating with MDD in a separate family, possibly indicating the presence of an unobserved, linked, rare variant in that particular family. Our results indicate that genes encoding transcription factors expressed in the brain might be an important group of MDD candidate genes and that rare variants in ZNF34 might contribute to susceptibility to MDD and perhaps other affective disorders.
目前尚无已知对重度抑郁症(MDD)易感性有重大影响的基因变异。虽然一种提议的研究方法是通过增加样本量来提高灵敏度,但另一种方法是关注有多个患病个体的家庭,以识别具有强烈效应的罕见或新变异基因。选择基于家庭的方法,我们对五个MDD家庭中的患病个体(n = 12)进行了全外显子组分析,每个家庭至少有五个患病个体,发病早且为青春期前诊断。我们鉴定出67个基因,其中新的有害变异在患病亲属中共享。基因本体分析表明,在这67个基因中,有18个编码转录调节因子,其中8个在人类大脑中表达,包括4个含KRAB - A盒的锌指抑制因子。其中一个,ZNF34,已被报道与双相情感障碍相关,并且与健康对照相比,在双相情感障碍患者中差异表达。我们在发现该变异的家庭中所有可用个体中发现了一个新的变异——在ZNF34蛋白的保守抑制结构域中编码非保守的P17R替换——该变异与MDD完全共分离。进一步分析表明,在另一个家庭中,一个常见的ZNF34编码插入缺失与MDD共分离,这可能表明在那个特定家庭中存在一个未观察到的、连锁的罕见变异。我们的结果表明,在大脑中表达的编码转录因子的基因可能是一组重要的MDD候选基因,并且ZNF34中的罕见变异可能导致对MDD以及可能其他情感障碍的易感性。