Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA, USA.
The Manton Center for Orphan Disease Research, Boston Children's Hospital, Boston, MA, USA.
Mol Psychiatry. 2021 May;26(5):1706-1718. doi: 10.1038/s41380-021-01035-y. Epub 2021 Feb 17.
Mendelian and early-onset severe psychiatric phenotypes often involve genetic variants having a large effect, offering opportunities for genetic discoveries and early therapeutic interventions. Here, the index case is an 18-year-old boy, who at 14 years of age had a decline in cognitive functioning over the course of a year and subsequently presented with catatonia, auditory and visual hallucinations, paranoia, aggression, mood dysregulation, and disorganized thoughts. Exome sequencing revealed a stop-gain mutation in RCL1 (NM_005772.4:c.370 C > T, p.Gln124Ter), encoding an RNA 3'-terminal phosphate cyclase-like protein that is highly conserved across eukaryotic species. Subsequent investigations across two academic medical centers identified eleven additional cases of RCL1 copy number variations (CNVs) with varying neurodevelopmental or psychiatric phenotypes. These findings suggest that dosage variation of RCL1 contributes to a range of neurological and clinical phenotypes.
孟德尔和早发性严重精神表型通常涉及具有较大影响的遗传变异,为遗传发现和早期治疗干预提供了机会。在这里,索引病例是一名 18 岁男孩,他在 14 岁时认知功能在一年内下降,随后出现紧张症、听觉和视觉幻觉、偏执、攻击性、情绪失调和思维混乱。外显子组测序显示 RCL1(NM_005772.4:c.370C>T,p.Gln124Ter)中的一个停止增益突变,该基因编码一种 RNA 3'-末端磷酸环化酶样蛋白,在真核生物中高度保守。随后在两个学术医疗中心的调查发现了另外 11 例 RCL1 拷贝数变异(CNVs),具有不同的神经发育或精神表型。这些发现表明 RCL1 的剂量变化导致了一系列神经和临床表型。