NIH Undiagnosed Diseases Program, Common Fund, Office of the Director, NIH, Bethesda, Maryland.
Office of the Clinical Director, NHGRI, NIH, Bethesda, Maryland.
Hum Mutat. 2019 Jan;40(1):42-47. doi: 10.1002/humu.23675. Epub 2018 Nov 18.
The genetic etiologies of many rare disorders, including early infantile epileptic encephalopathies, are largely undiagnosed. A 6-year-old girl was admitted to the National Institutes of Health Undiagnosed Diseases Program with profound intellectual disability, infantile-onset seizures, chronic respiratory failure, facial dysmorphisms, skeletal abnormalities, and atrial septum defect. A large region of homozygosity was discovered on chromosome 16, spanning 16q22.1-16q24.3' caused by uniparental disomy (UPD) that included a maternally inherited homozygous microdeletion covering exon 6 of WWOX (NM_016373.3). mRNA expression analysis revealed that the deletion led to nonsense-mediated decay of the NM_016373.3 transcript; the exon 6 of an alternative transcript (NM_130791.3), lacking the short-chain dehydrogenase, was utilized. The microdeletion in WWOX explains the seizures and intellectual disability, while pathogenic variants in another gene, HSPG2, are likely responsible for the patient's skeletal abnormalities. This report describes a rare autosomal recessive disorder with multiple genetic etiologies, one of which involves UPD.
许多罕见疾病的遗传病因,包括早发性婴儿癫痫性脑病,在很大程度上仍未得到诊断。一名 6 岁女孩因严重智力残疾、婴儿期发作的癫痫、慢性呼吸衰竭、面部畸形、骨骼异常和房间隔缺损,被收入美国国立卫生研究院未确诊疾病计划。在染色体 16 上发现了一个大的纯合区域,由单亲二体性(UPD)引起,跨越 16q22.1-16q24.3',包括一个母系遗传的纯合微缺失,覆盖 WWOX 的外显子 6(NM_016373.3)。mRNA 表达分析显示,该缺失导致 NM_016373.3 转录本的无意义介导的衰变;利用了另一个基因 HSPG2 的替代转录本(NM_130791.3)的外显子 6,其缺乏短链脱氢酶。WWOX 的微缺失解释了癫痫和智力残疾,而另一个基因 HSPG2 的致病性变异可能是导致患者骨骼异常的原因。本报告描述了一种罕见的常染色体隐性疾病,有多种遗传病因,其中一种涉及 UPD。