Langlois Sylvie, Tarailo-Graovac Maja, Sayson Bryan, Drögemöller Britt, Swenerton Anne, Ross Colin Jd, Wasserman Wyeth W, van Karnebeek Clara Dm
Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada.
Centre for Molecular Medicine and Therapeutics, Vancouver, BC, Canada.
Eur J Hum Genet. 2016 Jun;24(6):949-53. doi: 10.1038/ejhg.2015.217. Epub 2015 Oct 21.
PEHO syndrome (OMIM no. 260565) is characterized by myoclonic jerking and infantile spasms, profound psychomotor retardation with the absence of motor milestones and speech, absence or early loss of visual fixation with atrophy of optic discs by 2 years of age and progressive brain atrophy on neuroimaging. We describe the results of a genomic study of a girl with PEHO syndrome and review the literature on cases with a disease-causing variant in the same gene. Exome sequencing of the index and unaffected parents followed by Sanger confirmation identified nine candidate genes harboring nonsynonymous rare variants identified by trio whole-exome sequencing. The de novo variant, a missense variant (c.296C>T, p.(T99M)), affecting the motor domain of KIF1A was considered the pathogenic mutation. The literature review revealed 24 cases with disease-causing variants in the motor domain of KIF1A, of which three met all the criteria for PEHO syndrome and an additional patient with incomplete clinical data met four of the five criteria. If the criteria were modified to include cases with any convulsive disorder and less profound intellectual disability, a total of six patients met all five of the criteria, three patients met four of the criteria and six met three of the criteria. Our results indicate that the molecular basis for PEHO syndrome, in at least a subset of patients, is a dominant KIF1A variant affecting the motor domain of the protein. Variable expressivity is seen with recurrent variants causing the full phenotype of PEHO syndrome in some patients and in other patients, a partial or milder PEHO phenotype.
PEHO综合征(OMIM编号:260565)的特征为肌阵挛性抽搐和婴儿痉挛、严重精神运动发育迟缓,无运动里程碑和言语能力,2岁前无视觉注视或早期丧失视觉注视且视盘萎缩,神经影像学检查显示进行性脑萎缩。我们描述了一名患有PEHO综合征女孩的基因组研究结果,并回顾了关于同一基因中致病变异病例的文献。对先证者及其未受影响的父母进行外显子组测序,随后进行桑格验证,确定了9个含有非同义罕见变异的候选基因,这些变异是通过三联体全外显子组测序鉴定出来的。新发变异,即一个错义变异(c.296C>T,p.(T99M)),影响KIF1A的运动结构域,被认为是致病突变。文献回顾显示,有24例在KIF1A运动结构域存在致病变异的病例,其中3例符合PEHO综合征的所有标准,另有1例临床数据不完整的患者符合5项标准中的4项。如果将标准修改为包括任何惊厥性疾病和智力残疾程度较轻的病例,共有6例患者符合所有5项标准,3例患者符合4项标准,6例患者符合3项标准。我们的结果表明,至少在一部分患者中,PEHO综合征的分子基础是影响该蛋白运动结构域的显性KIF1A变异。在一些患者中,反复出现的变异导致PEHO综合征的完整表型,而在其他患者中则表现为部分或较轻的PEHO表型,存在可变表达性。