Dehghani MohammadReza, Mojarad Majid, Ghayoor Karimiani Ehsan, Vahidi Mehrjardi Mohammad Yahya, Sahebalzamani Afsaneh, Ashrafzadeh Farah, Beiraghi Toosi Mehran, Eslahi Atiyeh, Ahangari Najmeh, Yassini Seyed Mojtaba, Hassanbeigi Afsaneh, Rasti Azam, Kalantar Seyed Mehdi, Maroofian Reza
Medical Genetics Research Centre, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Public Health Genomics. 2017;20(3):188-193. doi: 10.1159/000477560. Epub 2017 Jul 19.
Joubert syndrome (JS) is a clinically and genetically heterogeneous group of rare neurodevelopmental disorder characterised by peculiar midbrain-hindbrain malformation, known as the "molar tooth" sign. JS can manifest a broad range of signs and symptoms. The most common features of JS are hypotonia, ataxia, developmental delay/intellectual disability, abnormal eye movements, and neonatal breathing abnormalities. To date, 29 genes have been shown to cause JS.
We employed whole-genome single nucleotide polymorphism genotyping in a group of Iranian families with JS and Sanger sequencing of a known mutation associated with JS located in a single homozygous regions shared by affected members of the families.
Homozygosity mapping uncovered a shared ∼2.2-Mb run of homozygosity on chromosome 8q21.3-q22.1 encompassing the known JS-causing TMEM67 gene. Sanger sequencing of a known mutation (NM_153704.5: c.725A>G; p.Asn242Ser) in TMEM67 identified from studying another Iranian family using whole-exome sequencing confirmed the presence of the homozygous mutation in 22 affected members of 12 nuclear families. "Molar tooth" sign of brain magnetic resonance imaging, moderate-to-severe neurodevelopmental delay, and abnormal eye movements were the most common features of affected individuals. In addition, liver disease, seizure, behavioural abnormalities, failure to thrive, and kidney disease were observed variably in some of the patients.
We propose that Asn242Ser is a founder mutation in the Iranian population, which might explain a significant proportion of JS cases from eastern Iran. Therefore, screening for this variant should be considered for genetic testing in Iranian patients with JS. In addition, this finding is important for developing population-specific genetic testing in Iran.
乔伯特综合征(JS)是一组临床和遗传异质性的罕见神经发育障碍,其特征为独特的中脑-后脑畸形,即“磨牙症”体征。JS可表现出广泛的体征和症状。JS最常见的特征是肌张力减退、共济失调、发育迟缓/智力残疾、异常眼球运动和新生儿呼吸异常。迄今为止,已有29个基因被证明可导致JS。
我们对一组患有JS的伊朗家庭进行了全基因组单核苷酸多态性基因分型,并对位于这些家庭受影响成员共享的单个纯合区域内与JS相关的已知突变进行了桑格测序。
纯合性定位发现8号染色体q21.3-q22.1区域存在一个约2.2Mb的共享纯合片段,其中包含已知的导致JS的TMEM67基因。对从另一个伊朗家庭通过全外显子测序鉴定出的TMEM67基因中的已知突变(NM_153704.5:c.725A>G;p.Asn242Ser)进行桑格测序,证实了12个核心家庭的22名受影响成员中存在纯合突变。脑磁共振成像的“磨牙症”体征、中度至重度神经发育迟缓以及异常眼球运动是受影响个体最常见的特征。此外,在一些患者中还不同程度地观察到了肝病、癫痫、行为异常、生长发育不良和肾病。
我们提出Asn242Ser是伊朗人群中的一个始祖突变,这可能解释了伊朗东部相当一部分JS病例。因此,对于伊朗JS患者的基因检测应考虑筛查该变异。此外,这一发现对于在伊朗开展针对特定人群的基因检测具有重要意义。