He Wen-Tao, Chen Chen, Pan Chu, Zhang Mu-Xun, Yu Xue-Feng, Wang Dao-Wen, Hu Shu-Hong
Department of Endocrinology and Metabolism, Wuhan, P. R. China.
Department of Cardiology, Wuhan, P. R. China.
Clin Genet. 2016 Feb;89(2):205-9. doi: 10.1111/cge.12655. Epub 2015 Sep 22.
Sclerosteosis, characterized by the hyperostosis of cranial and tubular bones, is a rare autosomal recessive hereditary disorder caused by mutation of SOST gene. Four nonsense mutations of SOST have been identified worldwide. Here, we report two affected siblings who carried a novel nonsense mutation of SOST in a consanguineous family from China. The proband manifested typical symptoms of sclerosteosis, whereas the symptoms were absent in another affected sibling. Two nucleotide substitutions in exon 2 of SOST were identified, c.444_445TC>AA, resulting in a premature stop codon, p.Cys148→Stop. This truncated mutation loses 66 amino acid residues which contain 3 cysteine residues of the cysteine-knot motif, leading to loss of function of SOST. The symptoms of sclerosteosis may be clinically heterogeneous in some patients, even with the same mutation. Our results support the notion that founder effects from the ancestors contribute to the disease onset.
骨硬化症以颅骨和管状骨的骨质增生为特征,是一种由SOST基因突变引起的罕见常染色体隐性遗传性疾病。在全球范围内已鉴定出SOST的四种无义突变。在此,我们报告了来自中国一个近亲家庭的两名患病兄弟姐妹,他们携带一种新的SOST无义突变。先证者表现出典型的骨硬化症症状,而另一名患病兄弟姐妹则没有症状。在SOST的第2外显子中鉴定出两个核苷酸替换,即c.444_445TC>AA,导致提前终止密码子p.Cys148→Stop。这种截短突变缺失了66个氨基酸残基,其中包含半胱氨酸结基序的3个半胱氨酸残基,导致SOST功能丧失。在一些患者中,即使具有相同的突变,骨硬化症的症状在临床上也可能具有异质性。我们的结果支持这样一种观点,即来自祖先的奠基者效应促成了疾病的发生。