Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy.
Laboratory of Molecular and Cell Biology, Istituto Dermopatico dell'Immacolata (IDI) IRCCS, Rome, Italy.
Eur J Hum Genet. 2018 Sep;26(9):1266-1271. doi: 10.1038/s41431-018-0183-6. Epub 2018 Jun 11.
A rare syndrome was first described in 1997 in a 17-year-old male patient presenting with Retinitis pigmentosa, HYpopituitarism, Nephronophthisis and Skeletal dysplasia (RHYNS). In the single reported familial case, two brothers were affected, arguing for X-linked or recessive mode of inheritance. Up to now, the underlying genetic basis of RHYNS syndrome remains unknown. Here we applied whole-exome sequencing in the originally described family with RHYNS to identify compound heterozygous variants in the ciliary gene TMEM67. Sanger sequencing confirmed a paternally inherited nonsense c.622A > T, p.(Arg208*) and a maternally inherited missense variant c.1289A > G, p.(Asp430Gly), which perturbs the correct splicing of exon 13. Overall, TMEM67 showed one of the widest clinical continuum observed in ciliopathies ranging from early lethality to adults with liver fibrosis. Our findings extend the spectrum of phenotypes/syndromes resulting from biallelic TMEM67 variants to now eight distinguishable clinical conditions including RHYNS syndrome.
一种罕见的综合征于 1997 年首次在一名 17 岁男性患者中描述,该患者表现为色素性视网膜炎、垂体功能减退、肾间质纤维化和骨骼发育不良(RHYNS)。在单报告的家族病例中,两名兄弟受到影响,提示 X 连锁或隐性遗传模式。迄今为止,RHYNS 综合征的潜在遗传基础仍不清楚。在这里,我们对最初描述的 RHYNS 家系进行了全外显子组测序,以鉴定出纤毛基因 TMEM67 中的复合杂合变异。Sanger 测序证实了一个父系遗传的无义 c.622A>T,p.(Arg208*)和一个母系遗传的错义变异 c.1289A>G,p.(Asp430Gly),这会干扰外显子 13 的正确剪接。总体而言,TMEM67 表现出纤毛病中观察到的最广泛的临床连续谱之一,从早期致死性到伴有肝纤维化的成年人。我们的发现将双等位基因 TMEM67 变异引起的表型/综合征谱扩展到现在的八种可区分的临床情况,包括 RHYNS 综合征。