Muru K, Kalev I, Teek R, Sõnajalg M, Kuuse K, Reimand T, Ounap K
Department of Genetics, United Laboratories, Tartu University Hospital, Tartu, Estonia.
Mol Syndromol. 2011 Sep;1(6):307-310. doi: 10.1159/000330109. Epub 2011 Aug 3.
Holt-Oram syndrome (HOS) is an autosomal dominant developmental defect involving preaxial radial ray upper limb deformity and variable cardiac defects. It has been demonstrated that HOS is caused by mutations in the T-box transcription factor gene TBX5. Numerous germline mutations (more than 60) of this gene produce preterminal stop codons, which lead to synthesis of a truncated nonfunctional TBX5 protein. The haplo-insufficiency of the TBX5 gene is the most significant cause of HOS. We report on a sporadic patient with clinical features of HOS. Our patient had a cardiac anomaly - a muscular ventricular and atrial septal defect, patent ductus arteriosus and a conduction defect (a first-step atrioventricular block). Upper limb anomalies in our patient were relatively mild and unusual to HOS - distally displaced thumbs, narrow shoulders and hypotrophy of the muscles in the shoulder region. Molecular analysis identified a novel and unusual heterozygous frameshift mutation - c.1304delT (p.Leu435fsX146) - in exon 9 of the TBX5 gene, which is predicted to cause an elongated TBX5 protein with 84 miscoding amino acids and 62 supernumerary C-terminal amino acids. To the best of our knowledge, only one such type of elongation mutation has thus far been reported in the TBX5 gene.
霍尔特-奥拉姆综合征(HOS)是一种常染色体显性发育缺陷,涉及上肢桡侧轴前射线畸形和多种心脏缺陷。已证实HOS是由T盒转录因子基因TBX5突变引起的。该基因的众多种系突变(超过60种)产生了提前终止密码子,导致截短的无功能TBX5蛋白的合成。TBX5基因的单倍体不足是HOS最主要的病因。我们报告了一名具有HOS临床特征的散发性患者。我们的患者存在心脏异常——肌性室间隔和房间隔缺损、动脉导管未闭以及传导缺陷(一度房室传导阻滞)。我们患者的上肢异常相对较轻,且与HOS不同寻常——拇指远侧移位、肩部狭窄以及肩部肌肉萎缩。分子分析在TBX5基因的第9外显子中鉴定出一种新的、不寻常的杂合移码突变——c.1304delT(p.Leu435fsX146),预计会导致一种延长的TBX5蛋白,带有84个错义氨基酸和62个额外的C末端氨基酸。据我们所知,迄今为止在TBX5基因中仅报道过一种此类延长突变。