Vreeburg M, de Zwart-Storm E A, Schouten M I, Nellen R G L, Marcus-Soekarman D, Devies M, van Geel M, van Steensel M A M
Department of Clinical Genetics, University Hospital Maastricht, Maastricht, The Netherlands.
Am J Med Genet A. 2007 Feb 15;143(4):360-3. doi: 10.1002/ajmg.a.31558.
Oculo-dento-digital dysplasia (ODDD, OMIM no.164210) is a pleiotropic disorder caused by mutations in the GJA1 gene that codes for the gap junction protein connexin 43. While the gene is highly expressed in skin, ODDD is usually not associated with skin symptoms. We recently described a family with ODDD and palmoplantar keratoderma. Interestingly, mutation carriers had a novel dinucleotide deletion in the GJA1 gene that resulted in truncation of part of the C-terminus. We speculated, that truncation of the C-terminus may be uniquely associated with skin disease in ODDD. Here, we describe a patient with ODDD and palmar hyperkeratosis caused by a novel dinucleotide deletion that truncates most of the connexin 43 C-terminus. Thus, our findings support the notion that such mutations are associated with the occurrence of skin symptoms in ODDD and provide the first evidence for the existence of a genotype-phenotype correlation.
眼-牙-指发育不全(ODDD,OMIM编号164210)是一种多效性疾病,由编码缝隙连接蛋白连接蛋白43的GJA1基因突变引起。虽然该基因在皮肤中高度表达,但ODDD通常与皮肤症状无关。我们最近描述了一个患有ODDD和掌跖角化病的家族。有趣的是,突变携带者在GJA1基因中有一个新的二核苷酸缺失,导致部分C末端截短。我们推测,C末端截短可能与ODDD中的皮肤疾病独特相关。在此,我们描述了一名患有ODDD和掌部角化过度的患者,其由一个新的二核苷酸缺失引起,该缺失截断了大部分连接蛋白43的C末端。因此,我们的发现支持了这样的观点,即此类突变与ODDD中皮肤症状的发生相关,并为基因型-表型相关性的存在提供了首个证据。