Dietz H C, Cutting G R, Pyeritz R E, Maslen C L, Sakai L Y, Corson G M, Puffenberger E G, Hamosh A, Nanthakumar E J, Curristin S M
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Nature. 1991 Jul 25;352(6333):337-9. doi: 10.1038/352337a0.
Marfan syndrome is an inherited disorder of connective tissue manifested in the ocular, skeletal and cardiovascular systems. It is inherited as an autosomal dominant with high penetrance, but has great clinical variability. Linkage studies have mapped the Marfan locus to chromosome 15q15-21.3. There have been no reports of genetic heterogeneity in the syndrome. Following the identification of fibrillin (a glycoprotein component of the extracellular microfibril), immunohistopathological quantification of the protein in skin and fibroblast culture, and examination of fibrillin synthesis, extracellular transport, and incorporation into the extracellular matrix (D. M. Milewicz, R.E.P., E. S. Crawford and P. H. Byers, manuscript in preparation) have demonstrated abnormalities of fibrillin metabolism in most patients. A portion of the complementary DNA encoding fibrillin has been cloned and mapped by in situ hybridization to chromosome 15. Here we report that the fibrillin gene is linked to the Marfan phenotype (theta = 0.00; logarithm of the odds (lod) = 3.9) and describe a de novo missense mutation in the fibrillin gene in two patients with sporadic disease. We thus implicate fibrillin as the protein defective in patients with the Marfan syndrome.
马方综合征是一种遗传性结缔组织疾病,表现在眼、骨骼和心血管系统。它以常染色体显性高外显率方式遗传,但具有很大的临床变异性。连锁研究已将马方综合征基因座定位于染色体15q15 - 21.3。该综合征尚无遗传异质性的报道。在鉴定出原纤蛋白(细胞外微原纤维的一种糖蛋白成分)后,对皮肤和培养的成纤维细胞中的该蛋白进行免疫组织病理学定量分析,以及对原纤蛋白的合成、细胞外转运和整合到细胞外基质的情况进行检测(D.M. 米莱维茨、R.E.P.、E.S. 克劳福德和P.H. 拜尔斯,正在准备的手稿)已证明大多数患者存在原纤蛋白代谢异常。编码原纤蛋白的部分互补DNA已被克隆,并通过原位杂交定位于染色体15。在此我们报道原纤蛋白基因与马方综合征表型相关(重组值θ = 0.00;优势对数(lod)= 3.9),并描述了两名散发性疾病患者原纤蛋白基因中的一个新发错义突变。因此,我们认为原纤蛋白是马方综合征患者中存在缺陷的蛋白质。