Singh Krishna Kumar, Elligsen Diana, Liersch Rüdiger, Schubert Stefanie, Pabst Brigitte, Arslan-Kirchner Mine, Schmidtke Jörg
Institute of Human Genetics, Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany.
J Mol Cell Cardiol. 2007 Feb;42(2):352-6. doi: 10.1016/j.yjmcc.2006.11.006. Epub 2006 Dec 26.
Marfan syndrome is caused by mutations in fibrillin-1, a large gene spanning approximately 200 kb of genomic DNA on chromosome 15q21. So far, more than 600 different mutations have been identified, accounting for 60-90% of all Marfan syndrome cases, the vast majority being single nucleotide exchanges as well as small deletions and insertions. Only four major rearrangements have been described in the literature so far. We have screened 11 individuals fulfilling the diagnostic criteria of Marfan syndrome but negative for point mutations in the fibrillin-1 gene by SSCP and/or direct sequencing, for large rearrangements. We report here the largest known de novo and out of frame deletion in the fibrillin-1 gene in a patient fulfilling the diagnostic criteria of Marfan syndrome. We identified the deletion breakpoints at the genomic and transcript levels and studied the expression of the mutated allele at the transcript and protein level. We conclude that large rearrangements may account for a non-negligible proportion of all Marfan cases.
马凡综合征由原纤蛋白-1的突变引起,原纤蛋白-1是一个大基因,跨越15号染色体q21上约200kb的基因组DNA。到目前为止,已鉴定出600多种不同的突变,占所有马凡综合征病例的60%-90%,绝大多数是单核苷酸交换以及小的缺失和插入。迄今为止,文献中仅描述了四种主要的重排。我们对11名符合马凡综合征诊断标准但通过单链构象多态性(SSCP)和/或直接测序检测原纤蛋白-1基因点突变为阴性的个体进行了大的重排筛查。我们在此报告一名符合马凡综合征诊断标准的患者中,原纤蛋白-1基因已知最大的新发框外缺失。我们在基因组和转录水平确定了缺失断点,并在转录和蛋白质水平研究了突变等位基因的表达。我们得出结论,大的重排在所有马凡综合征病例中所占比例可能不可忽略。