Betz Regina C, Planko Laura, Eigelshoven Sibylle, Hanneken Sandra, Pasternack Sandra M, Bussow Heinrich, Van Den Bogaert Kris, Wenzel Joerg, Braun-Falco Markus, Rutten Arno, Rogers Michael A, Ruzicka Thomas, Nöthen Markus M, Magin Thomas M, Kruse Roland
Institute of Human Genetics, University of Bonn, D-53111 Bonn, Germany.
Am J Hum Genet. 2006 Mar;78(3):510-9. doi: 10.1086/500850. Epub 2006 Jan 19.
Dowling-Degos disease (DDD) is an autosomal dominant genodermatosis characterized by progressive and disfiguring reticulate hyperpigmentation of the flexures. We performed a genomewide linkage analysis of two German families and mapped DDD to chromosome 12q, with a total LOD score of 4.42 ( theta =0.0) for marker D12S368. This region includes the keratin gene cluster, which we screened for mutations. We identified loss-of-function mutations in the keratin 5 gene (KRT5) in all affected family members and in six unrelated patients with DDD. These represent the first identified mutations that lead to haploinsufficiency in a keratin gene. The identification of loss-of-function mutations, along with the results from additional functional studies, suggest a crucial role for keratins in the organization of cell adhesion, melanosome uptake, organelle transport, and nuclear anchorage.
道林 - 迪戈斯病(DDD)是一种常染色体显性遗传性皮肤病,其特征为屈侧部位进行性且毁容性的网状色素沉着。我们对两个德国家庭进行了全基因组连锁分析,并将DDD定位到12号染色体长臂,标记D12S368的总LOD得分为4.42(θ = 0.0)。该区域包含角蛋白基因簇,我们对其进行了突变筛查。我们在所有患病家庭成员以及6名无关的DDD患者中鉴定出角蛋白5基因(KRT5)的功能丧失突变。这些是首次鉴定出的导致角蛋白基因单倍剂量不足的突变。功能丧失突变的鉴定以及其他功能研究的结果表明,角蛋白在细胞黏附、黑素体摄取、细胞器运输和核锚定的组织中起关键作用。