Thomas J T, Kilpatrick M W, Lin K, Erlacher L, Lembessis P, Costa T, Tsipouras P, Luyten F P
Craniofacial and Skeletal Diseases Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
Nat Genet. 1997 Sep;17(1):58-64. doi: 10.1038/ng0997-58.
Chondrodysplasia Grebe type (CGT) is an autosomal recessive disorder characterized by severe limb shortening and dysmorphogenesis. We have identified a causative point mutation in the gene encoding the bone morphogenetic protein (BMP)-like molecule, cartilage-derived morphogenetic protein-1 (CDMP-1). The mutation substitutes a tyrosine for the first of seven highly conserved cysteine residues in the mature active domain of the protein. We demonstrate that the mutation results in a protein that is not secreted and is inactive in vitro. It produces a dominant negative effect by preventing the secretion of other, related BMP family members. We present evidence that this may occur through the formation of heterodimers. The mutation and its proposed mechanism of action provide the first human genetic indication that composite expression patterns of different BMPs dictate limb and digit morphogenesis.
格里布型软骨发育不全(CGT)是一种常染色体隐性疾病,其特征为严重的肢体短小和形态发生异常。我们在编码骨形态发生蛋白(BMP)样分子——软骨衍生形态发生蛋白-1(CDMP-1)的基因中鉴定出一个致病点突变。该突变使蛋白质成熟活性结构域中七个高度保守的半胱氨酸残基中的第一个被酪氨酸取代。我们证明,该突变导致一种无法分泌且在体外无活性的蛋白质。它通过阻止其他相关BMP家族成员的分泌产生显性负效应。我们提供的证据表明,这可能是通过异二聚体的形成发生的。该突变及其提出的作用机制首次提供了人类遗传学证据,表明不同BMP的复合表达模式决定肢体和指(趾)的形态发生。