Brüchle Nadina Ortiz, Frank Jorge, Frank Valeska, Senderek Jan, Akar Ahmet, Koc Erol, Rigopoulos Dimitris, van Steensel Maurice, Zerres Klaus, Bergmann Carsten
Department of Human Genetics, RWTH Aachen University, Aachen, Germany.
J Invest Dermatol. 2008 Apr;128(4):791-6. doi: 10.1038/sj.jid.5701088. Epub 2007 Oct 4.
Congenital anonychia is a rare autosomal-recessive disorder characterized by the absence of finger- and toenails. Recently, we and others identified the secreted Wnt signaling ligand R-spondin 4 (RSPO4) as the first gene known to be responsible for inherited anonychia. R-spondins are secreted proteins that activate the Wnt/beta-catenin signaling pathway. This puts anonychia on the growing list of congenital malformation syndromes caused by Wnt signaling pathway defects. Here, we expand the RSPO4 mutational spectrum by identification of the previously unknown mutations c.190C>T (p.Arg64Cys) in exon 2 and c.301C>T (p.Gln101X) in exon 3, thereby corroborating R-spondin 4 as the major protein in autosomal-recessive anonychia. Almost all RSPO4 mutations detected so far affect the highly conserved exons 2 and 3. Thus, we postulate that RSPO4 mutations preferentially cluster in the furin-like cysteine-rich domains of R-spondin 4, which is in line with experimental data proposing that for beta-catenin stabilization, a shortened protein comprising just these two regions is sufficient.
先天性无甲症是一种罕见的常染色体隐性疾病,其特征为手指和脚趾甲缺失。最近,我们和其他研究人员鉴定出分泌型Wnt信号配体R-spondin 4(RSPO4)是首个已知的导致遗传性无甲症的基因。R-spondins是激活Wnt/β-连环蛋白信号通路的分泌蛋白。这使得无甲症被列入由Wnt信号通路缺陷引起的先天性畸形综合征的不断增加的列表中。在此,我们通过鉴定外显子2中先前未知的c.190C>T(p.Arg64Cys)突变和外显子3中c.301C>T(p.Gln101X)突变来扩展RSPO4突变谱,从而确证R-spondin 4是常染色体隐性无甲症的主要相关蛋白。到目前为止检测到的几乎所有RSPO4突变都影响高度保守的外显子2和3。因此,我们推测RSPO4突变优先聚集在R-spondin 4的弗林蛋白酶样富含半胱氨酸结构域中,这与实验数据一致,该数据表明为了实现β-连环蛋白的稳定,仅由这两个区域组成的缩短蛋白就足够了。