Department of Pediatrics, University Hospital Freiburg, Freiburg, Germany.
Nat Genet. 2011 Jan;43(1):79-84. doi: 10.1038/ng.727. Epub 2010 Dec 5.
Primary ciliary dyskinesia (PCD) is a genetically heterogeneous autosomal recessive disorder characterized by recurrent infections of the respiratory tract associated with the abnormal function of motile cilia. Approximately half of individuals with PCD also have alterations in the left-right organization of their internal organ positioning, including situs inversus and situs ambiguous (Kartagener's syndrome). Here, we identify an uncharacterized coiled-coil domain containing a protein, CCDC40, essential for correct left-right patterning in mouse, zebrafish and human. In mouse and zebrafish, Ccdc40 is expressed in tissues that contain motile cilia, and mutations in Ccdc40 result in cilia with reduced ranges of motility. We further show that CCDC40 mutations in humans result in a variant of PCD characterized by misplacement of the central pair of microtubules and defective assembly of inner dynein arms and dynein regulatory complexes. CCDC40 localizes to motile cilia and the apical cytoplasm and is required for axonemal recruitment of CCDC39, disruption of which underlies a similar variant of PCD.
原发性纤毛运动障碍(PCD)是一种遗传异质性常染色体隐性疾病,其特征是呼吸道反复感染,与运动纤毛的异常功能有关。大约一半的 PCD 患者的内脏器官位置的左右组织也发生改变,包括内脏逆位和 situs 不确定(Kartagener 综合征)。在这里,我们鉴定了一个未被描述的卷曲螺旋域,其中包含一个对小鼠、斑马鱼和人类的正确左右模式形成至关重要的蛋白 CCDC40。在小鼠和斑马鱼中,Ccdc40 在含有运动纤毛的组织中表达,Ccdc40 的突变导致纤毛的运动范围减小。我们进一步表明,人类 CCDC40 突变导致一种以中央对微管错位和内动力蛋白臂和动力蛋白调节复合物组装缺陷为特征的 PCD 变异型。CCDC40 定位于运动纤毛和顶细胞质,并且是 CCDC39 轴突招募所必需的,后者的破坏是类似的 PCD 变异型的基础。