University Hospital Freiburg, Hugstetter Strasse 55, Freiburg, Germany.
Kidney Int. 2010 May;77(10):891-6. doi: 10.1038/ki.2010.27. Epub 2010 Mar 3.
Nephronophthisis is a heterogenetic autosomal recessive disorder associated with multiple developmental abnormalities, including cystic kidney disease and retinal degeneration. Retinal dystrophies, in particular the X-linked forms, are believed to represent a distinct group of hereditary diseases; however, their genetic complexity and overlap with other syndromic diseases is increasingly apparent. In this study, we report that depletion of retinitis pigmentosa GTPase regulator (RPGR) during zebrafish embryogenesis causes developmental changes indistinguishable from the abnormalities caused by the depletion of nephrocystin-5 or nephrocystin-6. However, RPGR did not directly interact with either gene product. RPGR-interacting protein 1 was found to act as an adaptor connecting RPGR to nephrocystin-6, thereby linking it to the nephronophthisis protein network. This interaction was abolished by truncating mutations (c.1107delA) of the interacting protein. Our findings underline the importance of the interplay between the two protein networks, suggesting a phenotypic modulation in both retinitis pigmentosa and nephronophthisis.
先天性肾单位肾痨是一种常染色体隐性遗传性疾病,与多种发育异常有关,包括囊性肾病和视网膜变性。视网膜营养不良,特别是 X 连锁形式,被认为是一组独特的遗传性疾病;然而,它们的遗传复杂性和与其他综合征性疾病的重叠越来越明显。在这项研究中,我们报告说,在斑马鱼胚胎发生过程中消耗视杆细胞色素 GTP 酶调节因子(RPGR)会导致与消耗肾囊蛋白-5 或肾囊蛋白-6 引起的发育变化无法区分。然而,RPGR 并没有直接与这两种基因产物相互作用。发现 RPGR 相互作用蛋白 1 作为一种衔接蛋白,将 RPGR 连接到肾囊蛋白-6,从而将其连接到先天性肾单位肾痨蛋白网络。这种相互作用被截断突变(c.1107delA)所破坏。我们的研究结果强调了这两个蛋白网络之间相互作用的重要性,提示视杆细胞色素营养不良和先天性肾单位肾痨都存在表型调节。