Genetic evidence for selective transport of opsin and arrestin by kinesin-II in mammalian photoreceptors
Genetic evidence for selective transport of opsin and arrestin by kinesin-II in mammalian photoreceptors
复制标题
DOI：
10.1016/s0092-8674(00)00023-4
复制
发表时间：
2000-07-21
期刊：
影响因子：
64.5
通讯作者：
Goldstein, LSB
中科院分区：
文献类型：
--
作者：
Marszalek, JR;Liu, XR;Goldstein, LSB
为了测试激酶- ii在哺乳动物光感受器纤毛的运输中是否重要，并确定其潜在的货物，我们使用ccr - loxp诱变技术去除光感受器中的激酶- ii亚基KIF3A。KIF3A的完全缺失导致视蛋白、阻滞蛋白和膜在光感受器内段大量积聚，而cu-转导蛋白的定位不受影响。其他膜、细胞器和运输标记物以及视蛋白加工均正常。KIF3A缺失最终导致光感受器细胞凋亡，类似于已知的视蛋白转运突变体。这些数据表明，视蛋白和阻滞蛋白从内到外的运输途径需要驱动蛋白- ii，在视网膜色素变性中发现，这种运输途径的阻断会导致光感受器细胞死亡。
To test whether kinesin-II is important for transport in the mammalian photoreceptor cilium, and to identify its potential cargoes, we used Cre-loxP mutagenesis to remove the kinesin-II subunit, KIF3A, specifically from photoreceptors. Complete loss of KIF3A caused large accumulations of opsin, arrestin, and membranes within the photoreceptor inner segment, while the localization of cu-transducin was unaffected. Other membrane, organelle, and transport markers, as well as opsin processing appeared normal. Loss of KIF3A ultimately caused apoptotic photoreceptor cell death similar to a known opsin transport mutant. The data suggest that kinesin-II is required to transport opsin and arrestin from the inner to the outer segment and that blocks in this transport pathway lead to photoreceptor cell death as found in retinitis pigmentosa.