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Different roles for KIF17 and kinesin II in photoreceptor development and maintenance.

机译:KIF17和驱动蛋白II在感光器发育和维持中的不同作用。

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摘要

Kinesin 2 family members are involved in transport along ciliary microtubules. In Caenorhabditis elegans channel cilia, kinesin II and OSM-3 cooperate along microtubule doublets of the axoneme middle segment, whereas OSM-3 alone works on microtubule singlets to elongate the distal segment. Among sensory cilia, vertebrate photoreceptors share a similar axonemal structure with C. elegans channel cilia, and deficiency in either kinesin II or KIF17, the homologue of OSM-3, results in disruption of photoreceptor organization. However, direct comparison of the two effects is confounded by the use of different species and knockdown strategies in prior studies. Here, we directly compare the effects of dominant-negative kinesin II and KIF17 expression in zebrafish cone photoreceptors. Our data indicate that dominant-negative kinesin II disrupts function at the level of the inner segment and synaptic terminal and results in cell death. In contrast, dominant-negative KIF17 has no obvious effect on inner segment or synaptic organization but has an immediate impact on outer segment assembly.
机译:Kinesin 2家庭成员参与沿睫状微管的运输。在秀丽隐杆线虫通道纤毛中,驱动蛋白II和OSM-3沿着轴突中段的微管双峰协同作用,而OSM-3单独作用于微管单峰上以延长远端段。在感觉纤毛中,脊椎动物感光体与秀丽隐杆线虫纤毛具有相似的轴突结构,并且驱动蛋白II或OSM-3的同源物KIF17的缺乏导致感光体组织的破坏。但是,在先前的研究中,通过使用不同的物种和击倒策略,直接比较这两种效果是令人困惑的。在这里,我们直接比较在斑马鱼锥感光细胞中的显性负驱动蛋白II和KIF17表达的影响。我们的数据表明,显性-阴性驱动蛋白II破坏了内部区段和突触末端的功能,并导致细胞死亡。相比之下,显性负KIF17对内段或突触组织没有明显影响,但对外段组装具有直接影响。

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