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首页> 外文期刊>Current Biology: CB >Intraflagellar Transport Complex A Genes Differentially Regulate Cilium Formation and Transition Zone Gating
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Intraflagellar Transport Complex A Genes Differentially Regulate Cilium Formation and Transition Zone Gating

机译：内颗粒传输复合物的基因差异调节纤毛形成和过渡区门控

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摘要

Cilia are found on most eukaryotic cell types, serving motility, environment sensing, and signaling (cell-cell) functions, and defects cause genetic diseases (ciliopathies), affecting the development of many tissues []. Cilia are built by intraflagellar transport (IFT), a bidirectional microtubule-based motility driven by kinesin-2 anterograde (toward ciliary tip) and IFT-dynein retrograde (toward ciliary base) motors together with IFT-A and IFT-B cargo adaptor complexes that control retrograde and anterograde IFT, respectively []. Ciliary composition is also facilitated by the transition zone (TZ)?at the ciliary base and the associated Meckel-Gruber syndrome (MKS) and nephronophthisis (NPHP) modules that establish protein diffusion barriers and regulate cilium structure []. Although the molecular architecture of the IFT machine is?emerging [], how individual components contribute to cilium subtype formation and IFT remains relatively unexplored, especiallyin?vivo. In addition, little is known about functional interactions between IFT and TZ modules. Here, inCaenorhabditis elegans(roundworms), we identify cell-type-specific mechanisms by which IFT-A sculpts the structures of discrete ciliary subtypes and regulates IFT. We also uncover differential roles for IFT-A subunits in controlling the TZ restriction of MKS module components and ciliary exclusion (gating) of periciliary membrane proteins, with IFT-140 controlling their ciliary entry and IFT-43/121/139 controlling their ciliary removal. Furthermore, we determine that IFT-A and MKS module components synergistically interact to determine cilium structure. Overall, this work provides insight into the functional architecture of a metazoan IFT-A complex in different cell types and uncovers new relationships between ciliopathy-associated IFT-A and TZ modules.
机译：Cilia在大多数真核细胞类型，服务促使运动，环境感测和​​信号（细胞 - 细胞）功能，缺陷导致遗传疾病（纤毛病），影响许多组织的发展[]。 Cilia是由Intraflarar传输（IFT）构建的，由Kinesin-2 anterograde（朝向睫状体尖端）和IFT-Dynein逆行（朝向睫状硅IFT-B逆行的IFT-A和IFT-B货物适配器复合物驱动的双向微管的运动性该控制逆行和Anterograde IFT，分别[]。通过过渡区（TZ）（TZ）促进睫状体组合物在睫状碱和相关的Meckel-Gruber综合征（MKS）和肾细胞（NPHP）模块处，建立蛋白质扩散屏障和调节纤毛结构[]。虽然IFT机器的分子结构是？新兴[]，单个组分如何促成甲钙亚型形成，并且IFT仍然相对未探索，尤其是α体内。此外，关于IFT和TZ模块之间的功能相互作用几乎是众所周知的。在这里，Incaenorhabditis elegans（蛔虫），我们识别细胞类型特定机制，其中IFT-a雕刻离散纤毛亚型的结构并调节IFT。我们还揭示了IFT-A亚基的差分作用，用于控制MKS模块组分的TZ限制和筛选蛋白质蛋白的睫状体排斥（门控），IFT-140控制其睫状体入口和IFT-43 / 121/139控制它们的睫状体去除。此外，我们确定IFT-A和MKS模块组件协同相互作用以确定纤毛结构。总的来说，这项工作介绍了在不同小区类型中的Metazoan IFT-A复合物的功能架构的洞察力，并揭示了Cileopathy相关的IFT-A和TZ模块之间的新关系。

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