Defective ciliogenesis causes human developmental diseases termed ciliopathies. Microtubule (MT) asters originating from centrosomes in mitosis ensure the fidelity of cell division by positioning the spindle apparatus. However, the function of microtubule asters in interphase remains largely unknown. Here, we reveal an essential role of MT asters in transition zone (TZ) assembly during ciliogenesis. We demonstrate that the centrosome protein FSD1, whose biological function is largely unknown, anchors MT asters to interphase centrosomes by binding to microtubules. FSD1 knockdown causes defective ciliogenesis and affects embryonic development in vertebrates. We further show that disruption of MT aster anchorage by depleting FSD1 or other known anchoring proteins delocalizes the TZ assembly factor Cep290 from centriolar satellites, and causes TZ assembly defects. Thus, our study establishes FSD1 as a MT aster anchorage protein and reveals an important function of MT asters anchored by FSD1 in TZ assembly during ciliogenesis.

中文翻译：

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由FSD1锚定的微管紫苑控制着轴突组装和纤毛发生。

纤毛发生缺陷会导致人类发育疾病，称为纤毛病。源于有丝分裂中心体的微管（MT）紫by通过放置纺锤体来确保细胞分裂的保真度。然而，在相间的微管紫苑的功能仍然是很大程度上未知。在这里，我们揭示了纤毛在纤毛发生过程中过渡区（TZ）装配中的重要作用。我们证明，其生物学功能很大程度上未知的中心体蛋白FSD1通过结合微管将MT紫s锚定到相间中心体。FSD1组合式导致缺陷的纤毛发生并影响脊椎动物的胚胎发育。我们进一步表明，通过消耗FSD1或其他已知的锚定蛋白来破坏MT aster锚定会从中心粒卫星中解散TZ装配因子Cep290，并导致TZ组件缺陷。因此，我们的研究将FSD1建立为MT aster锚定蛋白，并揭示了纤毛形成过程中FSD1锚定的MT asters在TZ装配中的重要功能。