The primary cilium is a sensory organelle that receives specific signals from the extracellular environment important for vertebrate development and tissue homeostasis. Lamins, the major components of the nuclear lamina, are required to maintain the nuclear structure and are involved in most nuclear activities. In this study, we show that deficiency in lamin A/C causes defective ciliogenesis, accompanied by increased cytoplasmic accumulation of actin monomers and increased formation of actin filaments. Disruption of actin filaments by cytochalasin D rescues the defective ciliogenesis in lamin A/C‐depleted cells. Moreover, lamin A/C‐deficient cells display lower levels of nesprin 2 and defects in recruiting Arp2, myosin Va, and tau tubulin kinase 2 to the basal body during ciliogenesis. Collectively, our results uncover a functional link between nuclear lamina integrity and ciliogenesis and implicate the malfunction of primary cilia in the pathogenesis of laminopathy.

中文翻译：

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纤毛发生需要 Lamin A 介导的核膜完整性。

初级纤毛是一种感觉细胞器，它接收来自对脊椎动物发育和组织稳态很重要的细胞外环境的特定信号。纤层蛋白是核纤层的主要组成部分，需要维持核结构并参与大多数核活动。在这项研究中，我们表明缺乏 lamin A/C 会导致纤毛发生缺陷，伴随着肌动蛋白单体的细胞质积累增加和肌动蛋白丝形成增加。细胞松弛素 D 对肌动蛋白丝的破坏可挽救 lamin A/C 耗尽细胞中的纤毛发生缺陷。此外，核纤层蛋白 A/C 缺陷细胞显示出较低水平的 nesprin 2 和在纤毛发生过程中将 Arp2、肌球蛋白 Va 和 tau 微管蛋白激酶 2 募集到基体的缺陷。总的来说，