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Mixed-lineage leukemia protein 2 suppresses ciliary assembly by the modulation of actin dynamics and vesicle transport

机译：混合谱系白血病蛋白2通过调节肌动蛋白动力学和囊泡运输来抑制睫状体组件

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Primary cilia are critically involved in the coordination of diverse signaling pathways and ciliary defects are associated with a variety of human diseases. The past decades have witnessed great progress in the core machinery orchestrating ciliary assembly. However, the upstream epigenetic cues that direct ciliogenesis remain elusive. Herein, we demonstrate that mixed-lineage leukemia protein 2 (MLL2), a histone methyltransferase, plays a negative role in ciliogenesis. RNA-sequencing analysis reveals that the expression of five actin-associated proteins is significantly downregulated in MLL2-depleted cells. Overexpression of these proteins partially rescues ciliary abnormality elicited by MLL2 depletion. Our data also show that actin dynamics is remarkably changed in MLL2-depleted cells, resulting in the impairment of cell adhesion, spreading, and motility. In addition, MLL2 depletion promotes ciliary vesicle trafficking to the basal body in an actin-related manner. Together, these results reveal that MLL2 inhibits ciliogenesis by modulating actin dynamics and vesicle transport, and suggest that alteration of MLL2 may contribute to the pathogenesis of cilium-associated diseases.
机译：原发性纤毛主要涉及各种信号通路的协调，睫状缺陷与各种人类疾病有关。过去几十年目睹了核心机械协调睫毛组件的巨大进展。然而，直接纤氯的上游表观遗传线索仍然难以捉摸。在此，我们证明了混合谱系白血病蛋白2（MLL2），组蛋白甲基转移酶在纤西发生中起作用。 RNA测序分析表明，在MLL2耗尽的细胞中，五种肌动蛋白相关蛋白的表达显着下调。这些蛋白质的过表达部分抵押由MLL2耗竭引发的睫状体异常。我们的数据还表明，在MLL2耗尽的细胞中显着改变了肌动蛋白动态，导致细胞粘附，扩散和运动的损害。此外，MLL2耗竭以与肌动蛋白相关的方式促进睫状体囊泡贩运到基体。这些结果表明，MLL2通过调节肌动蛋白动态和囊泡运输来抑制纤西生成，并表明MLL2的改变可能有助于纤毛相关疾病的发病机制。

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