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Modulation of phosphatidylinositol 4-phosphate levels by CaBP7 controls cytokinesis in mammalian cells

机译:CaBP7调节磷脂酰肌醇4-磷酸水平控制哺乳动物细胞的胞质分裂

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摘要

Calcium and phosphoinositide signaling regulate cell division in model systems, but their significance in mammalian cells is unclear. Calcium-binding protein-7 (CaBP7) is a phosphatidylinositol 4-kinaseIII beta (PI4KIII beta) inhibitor required during cytokinesis in mammalian cells, hinting at a link between these pathways. Here we characterize a novel association of CaBP7 with lysosomes that cluster at the intercellular bridge during cytokinesis in HeLa cells. We show that CaBP7 regulates lysosome clustering and that PI4KIII beta is essential for normal cytokinesis. CaBP7 depletion induces lysosome mislocalization, extension of intercellular bridge lifetime, and cytokinesis failure. These data connect phosphoinositide and calcium pathways to lysosome localization and normal cytokinesis in mammalian cells.
机译:钙和磷酸肌醇信号传导调节模型系统中的细胞分裂,但它们在哺乳动物细胞中的意义尚不清楚。钙结合蛋白7(CaBP7)是哺乳动物细胞胞质分裂过程中所需的磷脂酰肌醇4激酶III beta(PI4KIII beta)抑制剂,提示这些途径之间存在联系。在这里,我们表征了CaBP7与溶酶体的新型关联,溶酶体在HeLa细胞胞质分裂过程中聚集在细胞间桥上。我们表明,CaBP7调节溶酶体簇和PI4KIII beta对于正常的胞质分裂是必不可少的。 CaBP7消耗诱导溶酶体错位,延长细胞间桥寿命和胞质分裂失败。这些数据将磷酸肌醇和钙途径连接到哺乳动物细胞中的溶酶体定位和正常胞质分裂。

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