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A Highlights from MBoC Selection: Compartmentalized nodes control mitotic entry signaling in fission yeast

机译:来自MBOC选择的亮点:分区节点控制裂变酵母中的有丝分类入口信号

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Cell cycle progression is coupled to cell growth, but the mechanisms that generate growth-dependent cell cycle progression remain unclear. Fission yeast cells enter into mitosis at a defined size due to the conserved cell cycle kinases Cdr1 and Cdr2, which localize to a set of cortical nodes in the cell middle. Cdr2 is regulated by the cell polarity kinase Pom1, suggesting that interactions between cell polarity proteins and the Cdr1-Cdr2 module might underlie the coordination of cell growth and division. To identify the molecular connections between Cdr1/2 and cell polarity, we performed a comprehensive pairwise yeast two-hybrid screen. From the resulting interaction network, we found that the protein Skb1 interacted with both Cdr1 and the Cdr1 inhibitory target Wee1. Skb1 inhibited mitotic entry through negative regulation of Cdr1 and localized to both the cytoplasm and a novel set of cortical nodes. Skb1 nodes were distinct structures from Cdr1/2 nodes, and artificial targeting of Skb1 to Cdr1/2 nodes delayed entry into mitosis. We propose that the formation of distinct node structures in the cell cortex controls signaling pathways to link cell growth and division.
机译:细胞周期进展偶联与细胞生长,但产生生长依赖性细胞周期进展的机制仍然尚不清楚。由于保守的细胞周期激酶CDR1和CDR2,裂变酵母细胞以限定的尺寸进入有丝分裂,该CDR1和CDR2定位在细胞中间的一组皮质节点。 CDR2由细胞极性激酶POM1调节,表明细胞极性蛋白和CDR1-CDR2模块之间的相互作用可能使细胞生长和分裂的协调具有强弱。为了鉴定CDR1 / 2和细胞极性之间的分子连接,我们进行了综合成对酵母双杂交筛。从所得到的相互作用网络中发现,蛋白质SKB1与CDR1和CDR1抑制靶标相互作用。 SKB1通过CDR1的负调节抑制有丝分裂,并局限于细胞质和一种新型皮质节点。 SKB1节点是来自CDR1 / 2节点的不同结构,SKB1至CDR1 / 2节点的人工靶向延迟进入有丝分裂。我们建议在细胞皮层中形成不同的节点结构,控制信号通路,以连接细胞生长和分裂。

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