SPAT-1/Bora acts with Polo-like kinase 1 to regulate PAR polarity and cell cycle progression
SPAT-1/Bora acts with Polo-like kinase 1 to regulate PAR polarity and cell cycle progression
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DOI：
10.1242/dev.055293
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发表时间：
2010-10-01
期刊：
影响因子：
4.6
通讯作者：
Gotta, Monica
中科院分区：
文献类型：
--
作者：
Noatynska, Anna;Panbianco, Costanza;Gotta, Monica
在不对称细胞分裂过程中，细胞极性和细胞周期进程是紧密协调的，但控制这两个事件的机制知之甚少。在这里，我们表明，Bora同源SPAT-1调节PAR极性和细胞周期进程在C。线虫胚胎我们发现，与哺乳动物细胞类似，SPAT-1与PLK-1起作用，而不与有丝分裂激酶Aurora A（AIR-1）起作用，如在果蝇中所示。SPAT-1与PLK-1结合，SPAT-1或PLK-1的缺失导致早期胚胎中类似的细胞分裂缺陷，这与AIR-1缺失引起的缺陷不同。此外，SPAT-1和PLK-1缺失导致极性受损，前和后PAR结构域长度异常，部分plk-1（RNAi）或spat-1（RNAi），但不是air-1（RNAi），可以挽救par-2突变体的致死性。SPAT-1在后部细胞中富集，并且这种富集依赖于PAR极性和PLK-1。综上所述，我们的数据表明，SPAT-1促进PLK-1的活性，以调节细胞极性和细胞周期定时在不对称细胞分裂的模型，提供了这两个过程之间的联系。
During asymmetric cell division, cell polarity and cell cycle progression are tightly coordinated, yet mechanisms controlling both these events are poorly understood. Here we show that the Bora homologue SPAT-1 regulates both PAR polarity and cell cycle progression in C. elegans embryos. We find that, similarly to mammalian cells, SPAT-1 acts with PLK-1 and not with the mitotic kinase Aurora A (AIR-1), as shown in Drosophila. SPAT-1 binds to PLK-1, and depletion of SPAT-1 or PLK-1 leads to similar cell division defects in early embryos, which differ from the defects caused by depletion of AIR-1. Additionally, SPAT-1 and PLK-1 depletion causes impaired polarity with abnormal length of the anterior and posterior PAR domains, and partial plk-1(RNAi) or spat-1(RNAi), but not air-1(RNAi), can rescue the lethality of a par-2 mutant. SPAT-1 is enriched in posterior cells, and this enrichment depends on PAR polarity and PLK-1. Taken together, our data suggest a model in which SPAT-1 promotes the activity of PLK-1 to regulate both cell polarity and cell cycle timing during asymmetric cell division, providing a link between these two processes.