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首页> 外文期刊>Cell cycle >Basal c-Jun N-terminal kinases promote mitotic progression through histone H3 phosphorylation.
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Basal c-Jun N-terminal kinases promote mitotic progression through histone H3 phosphorylation.

机译：基底c-Jun N末端激酶通过组蛋白H3磷酸化促进有丝分裂进程。

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摘要

Phosphorylation of histone H3 at serine 10 (S10) is essential for the onset of mitosis. Here, we show that basal c-Jun N-terminal kinases (JNKs) are required for mitotic histone H3-S10 phosphorylation in human primary fibroblast IMR90 cells. Inhibition of JNKs by specific pharmacologic inhibitors, expression of dominant-negative JNK1 and 2 mutants, or RNAi of JNK1 and 2 prevented phosphorylation of histone H3 at S10 in vivo. The JNK-specific inhibitor SP600125 blocked mitotic entry, as shown by its ability to prevent CDK1 dephosphorylation and cyclin A degradation. Basal JNK phosphorylation increased at G(2)/M phase, although total JNK protein levels remained unchanged. In addition, basal JNKs were localized in nuclei and centrosomes during this time, suggesting that the nuclear localization of JNKs during G(2)/M is tightly coupled with histone H3 phosphorylation. Basal JNKs were able to phosphorylate histone H3 in vitro and coprecipitation of histone H3 and JNKs was only detected at G(2)/M. Taken together, these data strongly suggest that basal JNKs play a key role in controlling histone H3 phosphorylation for mitotic entry at G(2)/M phase.
机译：组蛋白H3在丝氨酸10（S10）处的磷酸化对于有丝分裂的发生至关重要。在这里，我们显示人类原代成纤维细胞IMR90细胞中有丝分裂组蛋白H3-S10磷酸化需要基础c-Jun N末端激酶（JNKs）。特定药理抑制剂对JNK的抑制，显性阴性JNK1和2突变体的表达或JNK1和2的RNAi阻止了体内S10体内组蛋白H3的磷酸化。 JNK特异性抑制剂SP600125阻止有丝分裂进入，如其预防CDK1磷酸化和细胞周期蛋白A降解的能力所示。基础JNK磷酸化增加G（2）/ M阶段，尽管总JNK蛋白水平保持不变。此外，在此期间，基础JNKs定位在核和中心体中，表明在G（2）/ M期间JNKs的核定位与组蛋白H3磷酸化紧密相关。基底JNKs能够在体外磷酸化组蛋白H3，仅在G（2）/ M时检测到组蛋白H3和JNKs的共沉淀。两者合计，这些数据强烈表明基础JNKs在控制组蛋白H3磷酸化在G（2）/ M期有丝分裂进入中发挥关键作用。

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