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首页> 外文期刊>Cell cycle >Phosphorylation of histone H3 serine 10 in early mouse embryos: active phosphorylation at late S phase and differential effects of ZM447439 on first two embryonic mitoses.
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Phosphorylation of histone H3 serine 10 in early mouse embryos: active phosphorylation at late S phase and differential effects of ZM447439 on first two embryonic mitoses.

机译：早期小鼠胚胎中组蛋白H3丝氨酸10的磷酸化：ZM447439晚期S期的活性磷酸化和ZM447439对前两种胚胎瘤的差异效应。

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摘要

Cell division in mammalian cells is regulated by Aurora kinases. The activity of Aurora A is indispensable for correct function of centrosomes and proper spindle formation, while Aurora B for chromosome biorientation and separation. Aurora B is also responsible for the phosphorylation of histone H3 serine 10 (H3S10Ph) from G2 to metaphase. Data concerning the Aurora B activity and H3S10Ph in embryonic cells are limited to primordial and maturing oocytes and advanced pronuclei in zygotes. In the present study we have analyzed H3S10Ph in 1- and 2-cell mouse embryos. We show that H3S10 remains phosphorylated at anaphase and telophase of the second meiotic division, as well as during the anaphase and telophase of the first and second embryonic mitoses. At late G1 H3S10 is dephosphorylated and subsequently phosphorylated de novo at late S phase of the first and second cell cycle. These results show that the H3S10 phosphorylation/dephosphorylation cycle in embryonic cells is different than in somatic cells. The behaviour of thymocyte G0 nuclei introduced into ovulated oocytes and early 1-cell parthenogenotes confirms that kinases responsible for de novo H3S10 phosphorylation, most probably Aurora B, are active until G1 of the first cell cycle of mouse embryo. The inhibition of Aurora kinases by ZM447439 caused abnormalities both in the first and second mitoses. However, the disturbances in each division differed, suggesting important differences in the control of these mitoses. In ZM447439-treated mitotic zygotes Mad2 protein remained continuously present on kinetochores, what confirmed that spindle checkpoint remained active.
机译：哺乳动物细胞中的细胞分裂由极光激酶调节。 Aurora A的活性对于基于中心和适当的主轴形成的正确功能是必不可少的，而Aurora B用于染色体的嗜铬和分离。 Aurorab还负责从G2到中期的组蛋白H3丝氨酸10（H3S10ph）的磷酸化。关于胚胎细胞中的Aurora B活性和H3S10ph的数据仅限于Zygotes中的原始和成熟的卵母细胞和晚期前核。在本研究中，我们在1-和2细胞鼠胚胎中分析了H3S10ph。我们表明H3S10在第二减数分裂划分的后期和斑斑酶中仍然磷酸化，以及在第一和第二胚胎切片的后期和斑斑酶期间。在晚期G1 H3S10，在第一和第二细胞周期的晚期S期下，可去磷酸化并随后磷酸化De Novo。这些结果表明，胚胎细胞中的H3S10磷酸化/脱磷循环与体细胞不同。引入排卵的卵母细胞和早期1细胞疗法中胸腺细胞G0核的行为证实，对Novo H3S10磷酸化负责的激酶是活性的，直到小鼠胚胎的第一细胞周期的G1。通过ZM447439抑制Aurora激酶在第一和第二动弓织中引起异常。然而，每个分裂中的紊乱不同，表明对这些短暂的控制方面的重要差异。在ZM447439治疗的有丝分子型Zygotes Mad2蛋白在Kinetochores上连续存在，证实主轴检查点保持活跃。

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