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首页> 外文期刊>Cell cycle >Aurora kinase B-phosphorylated HP1 alpha functions in chromosomal instability
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Aurora kinase B-phosphorylated HP1 alpha functions in chromosomal instability

机译：Aurora激酶B-磷酸化HP1α在染色体不稳定性中的功能

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摘要

Heterochromatin Protein 1 alpha (HP1 alpha) associates with members of the chromosome passenger complex (CPC) during mitosis, at centromeres where it is required for full Aurora Kinase B (AURKB) activity. Conversely, recent reports have identified AURKB as the major kinase responsible for phosphorylation of HP1 alpha at Serine 92 (S92) during mitosis. Thus, the current study was designed to better understand the functional role of this posttranslationally modified form of HP1 alpha. We find that S92-phosphorylated HP1 alpha is generated in cells at early prophase, localizes to centromeres, and associates with regulators of chromosome stability, such as Inner Centromere Protein, INCENP. In mouse embryonic fibroblasts, HP1 alpha knockout alone or reconstituted with a non-phosphorylatable (S92A) HP1 alpha mutant results in mitotic chromosomal instability characterized by the formation of anaphase/telophase chromatin bridges and micronuclei. These effects are rescued by exogenous expression of wild type HP1 alpha or a phosphomimetic (S92D) variant. Thus, the results from the current study extend our knowledge of the role of HP1 alpha in chromosomal stability during mitosis.
机译：异铬蛋白蛋白1α（HP1α）在有丝分裂期间与染色体乘客综合体（CPC）的成员缔结，在焦粒子中，在碳纤维粒子需要全极光激酶B（AurkB）活性。相反，最近的报告已经将AurkB鉴定为负责在有丝分裂期间丝网92（S92）的HP1α的磷酸化的主要激酶。因此，目前的研究旨在更好地了解这种发生这种后期改性的HP1α的功能作用。我们发现S92-磷酸化的HP1α在早期预先存在的细胞中产生，定位为Centromeres，并与染色体稳定性的调节剂相关，如内厘米蛋白，INCENPP。在小鼠胚胎成纤维细胞中，单独的HP1α敲除或用非磷酸化（S92A）HP1α突变体重构有丝分裂染色体不稳定性，其特征在于形成所述后磷酸酶染色质桥和微核。通过野生型HP1α或磷酸化（S92D）变体的外源表达来抵抗这些效果。因此，目前研究的结果延长了在有丝分裂期间HP1α在染色体稳定性中的作用的了解。

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