Tetraploidy-associated centrosome overduplication in mouse early embryos
Tetraploidy-associated centrosome overduplication in mouse early embryos
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DOI：
10.1080/19420889.2018.1526605
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发表时间：
2018-07
影响因子：
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通讯作者：
Kan Yaguchi;Takahiro Yamamoto;R. Matsui;Masaya Shimada;Atsuko Shibanuma;Keiko Kamimura;T. Koda;Ryota Uehara
中科院分区：
文献类型：
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作者：
Kan Yaguchi;Takahiro Yamamoto;R. Matsui;Masaya Shimada;Atsuko Shibanuma;Keiko Kamimura;T. Koda;Ryota Uehara
摘要最近，我们观察到某些类型的人类癌细胞的四倍体化导致中心体复制周期的上调和额外中心体的慢性产生。在这里，我们调查是否四倍体连锁上调中心体复制也发生在非癌细胞使用四倍体孤雌生殖小鼠胚胎。在从头中心粒生物发生之前的早期胚胎阶段的胞质分裂阻断提供了独特的机会，其中可以诱导四倍化而不需要中心体数目的瞬时加倍。中心粒和中心体的额外数量更频繁地观察到在四倍体化的胚胎在囊胚阶段比在其二倍体对应物，证明了新发现的四倍体驱动的中心体过度复制在哺乳动物非癌症系统的一般性。
ABSTRACT Recently, we observed that tetraploidization of certain types of human cancer cells resulted in upregulation of centrosome duplication cycles and chronic generation of the extra centrosome. Here, we investigated whether tetraploidy-linked upregulation of centrosome duplication also occurs in non-cancer cells using tetraploidized parthenogenetic mouse embryos. Cytokinesis blockage at early embryonic stage before de novo centriole biogenesis provided the unique opportunity in which tetraploidization can be induced without transient doubling of centrosome number. The extra numbers of the centrioles and the centrosomes were observed more frequently in tetraploidized embryos during the blastocyst stage than in their diploid counterparts, demonstrating the generality of the newly found tetraploidy-driven centrosome overduplication in mammalian non-cancer systems.