Securin is required for chromosomal stability in human cells
Securin is required for chromosomal stability in human cells
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DOI：
10.1016/s0092-8674(01)00340-3
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发表时间：
2001-05-18
期刊：
影响因子：
64.5
通讯作者：
Lengauer, C
中科院分区：
文献类型：
--
作者：
Jallepalli, PV;Waizenegger, IC;Lengauer, C
染色体数目异常是癌症中最常见的遗传异常。因此，哺乳动物细胞中有丝分裂染色体传递保真度的调节机制引起了极大的兴趣。在这里，我们发现没有hSecurin基因的人类细胞以高频率丢失染色体。这种丢失与异常的后期有关，在此期间，细胞反复尝试分离染色体，但都没有成功。异常的有丝分裂与分离蛋白（姐妹分离蛋白酶）激活中的生化缺陷相关，使其无法有效切割粘附素亚基Scc 1。这些结果阐明了哺乳动物securin的功能，并表明它是维持整倍体所必需的。
Abnormalities of chromosome number are the most common genetic aberrations in cancer. The mechanisms regulating the fidelity of mitotic chromosome transmission in mammalian cells are therefore of great interest. Here we show that human cells without an hSecurin gene lose chromosomes at a high frequency. This loss was linked to abnormal anaphases during which cells underwent repetitive unsuccessful attempts to segregate their chromosomes. The abnormal mitoses were associated with biochemical defects in the activation of separin, the sister-separating protease, rendering it unable to cleave the cohesin subunit Scc1 efficiently. These results illuminate the function of mammalian securin and show that it is essential for the maintenance of euploidy.