Op De Beeck A, Caillet-Fauquet P
Department of Molecular Biology, Université Libre de Bruxelles, Rhode St Genèse, Belgium.
J Virol. 1997 Jul;71(7):5323-9. doi: 10.1128/JVI.71.7.5323-5329.1997.
The nonstructural protein NS1 of the autonomous parvovirus minute virus of mice interferes with cell division and can cause cell death, depending on the cell transformation state. Upon infection, the synthesis of NS1 protein is massively initiated during S phase. In this article, we show that minute virus of mice-infected cells accumulate in this phase. To investigate the link between NS1 accumulation and S-phase arrest, we have used stably transfected cells in which NS1 expression is under the control of a glucocorticoid-inducible promoter (the long terminal repeat of mouse mammary tumor virus). NS1 expression interferes with cell DNA replication, and consequently, the cell cycle stops in S phase. NS1 expression also induces nicks in the cell chromatin, as detected by an in situ nick translation assay. The nicks are observed several hours before any cell cycle perturbation. As cell cycle arrest is a common consequence of DNA damage, we propose that NS1 exerts its cytostatic activity by inducing lesions in cell chromatin.
自主细小病毒小鼠微小病毒的非结构蛋白NS1会干扰细胞分裂,并可能导致细胞死亡,这取决于细胞的转化状态。感染后,NS1蛋白的合成在S期大量启动。在本文中,我们表明感染小鼠微小病毒的细胞在这个阶段积累。为了研究NS1积累与S期停滞之间的联系,我们使用了稳定转染的细胞,其中NS1的表达受糖皮质激素诱导型启动子(小鼠乳腺肿瘤病毒的长末端重复序列)的控制。NS1的表达会干扰细胞DNA复制,因此,细胞周期在S期停止。如原位缺口平移试验所检测到的,NS1的表达还会诱导细胞染色质出现切口。在任何细胞周期扰动出现前数小时就能观察到这些切口。由于细胞周期停滞是DNA损伤的常见后果,我们提出NS1通过诱导细胞染色质损伤来发挥其细胞生长抑制活性。