The small ubiquitin-like modifier (SUMO) is essential in cell cycle regulation in Trypanosoma brucei
The small ubiquitin-like modifier (SUMO) is essential in cell cycle regulation in Trypanosoma brucei
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小泛素样修饰剂 (SUMO) 对于布氏锥虫的细胞周期调节至关重要
DOI：
10.1016/j.yexcr.2009.12.017
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发表时间：
2010-03-10
影响因子：
3.7
通讯作者：
Tu, Xiaoming
中科院分区：
文献类型：
--
作者：
Liao, Shanhui;Wang, Tao;Tu, Xiaoming
SUMO是一种可逆的蛋白质翻译后修饰物，在高等真核细胞生命的许多过程中发挥着重要作用。虽然SUMO在许多真核生物中已被发现，但在一些真核单细胞生物中，如布氏锥虫（Trypanosomabrucei，T brucei），SUMO和SUMO系统仍然是未知的。利用RNA干扰技术敲低布氏锥虫顺环型TbSUMO基因的表达。TbSUMO缺陷细胞的生长明显受到抑制，细胞阻滞于G（2）/M期，同时出现大量的ON 1 K细胞（zoids），染色体分离失败。这些结果表明，TbSUMO在细胞周期调控中是必不可少的，在有丝分裂中起重要作用。Zoids的富集表明有丝分裂的抑制并不阻止顺周期型布氏锥虫的细胞分裂。HA标记的TbSUMO在布氏锥虫中过表达，并显示在整个细胞周期中定位于细胞核，进一步揭示了其在细胞核中的独特功能。所有这些积累的数据意味着，一个SUMO系统调节细胞周期的进展可能存在于顺周期形式的布氏锥虫（c）2009爱思唯尔公司版权所有。
SUMO, a reversible post-translational protein modifier, plays important roles in many processes of higher eukaryotic cell life. Although SUMO has been identified in many eukaryotes, SUMO and SUMO system are still unknown in some eukaryotic unicellular organisms, such as Trypanosoma brucei (T brucei) In this study, only one SUMO homologue (TbSUMO) was identified in T brucei. Expression of TbSUMO was knocked down by using RNA interference technique in procyclic-form T brucei. The growth of TbSUMO-deficient cells was significantly inhibited TbSUMO-deficient cells were arrested in G(2)/M phase accompanied with an obvious increase of ON1K cells (zoids), and failed in chromosome segregation These results indicate that TbSUMO is essential in cell cycle regulation, with one important role in mitosis Meanwhile, the enrichment of zoids suggests the inhibition of mitosis does not prevent the cell division in procyclic-form T brucei. HA-tagged TbSUMO was overexpressed in T brucei and was shown to be localized to the nucleus through the whole cell cycle, further revealing its distinguished functions in nucleus. All these accumulated data imply that a SUMO system essential for regulating cell cycle progression might exist in the procyclic-form T brucei (c) 2009 Elsevier Inc All rights reserved.