Li Ziyin
Department of Microbiology & Molecular Genetics, University of Texas Medical School at Houston, TX, USA.
Eukaryot Cell. 2012 Oct;11(10):1180-90. doi: 10.1128/EC.00145-12. Epub 2012 Aug 3.
The cell division cycle is tightly regulated by the activation and inactivation of a series of proteins that control the replication and segregation of organelles to the daughter cells. During the past decade, we have witnessed significant advances in our understanding of the cell cycle in Trypanosoma brucei and how the cycle is regulated by various regulatory proteins. However, many other regulators, especially those unique to trypanosomes, remain to be identified, and we are just beginning to delineate the signaling pathways that drive the transitions through different cell cycle stages, such as the G(1)/S transition, G(2)/M transition, and mitosis-cytokinesis transition. Trypanosomes appear to employ both evolutionarily conserved and trypanosome-specific molecules to regulate the various stages of its cell cycle, including DNA replication initiation, spindle assembly, chromosome segregation, and cytokinesis initiation and completion. Strikingly, trypanosomes lack some crucial regulators that are well conserved across evolution, such as Cdc6 and Cdt1, which are involved in DNA replication licensing, the spindle motor kinesin-5, which is required for spindle assembly, the central spindlin complex, which has been implicated in cytokinesis initiation, and the actomyosin contractile ring, which is located at the cleavage furrow. Conversely, trypanosomes possess certain regulators, such as cyclins, cyclin-dependent kinases, and mitotic centromere-associated kinesins, that are greatly expanded and likely play diverse cellular functions. Overall, trypanosomes apparently have integrated unique regulators into the evolutionarily conserved pathways to compensate for the absence of those conserved molecules and, additionally, have evolved certain cell cycle regulatory pathways that are either different from its human host or distinct between its own life cycle forms.
细胞分裂周期受到一系列蛋白质激活和失活的严格调控,这些蛋白质控制细胞器向子细胞的复制和分离。在过去十年中,我们见证了对布氏锥虫细胞周期及其如何由各种调节蛋白调控的理解取得了重大进展。然而,许多其他调节因子,尤其是锥虫特有的调节因子,仍有待确定,而且我们才刚刚开始描绘驱动细胞周期不同阶段转换的信号通路,如G(1)/S转换、G(2)/M转换以及有丝分裂-胞质分裂转换。锥虫似乎利用进化上保守的分子和锥虫特有的分子来调控其细胞周期的各个阶段,包括DNA复制起始、纺锤体组装、染色体分离以及胞质分裂起始和完成。引人注目的是,锥虫缺乏一些在进化过程中高度保守的关键调节因子,如参与DNA复制许可的Cdc6和Cdt1、纺锤体组装所需的纺锤体马达驱动蛋白-5、与胞质分裂起始有关的中央纺锤体复合物以及位于分裂沟处的肌动球蛋白收缩环。相反,锥虫拥有某些调节因子,如细胞周期蛋白、细胞周期蛋白依赖性激酶和有丝分裂着丝粒相关驱动蛋白,这些调节因子大幅扩增,可能发挥多种细胞功能。总体而言,锥虫显然已将独特的调节因子整合到进化上保守的通路中,以弥补那些保守分子的缺失,此外,还进化出了某些与其人类宿主不同或在其自身生命周期形式之间不同的细胞周期调节通路。