Maple Jodi, Møller Simon Geir
Department of Mathematics and Natural Sciences, University of Stavanger, 4036 Stavanger, Norway.
Ann Bot. 2007 Apr;99(4):565-79. doi: 10.1093/aob/mcl249. Epub 2006 Nov 30.
The continuity of chloroplasts is maintained by division of pre-existing chloroplasts. Chloroplasts originated as bacterial endosymbionts; however, the majority of bacterial division factors are absent from chloroplasts and the eukaryotic host has added several new components. For example, the ftsZ gene has been duplicated and modified, and the Min system has retained MinE and MinD but lost MinC, acquiring at least one new component ARC3. Further, the mechanism has evolved to include two members of the dynamin protein family, ARC5 and FZL, and plastid-dividing (PD) rings were most probably added by the eukaryotic host.
Deciphering how the division of plastids is coordinated and controlled by nuclear-encoded factors is key to our understanding of this important biological process. Through a number of molecular-genetic and biochemical approaches, it is evident that FtsZ initiates plastid division where the coordinated action of MinD and MinE ensures correct FtsZ (Z)-ring placement. Although the classical FtsZ antagonist MinC does not exist in plants, ARC3 may fulfil this role. Together with other prokaryotic-derived proteins such as ARC6 and GC1 and key eukaryotic-derived proteins such as ARC5 and FZL, these proteins make up a sophisticated division machinery. The regulation of plastid division in a cellular context is largely unknown; however, recent microarray data shed light on this. Here the current understanding of the mechanism of chloroplast division in higher plants is reviewed with an emphasis on how recent findings are beginning to shape our understanding of the function and evolution of the components.
Extrapolation from the mechanism of bacterial cell division provides valuable clues as to how the chloroplast division process is achieved in plant cells. However, it is becoming increasingly clear that the highly regulated mechanism of plastid division within the host cell has led to the evolution of features unique to the plastid division process.
叶绿体的连续性通过已有叶绿体的分裂来维持。叶绿体起源于细菌内共生体；然而，叶绿体中不存在大多数细菌分裂因子，真核宿主添加了几个新成分。例如，ftsZ基因已被复制和修饰，Min系统保留了MinE和MinD，但失去了MinC，获得了至少一个新成分ARC3。此外，该机制已进化到包括动力蛋白家族的两个成员ARC5和FZL，质体分裂（PD）环很可能是由真核宿主添加的。
解读质体分裂如何由核编码因子协调和控制是我们理解这一重要生物学过程的关键。通过多种分子遗传学和生物化学方法，很明显FtsZ启动质体分裂，其中MinD和MinE的协同作用确保FtsZ（Z）环的正确定位。虽然植物中不存在经典的FtsZ拮抗剂MinC，但ARC3可能起到这一作用。这些蛋白质与其他原核来源的蛋白质如ARC6和GC1以及关键的真核来源的蛋白质如ARC5和FZL一起，构成了一个复杂的分裂机制。质体分裂在细胞环境中的调控在很大程度上尚不清楚；然而，最近的微阵列数据对此有所揭示。本文综述了目前对高等植物叶绿体分裂机制的理解，重点是最近的发现如何开始塑造我们对这些成分的功能和进化的理解。
从细菌细胞分裂机制推断为植物细胞中叶绿体分裂过程的实现提供了有价值的线索。然而，越来越清楚的是，宿主细胞内高度调控的质体分裂机制导致了质体分裂过程特有的特征的进化。
