Rao N N, Kornberg A
Department of Biochemistry, Stanford University School of Medicine, California 94305-5307, USA.
Prog Mol Subcell Biol. 1999;23:183-95. doi: 10.1007/978-3-642-58444-2_9.
The molecular mechanisms responsible for polyP accumulation in E. coli remain largely obscure. Based on the available data, a tentative model is proposed (Fig. 1; Ault-Riché et al. 1998). Inhibition by (p)ppGpp of PPX interrupts the dynamic balance between the synthesis of polyP by PPK and its hydrolysis by PPX, accounting for polyP accumulation. However, mutants lacking PhoB, the response regulator of the Pho regulon, fail to accumulate polyP even in the face of high levels of (p)ppGpp. Clearly, PhoB is required in some undefined manner. With regard to osmotic stress, the pathway to polyP accumulation is also distinct from the one identified with the activation of envZ and the associated changes in membrane functions. A tentative scheme attempting to describe the metabolic turnover of polyP is given in Fig. 4. [figure: see text] In adaptations to stress, cells must coordinate major changes in the rates of transcription, translation, and replication as well as make choices in the genes expressed (Kolter et al. 1993). PolyP could provide activated phosphates or coordinate an adaptive response by binding metals and/or specific proteins. Accumulation of polyP in E. coli and other organisms is commonly assumed to provide a reservoir of energy convertible to ATP. This seems implausible because of the turnover of ATP which consumes only a fraction of a second (Chapman and Atkinson 1977). Thus, other functions for polyP need to be considered, among them a regulatory role. PolyP, even at very low levels, is essential in E. coli for adaptations in stationary phase and for survival (Rao and Kornberg 1996). As a polyanionic polymer, polyP has chemical similarities to DNA and RNA in interactions with basic domains of proteins. Further investigation of the cellular location of polyP, its state of metabolic availability and identification of its binding partners are needed. In view of the ubiquity of polyP in eukaryotic cells (including dynamic turnover in the nuclei of some mammalian cells), studies similar to those undertaken in E. coli may reveal comparable functions.
大肠杆菌中多聚磷酸盐（polyP）积累的分子机制在很大程度上仍不清楚。基于现有数据，提出了一个初步模型（图1；Ault-Riché等人，1998年）。（p）ppGpp对PPX的抑制作用中断了PPK合成多聚磷酸盐与其被PPX水解之间的动态平衡，这解释了多聚磷酸盐的积累。然而，缺乏PhoB（Pho调控子的应答调节因子）的突变体即使面对高水平的（p）ppGpp也无法积累多聚磷酸盐。显然，PhoB以某种未明确的方式发挥作用。关于渗透胁迫，多聚磷酸盐积累的途径也不同于通过envZ激活及相关膜功能变化所确定的途径。图4给出了一个试图描述多聚磷酸盐代谢周转的初步方案。[图：见正文]在适应胁迫过程中，细胞必须协调转录、翻译和复制速率的重大变化，并在表达的基因中做出选择（Kolter等人，1993年）。多聚磷酸盐可以提供活化的磷酸盐，或者通过结合金属和/或特定蛋白质来协调适应性反应。通常认为大肠杆菌和其他生物体中多聚磷酸盐的积累提供了一个可转化为ATP的能量储备。但这似乎不太合理，因为ATP的周转只需要不到一秒钟的时间（Chapman和Atkinson，1977年）。因此，需要考虑多聚磷酸盐的其他功能，其中包括调节作用。多聚磷酸盐即使在非常低的水平下，对于大肠杆菌在稳定期的适应和生存也是必不可少的（Rao和Kornberg，1996年）。作为一种聚阴离子聚合物，多聚磷酸盐在与蛋白质碱性结构域的相互作用方面与DNA和RNA具有化学相似性。需要进一步研究多聚磷酸盐在细胞中的定位、其代谢可用性状态以及鉴定其结合伙伴。鉴于多聚磷酸盐在真核细胞中普遍存在（包括一些哺乳动物细胞核中的动态周转），类似于在大肠杆菌中进行的研究可能会揭示类似的功能。
