Molecular Mechanism of Bacterial Chromosome Partitioning dependent on a Centromere like site migS

我们在大肠杆菌基因组中发现了一个类似着丝粒的元件（migS）。我们搜索了与migS基因相互作用的基因产物。phoU转座子（Tn）插入突变在migS缺失突变下表现出生长缺陷。据报道，PhoU的功能在磷酸盐的吸收和细胞间的磷酸盐代谢，虽然一些人声称这些不是它的主要功能。phoU Tn插入突变体（phoU：：Tn）在phoU基因的羧基端缺失了几个氨基酸残基，无效突变体没有表现出与migS突变体相同的合成致死表型。phoU：：Tn细胞显示从细胞中心错置的类核，而在野生型细胞中，类核位于细胞的中心区域。在突变体中，子核在细胞分裂时没有明显分离。事实上，在phoU突变体中，无DNA细胞的频率增加。这种表型在slmA缺陷细胞中被夸大，其中隔膜抑制机制超过未分离的细胞核。 关于我们 eoids不存在。在ΔslmA中，phoU：:在双突变细胞中，与野生型细胞相比，无核细胞的频率增加，并出现了剪切型细胞。我们的结论是，截短的PhoU蛋白扰乱了子核的正确定位，这可能导致有丝分裂灾难。此外，我们想集中在细菌细胞中的DNA双极迁移的分子机制的研究。虽然肌动蛋白样蛋白已被发现在原核生物中，运动功能，以分区染色体到子细胞尚未被确定的双极迁移的染色体。据推测，一种马达蛋白参与了产生驱动力的过程。对migS依赖性迁移的分子机制的研究为推测的运动蛋白如何参与染色体分配提供了重要的新线索。蛋白质组学方法已经鉴定出两种蛋白质为migS结合蛋白。对编码migS结合蛋白的基因的进一步研究已经进行，结果表明这些基因可能参与migS的双极迁移。

We have found a centromere-like element (migS) on the Escherichia coli genome. We searched gene products that genetically interact with migS. Transposon (Tn) insertion mutations of phoU showed a growth defect under migS deletion mutation. It was reported that PhoU functions in phosphate uptake and intercellular phosphate metabolism, although several group claimed those were not its primary functions. The phoU Tn insertion mutant (phoU : : Tn) lacked a few amino acid residues from the carboxyl terminal of phoU gene, and the null mutant did not show the synthetic lethal phenotype with migS mutant. phoU::Tn cells showed mislocated nucleoid from centre of the cells, while in wild type cells have the nucleoid at central region of the cell. Daughter nucleoids were not clearly separated at cell division in the mutant. In fact, frequency of DNA-less cells increased in the phoU mutant. This phenotype was exaggerated in slmA deficient cells where septum inhibition mechanism over unseparated nucl … More eoids was absent. In ΔslmA, phoU : : Tn double mutant cells, frequency of anucleate cells were increased compared to the wild type cells and guillotine typed cells were appeared. We concluded that the truncated PhoU protein perturbed correct positioning of daughter nucleoids and this could lead mitotic catastroph. Furthermore, we would like to focus on study of the molecular mechanism for bipolar migration of DNA in a bacterial cell. Although actin-like proteins have been found in prokaryotes, a motor function to partition chromosomes into daughter cells has not yet been identified on bipolar migration of the chromsome. Presumably, a motor protein works on the process to generate a driving force. Investigation of the molecular mechanism of migS dependent migration is providing vital new clues as how the putative motor protein contributes to chromosome partitioning. Proteomics approaches have already been identified two proteins as migS binding proteins. Further investigation of the genes that encode the migS binding proteins have already been carried out, and the results indicates the genes would be involved in bipolar migration of migS Less