Katayama T, Takata M, Sekimizu K
Department of Microbiology, Kyushu University Faculty of Pharmaceutical Sciences, Fukuoka, Japan.
Mol Microbiol. 1997 Nov;26(4):687-97. doi: 10.1046/j.1365-2958.1997.5941967.x.
We isolated and characterized a new gene related to the control of cell division regulation in Escherichia coli. At 30 degrees C, the dnaAcos mutant causes over-replication of the chromosome, and colony formation is inhibited. We found that, at this temperature, the dnaAcos cells form filaments; therefore, septum formation is inhibited. This inhibition was independent of SfiA, an inhibitor of the septum-forming protein, FtsZ. To identify factors involved in this pathway of inhibition, we isolated seven multicopy suppressors for the cold-sensitive phenotype of the dnaAcos mutant. One of these proved to be a previously unknown gene, which we named cedA. This gene encoded a 12 kDa protein and resided at 38.9min on the E. coli genome map. A multicopy supply of the cedA gene to the dnaAcos cells did not repress over-replication of the chromosome but did stimulate cell division of the host, the result being growth of cells with an abnormally elevated chromosomal copy number. Therefore, the expression level of the cedA gene seems to be important for inhibiting cell division of the dnaAcos mutant at 30 degrees C. We propose that over-replication of the chromosome activates a pathway for inhibiting cell division and that the cedA gene modulates this division control. In the dnaA+ background, cedA also seems to affect cell division.
我们分离并鉴定了一个与大肠杆菌细胞分裂调控控制相关的新基因。在30摄氏度时，dnaAcos突变体导致染色体过度复制，菌落形成受到抑制。我们发现，在此温度下，dnaAcos细胞形成丝状；因此，隔膜形成受到抑制。这种抑制与隔膜形成蛋白FtsZ的抑制剂SfiA无关。为了鉴定参与这种抑制途径的因子，我们分离了七个多拷贝抑制子，用于dnaAcos突变体的冷敏感表型。其中一个被证明是一个以前未知的基因，我们将其命名为cedA。该基因编码一个12 kDa的蛋白质，位于大肠杆菌基因组图谱的38.9分钟处。将cedA基因多拷贝供应给dnaAcos细胞并没有抑制染色体的过度复制，但确实刺激了宿主的细胞分裂，结果是染色体拷贝数异常升高的细胞生长。因此，cedA基因的表达水平似乎对于在30摄氏度下抑制dnaAcos突变体的细胞分裂很重要。我们提出，染色体的过度复制激活了一条抑制细胞分裂的途径，并且cedA基因调节这种分裂控制。在dnaA+背景下，cedA似乎也影响细胞分裂。
