Jacobs C, Domian I J, Maddock J R, Shapiro L
Department of Developmental Biology, Stanford University School of Medicine, California 94305-5427, USA.
Cell. 1999 Apr 2;97(1):111-20. doi: 10.1016/s0092-8674(00)80719-9.
The master CtrA response regulator functions in Caulobacter to repress replication initiation in different phases of the cell cycle. Here, we identify an essential histidine kinase, CckA, that is responsible for CtrA activation by phosphorylation. Although CckA is present throughout the cell cycle, it moves to a cell pole in S phase, and upon cell division it disperses. Removal of the membrane-spanning region of CckA results in loss of polar localization and cell death. We propose that polar CckA functions to activate CtrA just after the initiation of DNA replication, thereby preventing premature reinitiations of chromosome replication. Thus, dynamic changes in cellular location of critical signal proteins provide a novel mechanism for the control of the prokaryote cell cycle.
主调控因子CtrA应答调节蛋白在柄杆菌中发挥作用,在细胞周期的不同阶段抑制复制起始。在此,我们鉴定出一种必需的组氨酸激酶CckA,它负责通过磷酸化激活CtrA。尽管CckA在整个细胞周期中都存在,但它在S期移动到细胞极,并且在细胞分裂时分散。去除CckA的跨膜区域会导致极性定位丧失和细胞死亡。我们提出,极性CckA的功能是在DNA复制起始后立即激活CtrA,从而防止染色体复制过早重新起始。因此,关键信号蛋白在细胞内位置的动态变化为原核细胞周期的控制提供了一种新机制。