A calcium flux at the termination of replication triggers cell division in Escherichia coli. Hypothesis
- PMID: 2695251
- DOI: 10.1016/0143-4160(89)90012-2
A calcium flux at the termination of replication triggers cell division in Escherichia coli. Hypothesis
Abstract
Cell division in Escherichia coli is coupled to chromosome replication. Even in the absence of known inducible division inhibitors, perturbations of chromosome replication affect cell division. Early studies suggested that a signal at the termination of replication might trigger subsequent division. Although later studies have suggested that fork encounter during termination is an active process involving specific termination sites and the tus protein, the coupling mechanism between termination and cell division remains to be elucidated. Recently it has been shown that the chromosome of a bacterium, Pseudomonas tabaci, contains a high proportion of calcium. E. coli maintains an intracellular concentration of free calcium identical to that of higher organisms and in dividing cells of E. coli a twenty-fold increase in the level of total calcium in the cytoplasm, a flux, occurs. In this article I propose that during the replication of the chromosome calcium entry balances calcium binding to DNA. At the termination of replication, there is a brief interval between the end of calcium binding to the chromosome and the end of calcium entry or release into the cytoplasm. During this interval the level of free calcium therefore rises. This rise may result in the observed flux by triggering the entry of calcium directly via voltage-gated calcium channels or indirectly via changes in phospholipid configurations. Mechanisms whereby these changes in calcium levels might be coupled to cell division and to a phospholipid control of the cell cycle are discussed.
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