Comparison of Two Models for Initiation of Replication in Escherichia coli

2020 ◽  
pp. 747-765
Author(s):  
Joseph M. Mahaffy ◽  
Judith W. Zyskind
1989 ◽  
Vol 140 (4) ◽  
pp. 453-477 ◽  
Author(s):  
Joseph M. Mahaffy ◽  
Judith W. Zyskind

Microbiology ◽  
2014 ◽  
Vol 160 (4) ◽  
pp. 703-710 ◽  
Author(s):  
Morigen Morigen ◽  
Ingvild Flåtten ◽  
Kirsten Skarstad

In Escherichia coli inhibition of replication leads to a block of cell division. This checkpoint mechanism ensures that no cell divides without having two complete copies of the genome to pass on to the two daughter cells. The chromosomal datA site is a 1 kb region that contains binding sites for the DnaA replication initiator protein, and which contributes to the inactivation of DnaA. An excess of datA sites provided on plasmids has been found to lead to both a delay in initiation of replication and in cell division during exponential growth. Here we have investigated the effect of datA on the cell division block that occurs upon inhibition of replication initiation in a dnaC2 mutant. We found that this checkpoint mechanism was aided by the presence of datA. In cells where datA was deleted or an excess of DnaA was provided, cell division occurred in the absence of replication and anucleate cells were formed. This finding indicates that loss of datA and/or excess of DnaA protein promote cell division. This conclusion was supported by the finding that the lethality of the division-compromised mutants ftsZ84 and ftsI23 was suppressed by deletion of datA, at the lowest non-permissive temperature. We propose that the cell division block that occurs upon inhibition of DNA replication is, at least in part, due to a drop in the concentration of the ATP–DnaA protein.


1966 ◽  
Vol 164 (995) ◽  
pp. 258-266 ◽  

In this paper I shall confine myself to only one aspect of chromosome replication in bacteria: its control and co-ordination with growth and cell division. The nature of the problem to be considered is made clear by two features of chromosome replication in Escherichia coli , First, under conditions of rapid growth, involving generation times of up to about one hour, DNA synthesis is essentially continuous; there is no detectable resting period corresponding to the G period typically found in higher organisms. Secondly, in glucose minimal media, as the data of Cairns (1963) and others have shown, a single replication point, or growth point, traverses the length of the chromosome during each cycle of replication. It follows that, although the rate of replication in E. coli might be determined by the supply of DNA precursors, the maintenance of the proper sequence of events cannot be controlled in this way since in a system in which DNA synthesis is continuous these precursors must be present at all times. Under the conditions mentioned above in E. coli , for example, the cell must have some means of ensuring that a new cycle of replication is not initiated until the previous one is complete. Consequently the important point of control of replication in bacteria must be over the initiation of replication rather than replication itself.


2007 ◽  
Vol 189 (23) ◽  
pp. 8660-8666 ◽  
Author(s):  
Henrik J. Nielsen ◽  
Brenda Youngren ◽  
Flemming G. Hansen ◽  
Stuart Austin

ABSTRACT Slowly growing Escherichia coli cells have a simple cell cycle, with replication and progressive segregation of the chromosome completed before cell division. In rapidly growing cells, initiation of replication occurs before the previous replication rounds are complete. At cell division, the chromosomes contain multiple replication forks and must be segregated while this complex pattern of replication is still ongoing. Here, we show that replication and segregation continue in step, starting at the origin and progressing to the replication terminus. Thus, early-replicated markers on the multiple-branched chromosomes continue to separate soon after replication to form separate protonucleoids, even though they are not segregated into different daughter cells until later generations. The segregation pattern follows the pattern of chromosome replication and does not follow the cell division cycle. No extensive cohesion of sister DNA regions was seen at any growth rate. We conclude that segregation is driven by the progression of the replication forks.


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