The bacterium Vibrio cholerae, the cause of the diarrhoeal disease cholera, has its genome divided between two chromosomes, a feature uncommon in the bacterial world. The two chromosomes are of dissimilar sizes, chromosome II consists of 1.07 million basepairs, while the large chromosome I consists of 2.96 million basepairs and hold most of the bacteria’s essential genes. The two chromosomes also have distinctly different origins of replication. The origin of chromosome I is homologues to that of Escherichia coli, while the origin of chromosome II is more plasmid like. It have been reported that the replication of the two chromosomes initiate at the same point in the cell cycle (Egan et al 2004 Curr. Biol. 14:R501-R502). The result was based on a rifampicin/cephalexin runout experiment. This finding did not agree with our early findings and recently published results showing that the two chromosomes of V. cholerae have independent mechanisms controlling the initiation of replication. The timing of chromosomal replication was therefore carefully reinvestigated by modelling flow cytometry data and marker frequency analysis based on quantitative PCR. The results show that the two chromosomes of V. cholerae does not initiate synchronously, rather chromosome II is replicated late in the C-period in such a way that the replication of the two chromosomes terminate at approximately the same time. Furthermore we report that treating V. cholerae with rifampicin produce an unexpected artefact, which have wrongly been interpreted as initiation synchrony. The artefact arises due to delayed rifampicin action on chromosome II, compared to chromosome I.
|Uddannelser||Molekylærbiologi, (Bachelor/kandidatuddannelse) Bachelor el. kandidat|
|Udgivelsesdato||1 jan. 2006|
- Vibrio cholerae