E-GEOD-41975 - Avoiding chromosome pathology when replication forks collide
Released on 22 July 2013, last updated on 3 May 2014
Chromosome duplication normally initiates via the assembly of replication fork complexes at defined origins. DNA synthesis by any one fork is thought to cease when it meets another travelling in the opposite direction, at which stage the replication machinery may simply dissociate before the nascent strands are finally ligated. But what actually happens is not clear. Here we present evidence consistent with the idea that every fork collision has the potential to trigger re-replication of the already replicated DNA, thus posing a threat to genomic integrity. In Escherichia coli this threat is kept at bay by the RecG DNA translocase. Without RecG, replication initiates where forks meet, establishing new forks with the potential to sustain cell growth and division in the absence of an active origin. The studies reported raise the question of how eukaryotic and archaeal cells are able to exploit multiple origins for the duplication of each chromosome without any apparent ill effect from the consequent multiple fork collisions. Measurement of replication dynamics (marker frequency analysis; MFA) for E. coli strains, including wild-type and various mutants.
Conrad A Nieduszynski <firstname.lastname@example.org>, Amy L Upton, Anna Stockum, Christian J Rudolph, Robert G Lloyd
Avoiding chromosome pathology when replication forks collide. Rudolph CJ, Upton AL, Stockum A, Nieduszynski CA, Lloyd RG. , Europe PMC 23892781