What is it about?
We studied what happens in Escherichia coli when two DNA-copying machines, called replication forks, meet as the chromosome is duplicated. We found that these fork collisions can trigger new rounds of DNA replication if RecG DNA translocase and DNA-trimming exonucleases are not there to control the DNA structures formed. This new replication used PriA and PriB, proteins normally involved in restarting replication at damaged or stalled forks, and in some settings also depended on recombination proteins. Strikingly, when barriers to fork movement were reduced and the chromosome remained circular, this collision-triggered replication could support growth even without the usual DnaA/oriC replication origin.
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Why is it important?
The work suggests that finishing chromosome replication is not simply a passive stopping point; it may be a moment that needs active control to protect genome stability. It supports a model in which RecG and 3′ single-strand DNA exonucleases help prevent already copied DNA from being copied again after fork collisions. This may help explain why cells need safeguards at replication termination, and it raises cautious questions about how organisms with many replication origins manage many such collisions.
Perspectives
What stands out to us is that a normal event in chromosome duplication, the meeting of two replication forks, could become harmful if the cleanup systems are missing. We connected genetic tests, genome-wide replication profiles, BrdU labelling, chromosome linearization, and two-origin chromosomes to build a consistent picture of collision-triggered replication. The paper is interesting to us because it places replication fork termination alongside initiation, repair, and restart as a process that must be carefully controlled.
Dr. Christian J Rudolph
Brunel University
Read the Original
This page is a summary of: Avoiding chromosome pathology when replication forks collide, Nature, July 2013, Nature,
DOI: 10.1038/nature12312.
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