What is it about?
We investigated how Escherichia coli controls chromosome replication when cells lack RecG, a DNA translocase linked to replication, repair and recombination. We found that DnaA-independent stable DNA replication, which can occur away from the normal chromosome origin, can copy regions across the chromosome and is greatly increased after UV damage in cells lacking RecG. This extra replication was associated with more replication fork activity, uncontrolled amplification of some chromosome regions, and branched DNA molecules containing few Holliday junctions. Our results support a model in which replication fork collisions create exposed 3′ DNA flaps that PriA can use to start inappropriate re-replication, feeding further recombination and replication.
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Why is it important?
The study helps explain why bacterial chromosome replication is normally arranged so that replication forks meet in a controlled terminus region. It suggests that RecG may protect E. coli not only by acting on recombination-related DNA structures, but also by limiting harmful re-replication after unscheduled fork collisions. This gives a more specific explanation for the chromosome segregation and cell division problems seen in recG mutants after DNA damage.
Perspectives
What stands out to us is how several lines of evidence converged on the same picture: chromosome-wide DNA labelling, fluorescent replication markers, origin–terminus tracking, and nuclease tests all pointed to pathological replication rather than simple accumulation of Holliday junctions. We were struck that once triggered by UV damage, the replication cascade could persist long after the original lesions should have been removed. This paper was useful for framing RecG as a factor that helps keep bacterial chromosome duplication orderly by preventing PriA-driven re-replication from getting out of control.
Dr. Christian J Rudolph
Brunel University
Read the Original
This page is a summary of: Replication fork collisions cause pathological chromosomal amplification in cells lacking RecG DNA translocase, Molecular Microbiology, October 2009, Wiley,
DOI: 10.1111/j.1365-2958.2009.06909.x.
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