What is it about?
In this perspective article, we examine the role of RecG, an E. coli protein that moves along DNA and can remodel branched DNA structures. RecG has been linked to DNA repair, replication restart, stable DNA replication and homologous recombination, but we ask whether several of these effects may reflect one underlying problem. We highlight evidence that, when RecG is absent, converging replication forks can generate DNA structures that allow unwanted re-replication, especially near the chromosome terminus. We also present genetic tests showing that the severe loss of recombinants in cells missing both RecG and the RuvABC junction-resolving complex is strongly eased when PriA helicase activity and the RecFOR pathway that loads RecA are also curtailed.
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Why is it important?
This work helps explain why bacterial chromosome copying must be tightly controlled when replication forks meet. It suggests that some effects previously interpreted as separate RecG functions may instead arise from uncontrolled replication at fork-fusion sites. The study also refines how we think about the balance between RecG, PriA, RecFOR, RecBCD and RuvABC in maintaining the E. coli chromosome.
Perspectives
From our perspective, the most interesting feature of this work is that a long list of RecG phenotypes can be re-examined through one problem: preventing pathological re-replication when replication forks meet. The paper combines a review of 25 years of RecG research with new genetic evidence from conjugational and tandem-repeat recombination assays. We do not rule out additional roles for RecG, but we suggest that controlling fork-fusion intermediates provides a useful way to make sense of many observations.
Dr. Christian J Rudolph
Brunel University
Read the Original
This page is a summary of: 25 years on and no end in sight: a perspective on the role of RecG protein, Current Genetics, April 2016, Springer Science + Business Media,
DOI: 10.1007/s00294-016-0589-z.
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