Figure 3.

Stabilisation of joint molecules by RuvABC and RecG. (A) DSBR intermediates visualised by 2D gel electrophoresis. RuvAB and RecG do not simply provide alternative pathways for the resolution of Holliday junctions, as previously suggested. Four‐way Holliday junction intermediates accumulate in the absence of RuvAB but not in the absence of RecG. The accumulation of Holliday junctions in the absence of RuvAB requires the presence of RecG 16. Data reproduced with permission from PLoS Genetics. (B) Role of RuvABC and RecG in the stability of joint molecules (i) Joint molecule stabilisation by RuvABC. In the absence of RecG, RuvAB migrates the Holliday junction away from the site of initiation of DSBR and leads to its cleavage by RuvC. Both branch migration and cleavage stabilise the joint molecule. (ii) Joint molecule stabilisation by RecG. In the absence of RuvABC, RecG manipulates the replication fork end of the D‐loop to allow PriA to bind in its 3′ end‐binding fork‐stabilising mode. This allows the initiation of DNA replication that stabilises the joint molecule. (iii) Joint molecule stabilisation by RuvABC and RecG. In the presence of both RuvABC and RecG, both the Holliday junction and replication fork ends of the D‐loop are stabilised.