An overview of homologous pairing and DNA strand exchange proteins

Eggleston, Angela K.; Kowalczykowski, S. C.

doi:10.1016/0300-9084(91)90199-b

Cited by 39 publications

(23 citation statements)

References 77 publications

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“…Although the core DNA strand exchange reaction is likely to proceed by a mechanism conserved since the divergence of prokaryotes and eukaryotes, certain biochemical properties are significantly different (Eggleston and Kowalczykowski 1991). Three biochemical differences are particularly relevant to the present study.…”

mentioning

confidence: 76%

“…Rad51 and Dmc1 share several properties with bacterial RecA, including the abilities to form helical presyn-aptic filaments and to promote strand exchange in purified systems (Eggleston and Kowalczykowski 1991;Sehorn and Sung 2004). All RecA-like recombinases are DNA-dependent ATPases, and all require ATP as a cofactor during DNA strand exchange; however, hydrolysis of ATP is not essential for homology recognition and DNA strand exchange (Menetski et al 1990;Sung and Stratton 1996;Campbell and Davis 1999a;Masson et al 1999;Hong et al 2001;Bugreev et al 2005).…”

mentioning

confidence: 99%

“…DNA strand exchange is the molecular process that defines homologous recombination (Roca and Cox 1990;Eggleston and Kowalczykowski 1991;Kowalczykowski 1991;Folta-Stogniew et al 2004). Members of the RecA family of recombinases promote DNA strand exchange by first assembling helical filaments on single-strand DNA (ssDNA).…”

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confidence: 99%

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Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin

Holzen¹,

Shah²,

Olivares³

et al. 2006

Genes Dev.

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The meiosis-specific recombinase Dmc1 plays a critical role in DNA strand exchange in budding yeast. Tid1/Rdh54, a member of the Swi2/Snf2 family of DNA translocases, has been shown to stimulate Dmc1-dependent recombination. Tid1 and its budding yeast paralog Rad54 have a variety of biochemical activities that may contribute to their biological function. Here we demonstrate that Dmc1 can associate with chromatin in the absence of DNA double-strand breaks (DSBs), and Tid1 suppresses this association. Chromatin immunoprecipitation experiments indicate that an activity shared by Tid1 and Rad54 is required for normal assembly of Dmc1 at DSB sites in preparation for recombination. These results lead to a model in which the ATP hydrolysis-dependent DNA translocase activity of Tid1 acts to promote dissociation of Dmc1 from nonrecombinogenic sites on chromatin, with Rad54 being able to substitute for this function in the absence of Tid1. The tendency of Dmc1 to form unproductive interactions with chromatin is proposed to be a consequence of the mechanism of strand exchange. The results raise the possibility that ATP hydrolysis-dependent disruption of nonproductive recombinase-DNA interactions is a feature shared with other homologous recombination systems.

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confidence: 76%

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confidence: 99%

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Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin

Holzen¹,

Shah²,

Olivares³

et al. 2006

Genes Dev.

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“…RecA binds single-stranded DNA with 3= overhangs (48). RecA rapidly polymerizes on DNA to form nucleoprotein filaments, the functional complexes that catalyze strand invasion (49).…”

Section: Discussionmentioning

confidence: 99%

Replication Restart after Replication-Transcription Conflicts Requires RecA in Bacillus subtilis

2015

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Efficient duplication of genomes depends on reactivation of replication forks outside the origin. Replication restart can be facilitated by recombination proteins, especially if single-or double-strand breaks form in the DNA. Each type of DNA break is processed by a distinct pathway, though both depend on the RecA protein. One common obstacle that can stall forks, potentially leading to breaks in the DNA, is transcription. Though replication stalling by transcription is prevalent, the nature of DNA breaks and the prerequisites for replication restart in response to these encounters remain unknown. Here, we used an engineered site-specific replication-transcription conflict to identify and dissect the pathways required for the resolution and restart of replication forks stalled by transcription in Bacillus subtilis. We found that RecA, its loader proteins RecO and AddAB, and the Holliday junction resolvase RecU are required for efficient survival and replication restart after conflicts with transcription. Genetic analyses showed that RecO and AddAB act in parallel to facilitate RecA loading at the site of the conflict but that they can each partially compensate for the other's absence. Finally, we found that RecA and either RecO or AddAB are required for the replication restart and helicase loader protein, DnaD, to associate with the engineered conflict region. These results suggest that conflicts can lead to both single-strand gaps and double-strand breaks in the DNA and that RecA loading and Holliday junction resolution are required for replication restart at regions of replication-transcription conflicts. IMPORTANCEHead-on conflicts between replication and transcription occur when a gene is expressed from the lagging strand. These encounters stall the replisome and potentially break the DNA. We investigated the necessary mechanisms for Bacillus subtilis cells to overcome a site-specific engineered conflict with transcription of a protein-coding gene. We found that the recombination proteins RecO and AddAB both load RecA onto the DNA in response to the head-on conflict. Additionally, RecA loading by one of the two pathways was required for both replication restart and efficient survival of the collision. Our findings suggest that both single-strand gaps and double-strand DNA breaks occur at head-on conflict regions and demonstrate a requirement for recombination to restart replication after collisions with transcription.

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“…Both pathways require RecA for homologous pairing and strand exchange (12,19). In addition to RecA, a number of other proteins are involved in homologous recombination in E. coli.…”

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confidence: 99%

Roles of therecJandrecNGenes in Homologous Recombination and DNA Repair Pathways ofNeisseria gonorrhoeae

2002

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The paradigm of homologous recombination comes from Escherichia coli, where the genes involved have been segregated into pathways. In the human pathogen Neisseria gonorrhoeae (the gonococcus), the pathways of homologous recombination are being delineated. To investigate the roles of the gonococcal recN and recJ genes in the recombination-based processes of the gonococcus, these genes were inactivated in the N. gonorrhoeae strain FA1090. We report that both recN and recJ loss-of-function mutants show decreased DNA repair ability. In addition, the recJ mutant was decreased in pilus-dependent colony morphology variation frequency but not DNA transformation efficiency, while the recN mutant was decreased in DNA transformation efficiency but not pilus-dependent variation frequency. We were able to complement all of these deficiencies by supplying an ectopic functional copy of either recJ or recN at an irrelevant locus. These results describe the role of recJ and recN in the recombination-dependent processes of the gonococcus and further define the pathways of homologous recombination in this organism.

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An overview of homologous pairing and DNA strand exchange proteins

Cited by 39 publications

References 77 publications

Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin

Tid1/Rdh54 promotes dissociation of Dmc1 from nonrecombinogenic sites on meiotic chromatin

Replication Restart after Replication-Transcription Conflicts Requires RecA in Bacillus subtilis

Roles of therecJandrecNGenes in Homologous Recombination and DNA Repair Pathways ofNeisseria gonorrhoeae

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