The RecB Nuclease Domain Binds to RecA-DNA Filaments: Implications for Filament Loading

Lucarelli, Debora; Wang, Ying A.; Galkin, Vitold E.; Xiong, Yong; Wigley, Dale B.

doi:10.1016/j.jmb.2009.06.042

Cited by 11 publications

(11 citation statements)

References 34 publications

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“…In the first pathway, end processing and RecA loading might be coupled: the AddAB complex in concert with SsbA, upon interaction with the chi site, might facilitate loading of RecA onto naked ssDNA (Kowalczykowski et al, 1994, Yeeles et al, 2011). The RecBCD Eco complex actively loads RecA Eco onto the exposed naked ssDNA (Anderson et al, 1999, Dillingham and Kowalczykowski, 2008, Lucarelli et al, 2009), but the AddAB-dependent RecA loading avenue remains to be documented (Yeeles and Dillingham, 2010). In the second pathway, end processing and RecA loading are uncoupled.…”

Section: Genetic Recombination Shares Some Steps With Recombinationalmentioning

confidence: 99%

The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

Kidane

Ayora

Sweasy

et al. 2012

Critical Reviews in Biochemistry and Molecular Biology

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Natural transformation is a programmed mechanism characterized by binding of free double-stranded (ds) DNA from the environment to the cell pole in rod-shaped bacteria. In Bacillus subtilis some competence proteins, which process the dsDNA and translocate single-stranded (ss) DNA into the cytosol, recruit a set of recombination proteins mainly to one of the cell poles. A subset of single-stranded binding proteins, working as “guardians”, protect ssDNA from degradation and limit the RecA recombinase loading. Then, the “mediators” overcome the inhibitory role of guardians, and recruit RecA onto ssDNA. A RecA·ssDNA filament searches for homology on the chromosome and, in a process that is controlled by “modulators”, catalyzes strand invasion with the generation of a displacement loop (D-loop). A D-loop resolvase or “resolver” cleaves this intermediate, limited DNA replication restores missing information and a DNA ligase seals the DNA ends. However, if any step fails, the “rescuers” will repair the broken end to rescue chromosomal transformation. If the ssDNA does not share homology with resident DNA, but it contains information for autonomous replication, guardian and mediator proteins catalyze plasmid establishment after inhibition of RecA. DNA replication and ligation reconstitute the molecule (plasmid transformation). In this review, the interacting network that leads to a cross talk between proteins of the uptake and genetic recombination machinery will be placed into prospective.

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Section: Genetic Recombination Shares Some Steps With Recombinationalmentioning

confidence: 99%

The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

Kidane

Ayora

Sweasy

et al. 2012

Critical Reviews in Biochemistry and Molecular Biology

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“…Biochemical data show that the RecBCD Eco complex, upon interaction with the chi site, activates RecB Eco to facilitate the loading of RecA Eco onto the exposed naked ssDNA (Anderson et al, 1999;Dillingham & Kowalczykowski, 2008;Yeeles & Dillingham, 2010). The activated RecB Eco domain also interacts with the RecA Eco nucleoprotein filament (Dillingham & Kowalczykowski, 2008;Lucarelli et al, 2009;Yeeles & Dillingham, 2010). It is unknown whether the RecBCD Eco paradigm for RecA Eco loading onto naked ssDNA, upon DSB and concomitant end-resection, can be extended to other members of the family (AddAB or AdnAB).…”

Section: Recombinase Loadingmentioning

confidence: 99%

Double-strand break repair in bacteria: a view fromBacillus subtilis

et al. 2011

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In all living organisms, the response to double-strand breaks (DSBs) is critical for the maintenance of chromosome integrity. Homologous recombination (HR), which utilizes a homologous template to prime DNA synthesis and to restore genetic information lost at the DNA break site, is a complex multistep response. In Bacillus subtilis, this response can be subdivided into five general acts: (1) recognition of the break site(s) and formation of a repair center (RC), which enables cells to commit to HR; (2) end-processing of the broken end(s) by different avenues to generate a 3'-tailed duplex and RecN-mediated DSB 'coordination'; (3) loading of RecA onto single-strand DNA at the RecN-induced RC and concomitant DNA strand exchange; (4) branch migration and resolution, or dissolution, of the recombination intermediates, and replication restart, followed by (5) disassembly of the recombination apparatus formed at the dynamic RC and segregation of sister chromosomes. When HR is impaired or an intact homologous template is not available, error-prone nonhomologous end-joining directly rejoins the two broken ends by ligation. In this review, we examine the functions that are known to contribute to DNA DSB repair in B. subtilis, and compare their properties with those of other bacterial phyla.

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“…The HR repair system in E.coli initiates DSB repair using the nuclease activity of the RecBCD complex to process the DNA ends and load RecA onto the ssDNA24. Further steps are required, and distinct from NHEJ, a homologous template is necessary for repair of the DSBs.…”

Section: Introductionmentioning

confidence: 99%

Pathways for Double-strand Break Repair in Genetically Unstable Z-DNA-forming Sequences

Kha

Wang

Natrajan

et al. 2010

Journal of Molecular Biology

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DNA can adopt many structures that differ from the canonical B-form, and several of these noncanonical DNA structures have been implicated in genetic instability associated with human disease. Previously, we found that Z-DNA causes DNA double-strand breaks (DSBs) in mammalian cells that can result in large-scale deletions and rearrangements. In contrast, the same Z-DNA-forming CG repeat in E.coli resulted in only small contractions or expansions within the repeat. This difference in the Z-DNA-induced mutation spectrum between mammals and bacteria may be due to different mechanisms for DSB repair; in mammalian cells non-homologous end-joining (NHEJ) is a major DSB repair pathway, while E.coli do not contain this system and typically use homologous recombination (HR) to process DSBs. To test the extent to which the different DSB repair pathways influenced the Z-DNA-induced mutagenesis, we engineered bacterial E.coli strains to express an inducible NHEJ system, to mimic the situation in mammalian cells. Mycobacterium tuberculosis NHEJ proteins Ku and Ligase D (LigD) were expressed in E.coli cells in the presence or absence of HR, and the Z-DNA-induced mutations were characterized. We found that the presence of the NHEJ mechanism markedly shifted the mutation spectrum from small deletions/insertions to large-scale deletions (from 2% to 24%). Our results demonstrate that NHEJ plays a role in the generation of Z-DNA-induced large-scale deletions, suggesting that this pathway is associated with DNA structureinduced destabilization of genomes from prokaryotes to eukaryotes.

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The RecB Nuclease Domain Binds to RecA-DNA Filaments: Implications for Filament Loading

Cited by 11 publications

References 34 publications

The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

Double-strand break repair in bacteria: a view fromBacillus subtilis

Pathways for Double-strand Break Repair in Genetically Unstable Z-DNA-forming Sequences

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