Evidence for Both 3’ and 5’ Single-Strand DNA Ends in Intermediates in Chi-Stimulated Recombination <i>In Vivo</i>

Razavy, Haide; Szigety, Susan K.; Rosenberg, Susan M.

doi:10.1093/genetics/142.2.333

Cited by 65 publications

(6 citation statements)

References 31 publications

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“…3B). Their distribution "outward" from dif implies degradation by other nucleases in the absence of RecB, as reported previously (22)(23)(24)(25).…”

Section: Recurrent Dsbs Near Terminal Hjssupporting

confidence: 81%

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Two mechanisms of chromosome fragility at replication-termination sites in bacteria

et al. 2021

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Chromosomal fragile sites are implicated in promoting genome instability, which drives cancers and neurological diseases. Yet, the causes and mechanisms of chromosome fragility remain speculative. Here, we identify three spontaneous fragile sites in the Escherichia coli genome and define their DNA damage and repair intermediates at high resolution. We find that all three sites, all in the region of replication termination, display recurrent four-way DNA or Holliday junctions (HJs) and recurrent DNA breaks. Homology-directed double-strand break repair generates the recurrent HJs at all of these sites; however, distinct mechanisms of DNA breakage are implicated: replication fork collapse at natural replication barriers and, unexpectedly, frequent shearing of unsegregated sister chromosomes at cell division. We propose that mechanisms such as both of these may occur ubiquitously, including in humans, and may constitute some of the earliest events that underlie somatic cell mosaicism, cancers, and other diseases of genome instability.

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“…3B). Their distribution "outward" from dif implies degradation by other nucleases in the absence of RecB, as reported previously (22)(23)(24)(25).…”

Section: Recurrent Dsbs Near Terminal Hjssupporting

confidence: 81%

“…3A) is most compatible with frequent formation of two-ended DSBs close to dif, followed by erosion of unrepaired DSB ends (Fig. 2K) (22)(23)(24)(25). However, we cannot rule out the possibility that equal numbers of one-ended DSBs occur on each side of dif in different cells in the population.…”

Section: Chromosome Segregation Failure and Fragilitymentioning

confidence: 89%

Two mechanisms of chromosome fragility at replication-termination sites in bacteria

et al. 2021

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“…However, examination of the effects of the elimination of exonuclease activities with different polarities suggests that 5′ ends also play a role in recombination and recombinational DNA repair (Razavy et al ., 1996). Rosenberg and Hastings (1991) have proposed a split‐end model for recombination (see also Razavy et al ., 1996) that might be applied to double‐strand break repair at a damaged fork. RecBCD requires nearly flush ends with <25 bp of ssDNA (Taylor and Smith, 1985).…”

Section: Discussionmentioning

confidence: 99%

The RecOR proteins modulate RecA protein function at 5' ends of single-stranded DNA

2001

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The Escherichia coli RecF, RecO and RecR pro teins have previously been implicated in bacterial recombinational DNA repair at DNA gaps. The RecOR-facilitated binding of RecA protein to single-stranded DNA (ssDNA) that is bound by single-stranded DNA-binding protein (SSB) is much faster if the ssDNA is linear, suggesting that a DNA end (rather than a gap) facilitates binding. In addition, the RecOR complex facilitates RecA protein-mediated D-loop formation at the 5' ends of linear ssDNAs. RecR protein remains associated with the RecA filament and its continued presence is required to prevent filament disassembly. RecF protein competes with RecO protein for RecR protein association and its addition destabilizes RecAOR filaments. An enhanced function of the RecO and RecR proteins can thus be seen in vitro at the 5' ends of linear ssDNA that is not as evident in DNA gaps. This function is countered by the RecF/RecO competition for association with the RecR protein.

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“…Plasmid vectors were described previously (Grueneberg et al, 1991). Strains are listed in Table 1 (Boiteux & Huisman, 1989;Palejwala et al, 1991;Joyce & Grindley, 1984;Czeczot et al, 1991;Howard-Flanders et al, 1966;Matijasevic et al, 1993;Cunningham et al, 1986;Lovett & Clark, 1984;Razaby et al, 1996;Joyce et al, 1985). Stains WM101 (AB1157 + uVrA::Tn10 alkA1 tag-1) and WM103 (AB1157 + uVrB::Tn10 alkA1 tag-1) were constructed by P1 transduction of the uVrA::Tn10 allele in BH200 and the uVrB5 allele in AB1885, which is closely linked to a Tn10 insertion, respectively, into strain MV1932 and selection on tetracycline.…”

Section: Methodsmentioning

confidence: 99%

Evidence for a Recombination-Independent Pathway for the Repair of DNA Interstrand Cross-Links Based on a Site-Specific Study with Nitrogen Mustard

1997

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DNA-DNA interstrand cross-links are thought to be important for the cytotoxicity of many chemotherapeutic agents. To study this more definitively, adduct site-specific methods are used to construct a plasmid with a single nitrogen mustard interstrand cross-link (inter-HN2-pTZSV28). Replication efficiency (RE = [colonies from (inter-HN2-pTZSV28)/(control with no cross-link)]) is approximately 0.3 following transformation into Escherichia coli, implying that the cross-link is repaired. The commonly accepted pathway for cross-link repair, which involves both nucleotide excision repair (NER) and recombination, is ruled out since RE is approximately 0.3 in a delta recA strain. Non-RecA-directed recombination such as copy-choice is also unlikely. However, NER is involved since RE was approximately 0.02 in strains deficient in NER. Base excision repair is not important since RE is approximately 0.3 in strains deficient in 3-methyladenine DNA glycosylases I and II, FAPY DNA glycosylase, both known apurinic/apyrimidinic endonucleases, or DNA deoxyribophosphodiesterase. Another hypothetical repair pathway hinging on a 5' --> 3' exonuclease activity is unlikely since RE is approximately 0.3 in cells deficient in either the 5' --> 3' exonuclease activities of DNA polymerase I, exonuclease VII, or RecJ. Thus, aside from NER, it is unclear what else participates in this recombination-independent repair pathway, although a pathway involing NER followed by replicative bypass of the lesion is the current working hypothesis. Psoralen interstrand cross-links appear not to be repairable by this second pathway, which may have implications for the relative cytotoxicity of interstrand cross-links from different agents.

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Evidence for Both 3’ and 5’ Single-Strand DNA Ends in Intermediates in Chi-Stimulated Recombination In Vivo

Cited by 65 publications

References 31 publications

Two mechanisms of chromosome fragility at replication-termination sites in bacteria

Two mechanisms of chromosome fragility at replication-termination sites in bacteria

The RecOR proteins modulate RecA protein function at 5' ends of single-stranded DNA

Evidence for a Recombination-Independent Pathway for the Repair of DNA Interstrand Cross-Links Based on a Site-Specific Study with Nitrogen Mustard

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