Fate of DNA replication fork encountering a single DNA lesion during <i>oriC</i> plasmid DNA replication <i>in vitro</i>

Higuchi, Kiyoshi; Katayama, Tsutomu; Iwai, Shigenori; Hidaka, Masaaki; Horiuchi, Takashi; Maki, Hisaji

doi:10.1046/j.1365-2443.2003.00646.x

Cited by 137 publications

(147 citation statements)

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“…For this we designed a DNA molecule to mimic the stalled replication fork structure observed most prominently in the limited studies carried out to date in vitro on the structure of forks stalled at leading strand lesions (19,20). Our construct features a long (2035 nucleotide) ssDNA gap on the leading strand (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Situational Repair of Replication Forks

Robu

Inman

Cox

2004

Journal of Biological Chemistry

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Replication forks often stall or collapse when they encounter a DNA lesion. Fork regression is part of several major paths to the repair of stalled forks, allowing nonmutagenic bypass of the lesion. We have shown previously that Escherichia coli RecA protein can promote extensive regression of a forked DNA substrate that mimics a possible structure of a replication fork stalled at a leading strand lesion. Using electron microscopy and gel electrophoresis, we demonstrate that another protein, E. coli RecG helicase, promotes extensive fork regression in the same system. The RecG-catalyzed fork regression is very efficient and faster than the

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Section: Resultsmentioning

confidence: 99%

“…The major stalled fork structure identified in two recent studies is one in which the leading strand has halted DNA synthesis at the site of a lesion, and lagging strand synthesis has continued for some distance (1 kbp or more) beyond that point (19,20). The resulting fork structure has a long single strand gap on the leading strand (Fig.…”

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confidence: 99%

Situational Repair of Replication Forks

Robu

Inman

Cox

2004

Journal of Biological Chemistry

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“…Subsequent work confirmed that sister polymerases are physically attached to one another (1). This colocalization is accompanied by coordination; blocking leading-strand replication stops the whole replisome (3)(4)(5).…”

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confidence: 86%

“…1E Center). This process is similar to the uncoupling of the leading polymerase in response to blocked laggingstrand replication (4,5). In a third possibility, the independent replisome factory model, there is no coupling between replisomes despite colocalization, and the replisomes may move at different rates (Fig.…”

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confidence: 89%

Independence of replisomes in Escherichia coli chromosomal replication

Breier

Cozzarelli

2005

Proc. Natl. Acad. Sci. U.S.A.

103

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In Escherichia coli DNA replication is carried out by the coordinated action of the proteins within a replisome. After replication initiation, the two bidirectionally oriented replisomes from a single origin are colocalized into higher-order structures termed replication factories. The factory model postulated that the two replisomes are also functionally coupled. We tested this hypothesis by using DNA combing and whole-genome microarrays. Nascent DNA surrounding oriC in single, combed chromosomes showed instead that one replisome, usually the leftward one, was significantly ahead of the other 70% of the time. We next used microarrays to follow replication throughout the genome by measuring DNA copy number. We found in multiple E. coli strains that the replisomes are independent, with the leftward replisome ahead of the rightward one. The size of the bias was strain-specific, varying from 50 to 130 kb in the array results. When we artificially blocked one replisome, the other continued unabated, again demonstrating independence. We suggest an improved version of the factory model that retains the advantages of threading DNA through colocalized replisomes at about equal rates, but allows the cell flexibility to overcome obstacles encountered during elongation.DNA combing ͉ microarrays ͉ initiation ͉ replication origin ͉ factory model C ellular DNA replication is almost always initiated in a bidirectional manner. Therefore, initiation of replication requires the recruitment of four polymerases and assorted auxiliary proteins at a replication origin (1). Before 1983, the dominant model was that the leading and lagging polymerases continually and repeatedly sped past each other (Fig. 1A) because of the antiparallel nature of duplex DNA. It was difficult to see how the polymerases could be coordinated to achieve synthesis of both DNA strands at about the same time. Alberts et al. (2) suggested an elegant solution, the trombone model, in which one strand is looped so that the two polymerases are colocalized and point in the same direction (Fig. 1B), forming a replisome that additionally contains the auxiliary proteins. Subsequent work confirmed that sister polymerases are physically attached to one another (1). This colocalization is accompanied by coordination; blocking leading-strand replication stops the whole replisome (3-5).A colocalization of the replisomes themselves was proposed in the factory model of DNA replication (6) and demonstrated cytologically (7). Instead of the left and right replisomes racing away from each other until they meet at the terminus (Fig. 1C), this model proposed that the replisomes have stationary positions in the center of the cell (7). Much as in the trombone model, colocalization is facilitated through looping of the DNA, which is fed through the factory (Fig. 1D). This model organizes replication to the cell's advantage (8,9). Extruding the two daughter chromosomes in opposite directions should greatly facilitate chromosome partitioning (10-12). Furthermore, resources such as dNT...

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“…The observation that the priA mutant undergoes replication fork reversal led us to conclude that the types of replication inactivation that cause replication fork reversal, such as a (34) RecBC, RecA, and RuvABC Replication-dependent linear DNA Overreplication (Fig. 4) UV irradiation (38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53) RecFOR and RecA Replication-dependent linear DNA Several models *In replication mutants or strains with ectopic Ter sites, because replication blockage is the only damage, the recombination proteins essential for viability are presumably essential for restart. In UV-irradiated cells, several types of damage occur, and all recombination proteins are required for full viability.…”

Section: Spontaneous Replication Fork Arrest: the Pria Mutantmentioning

confidence: 99%

Multiple pathways process stalled replication forks

Michel

Grompone

Flores

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

309

330

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Impairment of replication fork progression is a serious threat to living organisms and a potential source of genome instability. Studies in prokaryotes have provided evidence that inactivated replication forks can restart by the reassembly of the replication machinery. Several strategies for the processing of inactivated replication forks before replisome reassembly have been described. Most of these require the action of recombination proteins, with different proteins being implicated, depending on the cause of fork arrest. The action of recombination proteins at blocked forks is not necessarily accompanied by a strand-exchange reaction and may prevent rather than repair fork breakage. These various restart pathways may reflect different structures at stalled forks. We review here the different strategies of fork processing elicited by different kinds of replication impairments in prokaryotes and the variety of roles played by recombination proteins in these processes.W ork from several laboratories has established that in bacteria, a recombination event can lead to the establishment of a unidirectional replication fork (reviewed in refs. 1-3). These observations extend the concept of a direct recombination-replication connection, originally proposed Ϸ30 years ago from studies of bacteriophage T4 and replication. Furthermore, the existence of recombination-dependent replication in yeast suggests that this connection may be a widely distributed phenomenon (4, 5).Considering the tight control of replication initiation at chromosomal origins, the assembly of a complete replisome at recombination intermediates, independently of time and place, is paradoxical. One of the raisons d'être of this potentially dangerous process was revealed by the finding that recombination intermediates form at inactivated replication forks and are used for replication restart. However, studies of the replicationrecombination connection in Escherichia coli have indicated that recombination proteins do not necessarily catalyze strand exchange at blocked forks and rather act in a variety of reactions that depend on the origin of the arrest. We review here the diversity of fates of inactivated replication forks in bacteria, as well as our present knowledge of the roles played by recombination proteins during replication restart. DNA Double-Strand End Repair in BacteriaAlmost 30 years ago, Higgins et al. (6) proposed that blocked replication forks could be isomerized into a four-way Holliday junction (HJ) with a DNA double-strand end, which could permit DNA repair and then continuation of replication (Fig. 1, step A). The test of the model, performed by treatment of mammalian cells with a DNA-damaging agent, was inconclusive (7). However, more recent studies in E. coli suggest that such replication fork reversal plays a crucial role in replication restart in bacteria (8,9).A key aspect of the replication fork reversal model is that it generates a DNA double-strand end at blocked forks without chromosome breakage. In E. coli, the enzyme th...

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Fate of DNA replication fork encountering a single DNA lesion during oriC plasmid DNA replication in vitro

Cited by 137 publications

References 50 publications

Situational Repair of Replication Forks

Situational Repair of Replication Forks

Independence of replisomes in Escherichia coli chromosomal replication

Multiple pathways process stalled replication forks

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