FtsK-dependent and -independent pathways of Xer site-specific recombination

Recchia, Gavin D.; Aroyo, Mira; Wolf, Daniel; Blakely, Garry W.; Sherratt, David J.

doi:10.1093/emboj/18.20.5724

Cited by 102 publications

(107 citation statements)

References 51 publications

(93 reference statements)

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“…In the ⌬rtp ⌬spoIIIE mutant, RipX would, therefore, be less effective at dimer resolution. The carboxyl-terminal domain of E. coli FtsK is homologous to SpoIIIE (30) and is required for efficient chromosome dimer resolution via dif recombination (26)(27)(28)(29). Like SpoIIIE, FtsK localizes to the division septum (64).…”

Section: The Absence Of Rtp Probably Results In An Increase In Chromomentioning

confidence: 99%

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

Lemon

Kurtser²,

Grossman³

2000

Proceedings of the National Academy of Sciences

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Many circular genomes have replication termination systems, yet disruption of these systems does not cause an obvious defect in growth or viability. We have found that the replication termination system of Bacillus subtilis contributes to accurate chromosome partitioning. Partitioning of the terminus region requires that chromosome dimers, that have formed as a result of RecA-mediated homologous recombination, be resolved to monomers by the site-specific recombinase encoded by ripX. In addition, the chromosome must be cleared from the region of formation of the division septum. This process is facilitated by the spoIIIE gene product which is required for movement of a chromosome out of the way of the division septum during sporulation. We found that deletion of rtp, which encodes the replication termination protein, in combination with mutations in ripX or spoIIIE, led to an increase in production of anucleate cells. This increase in production of anucleate cells depended on recA, indicating that there is probably an increase in chromosome dimer formation in the absence of the replication termination system. Our results also indicate that SpoIIIE probably enhances the function of the RipX recombinase system. We also determined the subcellular location of the replication termination protein and found that it is a good marker for the position of the chromosome terminus.

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Section: The Absence Of Rtp Probably Results In An Increase In Chromomentioning

confidence: 99%

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

Lemon

Kurtser²,

Grossman³

2000

Proceedings of the National Academy of Sciences

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“…In E. coli, this 600-aa region is abundant in proline and glutamine residues. Cells lacking FtsK C form filaments and chains with mispositioned nucleoids (35,43,44) and are defective in Xer recombination at chromosomal and plasmid dif (34,35,37), but not at cer and psi sites (35). Most of the chromosome segregation defect is suppressed in a recA background (35), consistent with a major part of the chromosome segregation function of FtsK C being in its role in promoting Xer recombination at dif.…”

Section: I) Xerc Initiates Catalysis (Ii) To Form a Hj Intermediatementioning

confidence: 98%

“…There is normally a barrier to this conformational change, and XerC frequently catalyzes the conversion of the HJ back to substrate (ii). In recombination at psi, the proteins PepA and ArgA-P facilitate the HJ conformational change, whereas in recombination at dif, FtsK c is thought to facilitate this change (34,35) (40)(41)(42). The 500-aa C-terminal domain, FtsK C , is implicated in chromosome segregation (43,44) and is homologous to the C-terminal domain of the Bacillus subtilis SpoIIIE protein that functions in DNA transfer from the mother cell to the prespore (45).…”

Section: I) Xerc Initiates Catalysis (Ii) To Form a Hj Intermediatementioning

confidence: 99%

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Circles: The replication-recombination-chromosome segregation connection

Barre

Søballe²,

Michel³

et al. 2001

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

109

114

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Crossing over by homologous recombination between monomeric circular chromosomes generates dimeric circular chromosomes that cannot be segregated to daughter cells during cell division. In Escherichia coli, homologous recombination is biased so that most homologous recombination events generate noncrossover monomeric circular chromosomes. This bias is lost in ruv mutants. A novel protein, RarA, which is highly conserved in eubacteria and eukaryotes and is related to the RuvB and the DnaX proteins, ␥ and , may influence the formation of crossover recombinants. Those dimeric chromosomes that do form are converted to monomers by Xer site-specific recombination at the recombination site dif, located in the replication terminus region of the E. coli chromosome. The septum-located FtsK protein, which coordinates cell division with chromosome segregation, is required for a complete Xer recombination reaction at dif. Only correctly positioned dif sites present in a chromosomal dimer are able to access septum-located FtsK. FtsK acts by facilitating a conformational change in the Xer recombination Holliday junction intermediate formed by XerC recombinase. This change provides a substrate for XerD, which then completes the recombination reaction.homologous recombination ͉ Ruv͞Xer recombination ͉ dimer resolution ͉ FtsK B arbara McClintock, during her work on ring chromosomes in maize, inferred in 1932 that whereas crossing over between rod-shaped (linear) chromosomes does not alter their topology, crossing over between ring (circular) chromosomes generates larger ring chromosomes (circular dimers) that cannot be segregated normally at cell division (1). This topological complication arising from crossing over between circular chromosomes was largely ignored until the 1980s, when it was demonstrated that site-specific recombination systems act to convert dimeric plasmid molecules, formed by homologous recombination, to monomers, and thereby facilitate stable plasmid inheritance (2, 3). Subsequently, it was shown that one of these site-specific recombination systems, XerCD site-specific recombination, also functions in the conversion of dimeric Escherichia coli chromosomes to monomers (4-6). Xer recombination uses two related recombinases, XerC and XerD, belonging to the tyrosine recombinase family, each recombinase catalyzing the exchange of one pair of strands in a reaction that proceeds through a Holliday junction (HJ) intermediate (7)(8)(9). XerCD act at the recombination site dif, located in the replication terminus region of the E. coli chromosome and at related sites in multicopy plasmids, for example, psi in plasmid pSC101 and cer in ColE1 (3, 10).Here we outline the processes that limit dimer formation by homologous crossing over in E. coli. We also discuss the mechanism that restricts Xer recombination at chromosomal dif to converting dimers to monomers by making a part of the recombination machine only accessible to dif sites when they are present in chromosomal dimers at the time of cell division.Homologous recom...

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“…No such directionality-determining proteins are known for the chromosomal dimer resolution, suggesting that the chromosomal system is guided by a different kind of signal. Sherratt and others now report that FtsK protein, which is a part of the cell constriction machinery, is required for the XerD-catalyzed reaction (69,70). Yet, FtsK is likely to be a trigger of the final resolution rather than a signal determining the direction of the resolution.…”

Section: Homologous Recombination In Phage T4mentioning

confidence: 99%

DNA replication meets genetic exchange: Chromosomal damage and its repair by homologous recombination

Kuzminov

2001

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

198

126

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Proceedings of the National Academy of Sciences Colloquium on the roles of homologous recombination in DNA replication are summarized. Current findings in experimental systems ranging from bacteriophages to mammalian cell lines substantiate the idea that homologous recombination is a system supporting DNA replication when either the template DNA is damaged or the replication machinery malfunctions. There are several lines of supporting evidence: (i) DNA replication aggravates preexisting DNA damage, which then blocks subsequent replication; (ii) replication forks abandoned by malfunctioning replisomes become prone to breakage; (iii) mutants with malfunctioning replisomes or with elevated levels of DNA damage depend on homologous recombination; and (iv) homologous recombination primes DNA replication in vivo and can restore replication fork structures in vitro. The mechanisms of recombinational repair in bacteriophage T4, Escherichia coli, and Saccharomyces cerevisiae are compared. In vitro properties of the eukaryotic recombinases suggest a bigger role for single-strand annealing in the eukaryotic recombinational repair.

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FtsK-dependent and -independent pathways of Xer site-specific recombination

Cited by 102 publications

References 51 publications

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

Circles: The replication-recombination-chromosome segregation connection

DNA replication meets genetic exchange: Chromosomal damage and its repair by homologous recombination

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