FtsK is an essential cell division protein that is localized to the septum and induced as part of the SOS response

Wang, Lilin; Lutkenhaus, Joe

doi:10.1046/j.1365-2958.1998.00958.x

Cited by 163 publications

(175 citation statements)

References 37 publications

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“…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). The amino terminal portion of FtsK is required for cell division (26,64).…”

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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“…Members of a family of proteins, represented by B. subtilis SpoIIIE and E. coli FtsK, localize to the leading edge of the septum and function as ATP-dependent DNA pumps (Wu and Errington 1994;Wu et al 1995;Wang and Lutkenhaus 1998;Bath et al 2000). The amino-terminal domains of SpoIIIE and FtsK are required for localization to the leading edge of the division septum (Wu and Errington 1997;Wang and Lutkenhaus 1998). The carboxy-terminal cytoplasmic domain of SpoIIIE tracks along DNA in an ATP-dependent manner in vitro (Bath et al 2000).…”

Section: Post-septation Partitioningmentioning

confidence: 99%

The extrusion-capture model for chromosome partitioning in bacteria

Lemon¹,

Grossman²

2001

Genes Dev.

142

124

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“…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%

“…Whether localization of FtsK to a new septum at midcell leads to changes in its activity remains to be determined. FtsK levels are at least partly under control of the SOS regulon, which is induced in response to cellular DNA damage (40); indeed, FtsK is the only known essential gene to be under SOS control. The reasons for this are unclear, because after SOS induction there may be no functional FtsZ septal rings to which even increased levels of FtsK can localize.…”

Section: Xer Recombination At Dif Is Restricted To Dimer Resolution Amentioning

confidence: 99%

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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FtsK is an essential cell division protein that is localized to the septum and induced as part of the SOS response

Cited by 163 publications

References 37 publications

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

Effects of replication termination mutants on chromosome partitioning in Bacillussubtilis

The extrusion-capture model for chromosome partitioning in bacteria

Circles: The replication-recombination-chromosome segregation connection

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