2003
DOI: 10.1046/j.1365-2958.2003.03574.x
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Species specificity in the activation of Xer recombination at dif by FtsK

Abstract: SummaryIn Escherichia coli , chromosome dimers are resolved to monomers by the addition of a single cross-over at a specific locus on the chromosome, dif . Recombination is performed by two tyrosine recombinases, XerC and XerD, and requires the action of an additional protein, FtsK. We show that Haemophilus influenzae FtsK activates recombination by H. influenzae XerCD at H. influenzae dif . However, it cannot activate recombination by E. coli XerCD. Reciprocally, E. coli FtsK cannot activate recombination by … Show more

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Cited by 52 publications
(71 citation statements)
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References 39 publications
(53 reference statements)
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“…4). E. coli FtsK can activate XerCD Ng /dif Ng recombination, although inefficiently, suggesting that activation is partly species-specific, as previously reported for E. coli and Haemophilus influenzae (26). The dif GGI site differs from dif Ng at four positions all included in the XerD-binding site (Fig.…”
Section: Discussionsupporting
confidence: 70%
“…4). E. coli FtsK can activate XerCD Ng /dif Ng recombination, although inefficiently, suggesting that activation is partly species-specific, as previously reported for E. coli and Haemophilus influenzae (26). The dif GGI site differs from dif Ng at four positions all included in the XerD-binding site (Fig.…”
Section: Discussionsupporting
confidence: 70%
“…This is composed of two paralogous tyrosine recombinases (integrases), XerC and XerD, which cooperatively catalyze strand exchanges at a 28-bp DNA sequence, the dif site, which must be located at the junction of the two replichores to be functional [3,68]. Xer recombination is intimately coupled to cell division [9] through the septal protein FtsK [1012], a DNA translocase [8] with an essential N-terminal transmembrane domain involved in its localization at the septum [13], and a C-terminal DNA motor domain involved in positioning and synapsing the two dif sites of the chromosome dimer at the division septum [12,1419] as well as in activating the strand exchange [8] by direct interaction with XerD [20,21]. …”
Section: Introductionmentioning
confidence: 99%
“…influenzae obeys the E. coli paradigm [21], whereas in B. subtilis, the model bacteria for firmicutes (formerly known as low GC-content Gram-positive bacteria), neither of the two FtsK analogs (SpoIIIE and YtpT) appears able to drive Xer recombination [26]. Several attempts have been made to identify the Xer recombination machinery in Streptococci, a taxonomic group belonging to firmicutes and comprising major pathogens [29] as well as innocuous food-grade species of major industrial importance [30,31].…”
Section: Introductionmentioning
confidence: 99%
“…This step strictly requires FtsKγ [Yates et al, 2003. Consistently, FtsKγ can activate recombination in the absence of FtsKαβ [Grainge et al, 2011;Nolivos et al, 2010].…”
Section: Activating Xer Recombinationmentioning
confidence: 62%
“…It can be further subdivided into α-, β-and γ-subdomains ( fig. 1 ) [Yates et al, 2003]. The α-and β-subdomains form the DNA pump [Massey et al, 2006], while the γ-subdomain acts as a control module .…”
mentioning
confidence: 99%