Chromosome Dimer Resolution

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General Description

. This figure is taken from Lesterlin et al. (2004)[1]


Uneven numbers of Sister Chromatid Exchanges (SCE), or homologous recombination events between replicating chromosomes lead to the conjoining of the 2 daughter chromosomes as a single circle. This "chromosome dimer" must be resolved so each daughter cell receives a complete copy of the genome.

  • Chromosome dimer resolution is abbreviated CDR.

In growing wild-type bacteria, chromosome dimers due to homologous recombination form in about 15% of the cells[2][3].

Components

The main recombinase consists of monomers of XerC and XerD[4][5]. FtsK is required to position dif and activate the strand exchange by XerD[6][7][8]. The binding of both XerC and XerD is highly cooperative[5].

Function

XerC binds the dif left half site and XerD binds the dif right half site[5]. Kennedy et al. (2008) contains a very good figure describing chromosome dimer formation and resolution[9]. The substrate for XerCD consists of a central core sequence of between 6-8 bases flanked by the binding sites for XerC and XerD[10].

Regulation

Site- specific recombination involving XerCD is restricted to the septal ring via an interaction with the C-terminal domain of FtsK. FtsK pumps the DNA towards the dif locus and will stop this translocation when it comes into contact with the XerCD recombinase-bound dif[11]. The interaction of FtsK's C-terminal domain is sufficient to activate the exchange of the second pair of DNA strands by XerD[8][12]. A model for the control of XerCD's catalytic activity on DNA is shown in Ferreira et al. (2003)[13].

Cell Biology

The dimers are resolved via the transient Holliday Junction by XerCD at the chromosomal dif site[8]. The morphological defects in cells lacking the C-terminal domain of FtsK are due to the failure to resolve chromosome dimers by Xer recombination[12].

Experimental Resources

  • Xer/site-specific recombination assays are described in Bigot et al. (2005)[14], Steiner et al. (1999)[7], and Massey et al. (2004)[15].
  • Functional replacement of dif with other core sequences leads to the uncoupling of recombination with Chromosome Dimer Resolution (CDR)[16].
  • A list of dif reporters may be found on the dif page in EcoliWiki.

Comparison with other organisms

Notes

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If the dif region has been removed (including dif and hipA), then dimers cannot be resolved and the regulation of septal ring constriction is lost. Cell division will continue over the nucleoid, guillotining the chromosome. Such an event causes DNA damage, induction of the SOS response, and ultimately the formation of a "twin filament," as described in Hendricks et al. (2000)[17].

Related GO Terms

References

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  1. ↑ Lesterlin, C et al. (2004) Genetic recombination and the cell cycle: what we have learned from chromosome dimers. Mol. Microbiol. 54 1151-60 PubMed
  2. ↑ Steiner, WW & Kuempel, PL (1998) Sister chromatid exchange frequencies in Escherichia coli analyzed by recombination at the dif resolvase site. J. Bacteriol. 180 6269-75 PubMed
  3. ↑ Steiner, WW & Kuempel, PL (1998) Cell division is required for resolution of dimer chromosomes at the dif locus of Escherichia coli. Mol. Microbiol. 27 257-68 PubMed
  4. ↑ Blakely, G et al. (1991) Escherichia coli XerC recombinase is required for chromosomal segregation at cell division. New Biol. 3 789-98 PubMed
  5. ↑ 5.0 5.1 5.2 Blakely, G et al. (1993) Two related recombinases are required for site-specific recombination at dif and cer in E. coli K12. Cell 75 351-61 PubMed
  6. ↑ Kuempel, PL et al. (1991) dif, a recA-independent recombination site in the terminus region of the chromosome of Escherichia coli. New Biol. 3 799-811 PubMed
  7. ↑ 7.0 7.1 Steiner, W et al. (1999) The cytoplasmic domain of FtsK protein is required for resolution of chromosome dimers. Mol. Microbiol. 31 579-83 PubMed
  8. ↑ 8.0 8.1 8.2 Barre, FX et al. (2000) FtsK functions in the processing of a Holliday junction intermediate during bacterial chromosome segregation. Genes Dev. 14 2976-88 PubMed
  9. ↑ Kennedy, SP et al. (2008) Delayed activation of Xer recombination at dif by FtsK during septum assembly in Escherichia coli. Mol. Microbiol. 68 1018-28 PubMed
  10. ↑ Sherratt, DJ et al. (1995) Site-specific recombination and circular chromosome segregation. Philos. Trans. R. Soc. Lond., B, Biol. Sci. 347 37-42 PubMed
  11. ↑ Graham, JE et al. (2010) FtsK translocation on DNA stops at XerCD-dif. Nucleic Acids Res. 38 72-81 PubMed
  12. ↑ 12.0 12.1 Recchia, GD et al. (1999) FtsK-dependent and -independent pathways of Xer site-specific recombination. EMBO J. 18 5724-34 PubMed
  13. ↑ Ferreira, H et al. (2003) Functional analysis of the C-terminal domains of the site-specific recombinases XerC and XerD. J. Mol. Biol. 330 15-27 PubMed
  14. ↑ Bigot, S et al. (2005) KOPS: DNA motifs that control E. coli chromosome segregation by orienting the FtsK translocase. EMBO J. 24 3770-80 PubMed
  15. ↑ Massey, TH et al. (2004) Asymmetric activation of Xer site-specific recombination by FtsK. EMBO Rep. 5 399-404 PubMed
  16. ↑ Capiaux, H et al. (2002) A dual role for the FtsK protein in Escherichia coli chromosome segregation. EMBO Rep. 3 532-6 PubMed
  17. ↑ Hendricks, EC et al. (2000) Cell division, guillotining of dimer chromosomes and SOS induction in resolution mutants (dif, xerC and xerD) of Escherichia coli. Mol. Microbiol. 36 973-81 PubMed
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