大约10%~15%的大肠杆菌在染色体复制过程中会形成染色体二聚体。大肠杆菌染色体编码的重组酶XerC和XerD作用于染色体复制终点区的dif序列, 以同源重组的方式将染色体二聚体解离为单体, 使细菌得以正常复制分裂。编码霍乱毒素的噬菌体CTXΦ以位点特异的方式整合入霍乱弧菌染色体, 但其基因组中不含有任何重组酶基因, 其整合过程需要细菌染色体编码的XerC和XerD重组酶, 且整合位点与大肠杆菌dif序列相似。XerCD重组酶基因和dif位点在细菌染色体广泛存在, 表明其可能是染色体二聚体解离, 噬菌体及其他外源基因成分整合入染色体过程中一种广泛存在的途径。文章对XerCD/dif位点特异性重组在细菌染色体二聚体解离、外源基因整合的研究进展进行综述。
In Escherichia coli, 10% to 15% of growing bacteria produce chromosome dimers during DNA replication. These dimers are resolved by XerC and XerD, two chromosome recombinases that target the dif sequence in the replication terminus of chromosome. Phage CTXΦ integrates into vibrio cholerae chromosome in a site-speci?c manner. However, CTXΦ genome does not encode any recombinase, while recombinase XerC and XerD, which is coded by vibrio cholerae chromosome are required for the integration of CTXΦ into the vibrio cholerae chromosome. The CTXΦ integration site overlaps with the dif site. The wide distribution of XerCD recombinase and dif site among bacteria genome suggests that it may be universal in resolve of chromosome dimers and phage integration. In this article, we reviewed the research progresses on chromosome dimer resolve and phage integration through XerCD/dif site-speci?c recombination.
[1] Higgins NP. Mutational bias suggests that replication ter-mination occurs near the dif site, not at Ter sites: what's the Dif? Mol Microbiol, 2007, 64(1): 1-4.
[2] Mulcair MD, Schaeffer PM, Oakley AJ, Cross HF, Neylon C, Hill TM, Dixon NE. A molecular mousetrap determines polarity of termination of DNA replication in E. coli. Cell, 2006, 125(7): 1309-1319.
[3] Kuempel PL, Henson JM, Dircks L, Tecklenburg M, Lim DF. dif, a recA-independent recombination site in the terminus region of the chromosome of Escherichia coli. New Biol, 1991, 3(8): 799-811.
[4] Lesterlin C, Barre FX, Cornet F. Genetic recombination and the cell cycle: what we have learned from chromosome dimers. Mol Microbiol, 2004, 54(5): 1151-1160.
[5] Kennedy SP, Chevalier F, Barre FX. Delayed activation of Xer recombination at dif by FtsK during septum assembly in Escherichia coli. Mol Microbiol, 2008, 68(4): 1018-1028.
[6] Blakely G, May G, McCulloch R, Arciszewska LK, Burke M, Lovett ST, Sherratt DJ. Two related recombinases are required for site-specific recombination at dif and cer in Escherichia coli K12. Cell, 1993, 75(2): 351-361.
[7] Recchia GD, Sherratt DJ. Conservation of xer site-specific recombination genes in bacteria. Mol Microbiol, 1999, 34(5): 1146-1148.
[8] Subramanya HS, Arciszewska LK, Baker RA, Bird LE, Sherratt DJ, Wigley DB. Crystal structure of the site-specific recombinase, XerD. EMBO J, 1997, 16(17): 5178-5187.
[9] Carnoy C, Roten CA. The dif/Xer recombination systems in proteobacteria. PLoS One, 2009, 4(9): e6531.
[10] Tecklenburg M, Naumer A, Nagappan O, Kuempel P. The dif resolvase locus of the Escherichia coli chromosome can be replaced by a 33-bp sequence, but function depends on location. Proc Natl Acad Sci USA, 1995, 92(5): 1352-1356.
[11] Bigot S, Sivanathan V, Possoz C, Barre FX, Cornet F. FtsK, a literate chromosome segregation machine. Mol Micro-biol, 2007, 64(6): 1434-1441.
[12] Kono N, Arakawa K, Tomita M. Comprehensive prediction of chromosome dimer resolution sites in bacterial genomes. BMC Genomics, 2011, 12(1): 19.
[13] Huber KE, Waldor MK. Filamentous phage integration requires the host recombinases XerC and XerD. Nature, 2002, 417(6889): 656-659.
[14] McLeod SM, Kimsey HH, Davis BM, Waldor MK. CTXphi and Vibrio cholerae: exploring a newly recognized type of phage-host cell relationship. Mol Microbiol, 2005, 57(2): 347-356.
[15] McLeod SM, Waldor MK. Characterization of XerC-and XerD-dependent CTX phage integration in Vibrio cholerae. Mol Microbiol, 2004, 54(4): 935-947.
[16] Val ME, Bouvier M, Campos J, Sherratt D, Cornet F, Mazel D, Barre FX. The single-stranded genome of phage CTX is the form used for integration into the genome of Vibrio cholerae. Mol Cell, 2005, 19(4): 559-566.
[17] Boyd EF. Efficiency and specificity of CTXΦ chromosomal integration: dif makes all the difference. Proc Natl Acad Sci USA, 2010, 107(9): 3951-3952.
[18] Das B, Bischerour J, Barre FX. VGJphi integration and excision mechanisms contribute to the genetic diversity of Vibrio cholerae epidemic strains. Proc Natl Acad Sci USA, 2011, 108(6): 2516-2521.
[19] Dominguez NM, Hackett KT, Dillard JP. XerCD-mediated site-specific recombination leads to loss of the 57-kilobase gonococcal genetic island. J Bacteriol, 2011, 193(2): 377-388.
[20] Summers DK, Sherratt DJ. Multimerization of high copy number plasmids causes instability: CoIE1 encodes a determinant essential for plasmid monomerization and sta-bility. Cell, 1984, 36(4): 1097-1103.
[21] Le Bourgeois P, Bugarel M, Campo N, Daveran-Mingot ML, Labonté J, Lanfranchi D, Lautier T, Pagès C, Ritzenthaler P. The unconve
