Louarn J, Cornet F, François V, Patte J, Louarn J M
Laboratoire de Microbiologie et de Génétique Moléculaires du Centre National de la Recherche Scientifique, Toulouse, France.
J Bacteriol. 1994 Dec;176(24):7524-31. doi: 10.1128/jb.176.24.7524-7531.1994.
The terminus region of the Escherichia coli chromosome is the scene of frequent homologous recombination. This can be demonstrated by formation of deletions between directly repeated sequences which flank a genetic marker whose loss can be easily detected. We report here that terminal recombination events are restricted to a relatively large terminal recombination zone (TRZ). On one side of the TRZ, the transition from the region with a high excision rate to the normal (low) excision rates of the rest of the chromosome occurs along a DNA stretch of less than 1 min. No specific border of this domain has been defined. To identify factors inducing terminal recombination, we examined its relation to two other phenomena affecting the same region, site-specific recombination at the dif locus and site-specific replication pausing. Both the location and the efficiency of terminal recombination remained unchanged after inactivation of the dif-specific recombination system. Similarly, inactivation of site-specific replication pausing or displacement of the replication fork trap so that termination occurs about 200 kb away from the normal region had no clear effect on this phenomenon. Therefore, terminal recombination is not a direct consequence of either dif-specific recombination or replication termination. Furthermore, deletions encompassing the wild-type TRZ do not eliminate hyperrecombination. Terminal recombination therefore cannot be attributed to the activity of some unique sequence of the region. A possible explanation of terminal hyperrecombination involves nucleoid organization and its remodeling after replication: we propose that post replicative reconstruction of the nucleoid organization results in a displacement of the catenation links between sister chromosomes to the last chromosomal domain to be rebuilt. Unrelated to replication termination, this process would facilitate interactions between the catenated molecules and would make the domain highly susceptible to recombination between sister chromosomes.
大肠杆菌染色体的末端区域是频繁发生同源重组的场所。这可以通过在直接重复序列之间形成缺失来证明,这些重复序列位于一个遗传标记的两侧,该标记的缺失很容易被检测到。我们在此报告,末端重组事件局限于一个相对较大的末端重组区(TRZ)。在TRZ的一侧,从高切除率区域到染色体其余部分正常(低)切除率区域的转变沿着不到1分钟的DNA片段发生。该区域没有明确的边界。为了确定诱导末端重组的因素,我们研究了它与影响同一区域的另外两种现象的关系,即dif位点的位点特异性重组和位点特异性复制暂停。dif特异性重组系统失活后,末端重组的位置和效率均保持不变。同样,位点特异性复制暂停失活或复制叉陷阱移位,使得终止发生在距正常区域约200 kb处,对这一现象也没有明显影响。因此,末端重组不是dif特异性重组或复制终止的直接结果。此外,包含野生型TRZ的缺失并不能消除高重组率。因此,末端重组不能归因于该区域某些独特序列的活性。对末端高重组率的一种可能解释涉及类核组织及其复制后的重塑:我们提出,类核组织的复制后重建导致姐妹染色单体之间的连环连接移位到最后一个要重建的染色体区域。与复制终止无关,这一过程将促进连环分子之间的相互作用,并使该区域极易发生姐妹染色单体之间的重组。