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重组位点dif的活性限制在大肠杆菌染色体的一个小区域内。

Restriction of the activity of the recombination site dif to a small zone of the Escherichia coli chromosome.

作者信息

Cornet F, Louarn J, Patte J, Louarn J M

机构信息

Laboratoire de Microbiologie et de Génétique Moléculaire, Centre National de la Recherche Scientifique, 31062 Toulouse, Cedex, France.

出版信息

Genes Dev. 1996 May 1;10(9):1152-61. doi: 10.1101/gad.10.9.1152.

Abstract

The recombination site dif is the target on the Escherichia coli chromosome of the site-specific recombinases XerC and XerD. The dif/XerC-D system plays a role during the cell cycle, probably by favoring sister chromosome monomerization or separation. A phenomenon of regional control over dif activity, also analyzed in this issue, is demonstrated here by translocation of dif to a series of loci close to the normal locus. We found that the site is physiologically active only within a narrow zone around its natural position. Competence for dif activity does not depend on the sequence of the normal dif activity zone (DAZ), because delta(dif) deletions larger than the DAZ result in Dif+ bacteria when dif is reinserted at the junction point. Although dif maps where replication normally terminates, termination of replication is not the elicitor. A strain with a large inversion that places dif and its surrounding region close to oriC remains Dif+, even when a Tus- mutation allows replication to terminate far away from it. Preliminary data suggest the possibility that specialized sequences separate the competent zone from the rest of the chromosome. We suspect that these sequences are members of a set of sequences involved in a polarized process of postreplicative reconstruction of the nucleoid structure. We propose that this reconstruction forces catenation links between sister chromosomes to accumulate within the DAZ, where they eventually favor recombination at dif.

摘要

重组位点dif是位点特异性重组酶XerC和XerD在大肠杆菌染色体上的作用靶点。dif/XerC-D系统在细胞周期中发挥作用,可能是通过促进姐妹染色体单体化或分离来实现的。本文还分析了对dif活性的区域控制现象,通过将dif易位到一系列靠近正常位点的基因座上得以证明。我们发现该位点仅在其天然位置周围的狭窄区域内具有生理活性。dif活性的能力并不取决于正常dif活性区(DAZ)的序列,因为当dif在连接点重新插入时,大于DAZ的δ(dif)缺失会产生Dif+细菌。尽管dif定位在复制通常终止的位置,但复制终止并非引发因素。一个具有大的倒位从而使dif及其周围区域靠近oriC的菌株仍然是Dif+,即使Tus-突变允许复制在远离它的位置终止。初步数据表明,可能存在专门的序列将活性区与染色体的其余部分分隔开。我们怀疑这些序列是参与类核结构复制后极化重建过程的一组序列的成员。我们提出,这种重建促使姐妹染色体之间的连环连接在DAZ内积累,最终在那里促进dif处的重组。

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