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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Prophage λ Induces Terminal Recombination in Escherichia coli by Inhibiting Chromosome Dimer Resolution: An Orientation-Dependent cis-Effect Lending Support to Bipolarization of the Terminus
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Prophage λ Induces Terminal Recombination in Escherichia coli by Inhibiting Chromosome Dimer Resolution: An Orientation-Dependent cis-Effect Lending Support to Bipolarization of the Terminus

机译:噬菌体λ通过抑制染色体二聚体分辨率诱导大肠埃希氏菌的重组:定向依赖顺式效应支持总双极化。

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A prophage λ inserted by homologous recombination near dif , the chromosome dimer resolution site of Escherichia coli , is excised at a frequency that depends on its orientation with respect to dif. In wild-type cells, terminal hyper-(TH) recombination is prophage specific and undetectable by a test involving deletion of chromosomal segments between repeats identical to those used for prophage insertion. TH recombination is, however, detected in both excision and deletion assays when Δ dif , xerC , or ftsK mutations inhibit dimer resolution: lack of specialized resolution apparently results in recombinogenic lesions near dif. We also observed that the presence near dif of the prophage, in the orientation causing TH recombination, inhibits dif resolution activity. By its recombinogenic effect, this inhibition explains the enhanced prophage excision in wild-type cells. The primary effect of the prophage is probably an alteration of the dimer resolution regional control, which requires that dif is flanked by suitably oriented (polarized) stretches of DNA. Our model postulates that the prophage inserted near dif in the deleterious orientation disturbs chromosome polarization on the side of the site where it is integrated, because λ DNA, like the chromosome, is polarized by sequence elements. Candidate sequences are oligomers that display skewed distributions on each oriC - dif chromosome arm and on λ DNA.
机译:通过在dif(大肠杆菌的染色体二聚体分辨位点)附近通过同源重组插入的噬菌体λ,以取决于其相对于dif取向的频率被切除。在野生型细胞中,末端超-(TH)重组是原噬菌体特异性的,并且不能通过涉及删除与原噬菌体插入相同的重复序列之间的染色体区段的测试来检测。但是,当Δdif,xerC或ftsK突变抑制二聚体分辨率时,在切除和缺失分析中均可检测到TH重组:缺乏专门的分辨率显然会导致在dif附近产生重组病变。我们还观察到,在引起TH重组的方向上,在噬菌体的dif附近存在抑制了dif分离活性。通过其重组作用,这种抑制作用解释了野生型细胞中原噬菌体切除的增强。噬菌体的主要作用可能是二聚体分辨率区域控制的改变,这要求dif的侧面是适当定向的(极化的)DNA片段。我们的模型假设,以有害方向靠近dif插入的噬菌体干扰了整合位点一侧的染色体极化,因为λDNA与染色体一样被序列元件极化。候选序列是在每个oriC-dif染色体臂和λDNA上显示偏态分布的寡聚体。

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