首页> 美国卫生研究院文献>Genetics >Prophage lambda 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 lambda 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杆菌中的末端重组。方向依赖性顺式作用支持末端的双极化。

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摘要

A prophage lambda 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 Deltadif, 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 lambda 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 lambda DNA.
机译:通过在dif(大肠杆菌的染色体二聚体解析位点)附近通过同源重组插入的前噬菌λ被切除,其频率取决于其相对于dif的取向。在野生型细胞中,末端超(TH)重组是原噬菌体特异性的,并且不能通过涉及与用于原噬菌体插入的重复序列相同的重复之间的染色体区段缺失的测试来检测。但是,当Deltadif,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重组生成的病变接近dif。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,这种抑制作用可以解释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的两侧是适当定向的(极化的)DNA片段。我们的模型假设,以有害取向插入到dif附近的噬菌体会干扰整合位点一侧的染色体极化,因为lambda DNA(如染色体)被序列元件极化了。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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