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IS10 promotes adjacent deletions at low frequency.IS10在低频情况下促进相邻缺失。
Genetics. 1991 May;128(1):37-43. doi: 10.1093/genetics/128.1.37.
2
Intermolecular transposition of IS10 causes coupled homologous recombination at the transposition site.IS10的分子间转座导致转座位点处的耦合同源重组。
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3
A comparison of intramolecular rearrangements promoted by transposons Tn5 and Tn10.转座子Tn5和Tn10促进的分子内重排的比较。
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4
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5
Replicative and conservative transpositional recombination of insertion sequences.插入序列的复制性和保守性转座重组
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6
IS10/Tn10 transposition efficiently accommodates diverse transposon end configurations.IS10/Tn10转座能有效地适应多种转座子末端构型。
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7
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Transposon Tn10: genetic organization, regulation, and insertion specificity.转座子Tn10:遗传组织、调控及插入特异性
Fed Proc. 1982 Aug;41(10):2649-52.

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9
Intermolecular transposition of IS10 causes coupled homologous recombination at the transposition site.IS10的分子间转座导致转座位点处的耦合同源重组。
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10
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本文引用的文献

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Multiple IS10 rearrangements in Escherichia coli.大肠杆菌中多个IS10重排
J Mol Biol. 1984 Mar 15;173(4):437-61. doi: 10.1016/0022-2836(84)90390-5.
2
Translational control of IS10 transposition.IS10转座的翻译调控
Cell. 1983 Sep;34(2):683-91. doi: 10.1016/0092-8674(83)90401-4.
3
Three promoters near the termini of IS10: pIN, pOUT, and pIII.IS10末端附近的三个启动子:pIN、pOUT和pIII。
Cell. 1983 Sep;34(2):673-82. doi: 10.1016/0092-8674(83)90400-2.
4
New Tn10 derivatives for transposon mutagenesis and for construction of lacZ operon fusions by transposition.用于转座子诱变及通过转座构建lacZ操纵子融合体的新型Tn10衍生物。
Gene. 1984 Dec;32(3):369-79. doi: 10.1016/0378-1119(84)90012-x.
5
The galactose operon of E. coli K-12. I. Structural and pleiotropic mutations of the operon.大肠杆菌K-12的半乳糖操纵子。I. 操纵子的结构和多效性突变
Genetics. 1969 Jun;62(2):231-47. doi: 10.1093/genetics/62.2.231.
6
Physical analysis of Tn10- and IS10-promoted transpositions and rearrangements.Tn10和IS10介导的转座及重排的物理分析
Genetics. 1987 Jul;116(3):359-69. doi: 10.1093/genetics/116.3.359.
7
IS10 transposition is regulated by DNA adenine methylation.IS10转座受DNA腺嘌呤甲基化调控。
Cell. 1985 Nov;43(1):117-30. doi: 10.1016/0092-8674(85)90017-0.
8
Cointegrate formation by IS50 requires multiple donor molecules.IS50形成共整合体需要多个供体分子。
Mol Gen Genet. 1988 Feb;211(2):244-51. doi: 10.1007/BF00330600.
9
Insertion sequence IS10 anti-sense pairing initiates by an interaction between the 5' end of the target RNA and a loop in the anti-sense RNA.插入序列IS10反义配对通过靶标RNA的5'端与反义RNA中的一个环之间的相互作用启动。
J Mol Biol. 1989 Dec 5;210(3):561-72. doi: 10.1016/0022-2836(89)90132-0.
10
Dissection of the transposition process: a transposon-encoded site-specific recombination system.
Mol Gen Genet. 1979 Oct 1;175(3):267-74. doi: 10.1007/BF00397226.

IS10在低频情况下促进相邻缺失。

IS10 promotes adjacent deletions at low frequency.

作者信息

Roberts D E, Ascherman D, Kleckner N

机构信息

Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.

出版信息

Genetics. 1991 May;128(1):37-43. doi: 10.1093/genetics/128.1.37.

DOI:10.1093/genetics/128.1.37
PMID:1648003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1204451/
Abstract

Some transposable elements move by a replicative mechanism involving cointegrate formation. Intramolecular cointegration can generate a product called an "adjacent deletion" in which a contiguous chromosomal segment adjacent to the transposon is deleted while the element responsible remains intact. Insertion sequence IS10 is thought to transpose by a nonreplicative mechanism. In the simplest models, nonreplicative transposition cannot give rise to an adjacent deletion because an intrinsic feature of such transposition is excision of the IS element from the donor location. We report here that IS10 can generate adjacent deletions, but at a frequency which is approximately 1/30th the frequency of transposition for the same element. We suggest that these deletions might arise either by nonreplicative transposition events that involve two IS10 elements located on sister chromosomes or by aberrant nonreplicative events involving cleavage and ligation at only one end of the element.

摘要

一些转座元件通过涉及共整合体形成的复制机制移动。分子内共整合可产生一种称为“相邻缺失”的产物,其中转座子相邻的连续染色体片段被删除,而负责的元件保持完整。插入序列IS10被认为通过非复制机制转座。在最简单的模型中,非复制转座不会导致相邻缺失,因为这种转座的一个内在特征是IS元件从供体位置切除。我们在此报告,IS10可产生相邻缺失,但其频率约为同一元件转座频率的1/30。我们认为这些缺失可能是由涉及位于姐妹染色体上的两个IS10元件的非复制转座事件引起的,或者是由仅涉及元件一端的切割和连接的异常非复制事件引起的。