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转座子Tn10的基因组织

Genetic organization of transposon Tn10.

作者信息

Foster T J, Davis M A, Roberts D E, Takeshita K, Kleckner N

出版信息

Cell. 1981 Jan;23(1):201-13. doi: 10.1016/0092-8674(81)90285-3.

DOI:10.1016/0092-8674(81)90285-3
PMID:6260375
Abstract

Transposon Tn10 is 9300 bp in length, with 1400 bp inverted repeats at its ends. The inverted repeats are structurally intact IS-like sequences (Ross et al., 1979). Analysis of deletion mutants and structural variants of Tn10, reported below, shows that the two IS10 segments contain all of the Tn10-encoded genetic determinants, both sites and functions, that are required for transposition. Furthermore, the two repeats (IS10-Right and IS10-Left) are not functionally equivalent: IS10-Right is fully functional and is capable by itself of promoting normal levels of Tn10 transposition; IS10-Left functions only poorly by itself, promoting transposition at a very low level when IS10-Right is inactivated. Complementation analysis shows that IS10-Right encodes at least one function, required for Tn10 transposition, which can act in trans and which works at the ends of the element. Also, all of the sites specifically required for normal Tn10 transposition have been localized to the outermost 70 bp at each end of the element; there is no evidence that specific sites internal to the element play an essential role. Finally, Tn10 modulates its own transposition in such a way that transposition-defective point mutants, unlike deletion mutants, are not complemented by functions provided in trans; and wild-type Tn10, unlike deletion mutants, is not affected by functions provided in trans from a "high hopper" Tn10 element.

摘要

转座子Tn10长度为9300碱基对,其末端有1400碱基对的反向重复序列。这些反向重复序列是结构完整的类插入序列(IS)(罗斯等人,1979年)。下面报道的对Tn10缺失突变体和结构变体的分析表明,两个IS10片段包含了转座所需的所有Tn10编码的遗传决定因素,包括位点和功能。此外,两个重复序列(IS10-右和IS10-左)在功能上并不等同:IS10-右功能完全正常,能够自身促进正常水平的Tn10转座;IS10-左自身功能很差,当IS10-右失活时,它只能促进极低水平的转座。互补分析表明,IS10-右编码至少一种Tn10转座所需的功能,该功能可以反式作用,并且在元件末端起作用。此外,正常Tn10转座所需的所有位点都已定位到元件两端最外侧的70碱基对;没有证据表明元件内部的特定位点起关键作用。最后,Tn10以这样一种方式调节自身的转座,即与缺失突变体不同,转座缺陷型点突变体不能被反式提供的功能互补;与缺失突变体不同,野生型Tn10不受来自“高跳跃者”Tn10元件的反式提供的功能的影响。

相似文献

1
Genetic organization of transposon Tn10.转座子Tn10的基因组织
Cell. 1981 Jan;23(1):201-13. doi: 10.1016/0092-8674(81)90285-3.
2
DNA sequence organization of IS10-right of Tn10 and comparison with IS10-left.Tn10右侧IS10的DNA序列组织及其与IS10左侧的比较。
Proc Natl Acad Sci U S A. 1982 Apr;79(8):2608-12. doi: 10.1073/pnas.79.8.2608.
3
Essential sites at transposon Tn 10 termini.转座子Tn10末端的必需位点。
Proc Natl Acad Sci U S A. 1984 Jun;81(11):3452-6. doi: 10.1073/pnas.81.11.3452.
4
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.
5
Negative and positive regulation of Tn10/IS10-promoted recombination by IHF: two distinguishable processes inhibit transposition off of multicopy plasmid replicons and activate chromosomal events that favor evolution of new transposons.整合宿主因子(IHF)对Tn10/IS10促进的重组的负调控和正调控:两个可区分的过程抑制多拷贝质粒复制子上的转座并激活有利于新转座子进化的染色体事件。
Genes Dev. 1995 May 1;9(9):1123-36. doi: 10.1101/gad.9.9.1123.
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/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。
EMBO J. 1996 Sep 16;15(18):5112-22.
8
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.
9
Analysis of the complete nucleotide sequence of the tetracycline-resistance transposon Tn10.四环素抗性转座子Tn10的完整核苷酸序列分析。
Plasmid. 2000 May;43(3):235-9. doi: 10.1006/plas.1999.1458.
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Genome rearrangements by residual IS10 elements in strains of Escherichia coli K-12 which had undergone Tn10 mutagenesis and fusaric acid selection.在经过Tn10诱变和镰孢菌酸筛选的大肠杆菌K-12菌株中,残留IS10元件引起的基因组重排。
Gene. 1993 Oct 29;133(1):17-22. doi: 10.1016/0378-1119(93)90219-s.

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