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通过γδ末端的突变使转座免疫与γδ转座解偶联。

Uncoupling of transpositional immunity from gamma delta transposition by a mutation at the end of gamma delta.

作者信息

Wiater L A, Grindley N D

机构信息

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06510.

出版信息

J Bacteriol. 1990 Sep;172(9):4959-63. doi: 10.1128/jb.172.9.4959-4963.1990.

Abstract

The transposon gamma delta, in common with other members of the Tn3 family, confers transpositional immunity, a phenomenon by which plasmids containing a single transposon end show reduced activity as targets for further insertion by the same element. We found that a copy of a mutant delta end, in which the two terminal base pairs (5' GG) were substituted with cytosines, conferred the same degree of immunity as the unaltered delta end. However, a transposon analog with the mutant delta end as its termini could not transpose. These results suggest that the binding of transposase to a site on a target replicon is sufficient to confer immunity and that immunity does not involve subsequent DNA transactions at the bound target site, analogous to the catalytic processes that occur at the transposon ends during transposition.

摘要

转座子γδ与Tn3家族的其他成员一样,具有转座免疫性,即含有单个转座子末端的质粒作为同一元件进一步插入的靶标时,其活性会降低。我们发现,一个突变δ末端的拷贝(其中两个末端碱基对(5' GG)被胞嘧啶取代)赋予了与未改变的δ末端相同程度的免疫性。然而,以突变δ末端为末端的转座子类似物不能转座。这些结果表明,转座酶与靶复制子上的位点结合足以赋予免疫性,并且免疫不涉及在结合的靶位点上随后的DNA交易,这类似于转座过程中转座子末端发生的催化过程。

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本文引用的文献

1
Control of Tn7 transposition.Tn7转座的控制
Mol Gen Genet. 1984;194(1-2):149-58. doi: 10.1007/BF00383510.
10
Bacteriophage Mu sites required for transposition immunity.转座免疫所需的噬菌体Mu位点。
Proc Natl Acad Sci U S A. 1988 Sep;85(18):6826-30. doi: 10.1073/pnas.85.18.6826.

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