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布氏锥虫抗原基因库通过不同DNA重组机制的修饰。

Modifications of a Trypanosoma b. brucei antigen gene repertoire by different DNA recombinational mechanisms.

作者信息

Pays E, Delauw M F, Van Assel S, Laurent M, Vervoort T, Van Meirvenne N, Steinert M

出版信息

Cell. 1983 Dec;35(3 Pt 2):721-31. doi: 10.1016/0092-8674(83)90105-8.

DOI:10.1016/0092-8674(83)90105-8
PMID:6197182
Abstract

In the Trypanosoma b. brucei AnTat 1.1C clone, the gene coding for the variant-specific surface antigen is telomeric and appears as a hybrid sequence, partially modified by gene conversion. This conversion is very similar to that observed in another AnTat 1.1-expressor clone (AnTat 1.1B). This sequence is not activated by duplicative transposition, although it could be activated by duplication in another clone (AnTat 1.10). Instead activation of the AnTat 1.1C gene seems operated by reciprocal recombination between its own telomere and the telomere carrying the previous (AnTat 1.16) ELC. Indeed, from the switch to AnTat 1.1C onward, the AnTat 1.16 ELC becomes a new silent member of its gene family, whereas in the variant directly derived from AnTat 1.1C (AnTat 1.3B), the AnTat 1.1C-containing telomere is lost, probably replaced by a large duplicate, at least 40 kb long, of the AnTat 1.3 gene-containing telomere. Different DNA rearrangement mechanisms used by the trypanosome to change its antigenic type thus contribute, by gain and loss of genes, to the evolution of the repertoire for surface antigens.

摘要

在布氏锥虫AnTat 1.1C克隆中,编码变异特异性表面抗原的基因位于端粒处,呈现为一种杂合序列,部分通过基因转换进行了修饰。这种转换与在另一个表达AnTat 1.1的克隆(AnTat 1.1B)中观察到的转换非常相似。该序列不是通过复制转座激活的,尽管它可能在另一个克隆(AnTat 1.10)中通过复制被激活。相反,AnTat 1.1C基因的激活似乎是通过其自身端粒与携带先前(AnTat 1.16)ELC的端粒之间的相互重组来实现的。事实上,从转换到AnTat 1.1C开始,AnTat 1.16 ELC成为其基因家族的一个新的沉默成员,而在直接从AnTat 1.1C衍生的变异体(AnTat 1.3B)中,含有AnTat 1.1C的端粒丢失了,可能被至少40 kb长的AnTat 1.3基因端粒的一个大重复片段所取代。锥虫用于改变其抗原类型的不同DNA重排机制因此通过基因的获得和丢失,对表面抗原库的进化做出了贡献。

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1
Modifications of a Trypanosoma b. brucei antigen gene repertoire by different DNA recombinational mechanisms.布氏锥虫抗原基因库通过不同DNA重组机制的修饰。
Cell. 1983 Dec;35(3 Pt 2):721-31. doi: 10.1016/0092-8674(83)90105-8.
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