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端粒酶缺陷型布氏锥虫中活性VSG表达位点处端粒缩短的后果。

Consequences of telomere shortening at an active VSG expression site in telomerase-deficient Trypanosoma brucei.

作者信息

Dreesen Oliver, Cross George A M

机构信息

Laboratory of Molecular Parasitology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6307, USA.

出版信息

Eukaryot Cell. 2006 Dec;5(12):2114-9. doi: 10.1128/EC.00059-06. Epub 2006 Oct 27.

Abstract

Trypanosoma brucei evades the host immune response by sequential expression of a large family of variant surface glycoproteins (VSG) from one of approximately 20 subtelomeric expression sites (ES). VSG transcription is monoallelic, and little is known about the regulation of antigenic switching. To explore whether telomere length could affect antigenic switching, we created a telomerase-deficient cell line, in which telomeres shortened at a rate of 3 to 6 bp at each cell division. Upon reaching a critical length, short silent ES telomeres were stabilized by a telomerase-independent mechanism. The active ES telomere progressively shortened and frequently broke. Upon reaching a critical length, the short active ES telomere stabilized, but the transcribed VSG was gradually lost from the population and replaced by a new VSG through duplicative gene conversion. We propose a model in which subtelomeric-break-induced replication-mediated repair at a short ES telomere leads to duplicative gene conversion and expression of a new VSG.

摘要

布氏锥虫通过从大约20个亚端粒表达位点(ES)之一顺序表达一大类可变表面糖蛋白(VSG)来逃避宿主免疫反应。VSG转录是单等位基因的,关于抗原转换的调控知之甚少。为了探究端粒长度是否会影响抗原转换,我们创建了一个端粒酶缺陷细胞系,其中端粒在每次细胞分裂时以3至6个碱基对的速度缩短。达到临界长度后,短的沉默ES端粒通过一种不依赖端粒酶的机制得以稳定。活跃的ES端粒逐渐缩短并频繁断裂。达到临界长度后,短的活跃ES端粒稳定下来,但转录的VSG逐渐从群体中丢失,并通过重复基因转换被新的VSG取代。我们提出了一个模型,其中短ES端粒处的亚端粒断裂诱导复制介导的修复导致重复基因转换和新VSG的表达。

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