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C模块结合因子支持盘基网柄菌基因组中TRE5-A逆转座子的扩增。

The C-module-binding factor supports amplification of TRE5-A retrotransposons in the Dictyostelium discoideum genome.

作者信息

Bilzer Annika, Dölz Heike, Reinhardt Alexander, Schmith Anika, Siol Oliver, Winckler Thomas

机构信息

School of Biology and Pharmacy, Institute of Pharmacy, Department of Pharmaceutical Biology, University of Jena, Semmelweisstrasse 10, 07743 Jena, Germany.

出版信息

Eukaryot Cell. 2011 Jan;10(1):81-6. doi: 10.1128/EC.00205-10. Epub 2010 Nov 12.

Abstract

Retrotransposable elements are molecular parasites that have invaded the genomes of virtually all organisms. Although retrotransposons encode essential proteins to mediate their amplification, they also require assistance by host cell-encoded machineries that perform functions such as DNA transcription and repair. The retrotransposon TRE5-A of the social amoeba Dictyostelium discoideum generates a notable amount of both sense and antisense RNAs, which are generated from element-internal promoters, located in the A module and the C module, respectively. We observed that TRE5-A retrotransposons depend on the C-module-binding factor (CbfA) to maintain high steady-state levels of TRE5-A transcripts and that CbfA supports the retrotransposition activity of TRE5-A elements. The carboxy-terminal domain of CbfA was found to be required and sufficient to mediate the accumulation of TRE5-A transcripts, but it did not support productive retrotransposition of TRE5-A. This result suggests different roles for CbfA protein domains in the regulation of TRE5-A retrotransposition frequency in D. discoideum cells. Although CbfA binds to the C module in vitro, the factor regulates neither C-module nor A-module promoter activity in vivo. We speculate that CbfA supports the amplification of TRE5-A retrotransposons by suppressing the expression of an as yet unidentified component of the cellular posttranscriptional gene silencing machinery.

摘要

逆转座元件是侵入了几乎所有生物体基因组的分子寄生物。尽管逆转座子编码介导其扩增的必需蛋白质,但它们也需要宿主细胞编码的机制提供协助,这些机制执行诸如DNA转录和修复等功能。社会性变形虫盘基网柄菌的逆转座子TRE5-A产生了大量的正义和反义RNA,它们分别由位于A模块和C模块中的元件内部启动子产生。我们观察到,TRE5-A逆转座子依赖C模块结合因子(CbfA)来维持TRE5-A转录本的高稳态水平,并且CbfA支持TRE5-A元件的逆转座活性。发现CbfA的羧基末端结构域是介导TRE5-A转录本积累所必需且足够的,但它不支持TRE5-A的有效逆转座。这一结果表明CbfA蛋白结构域在盘基网柄菌细胞中TRE5-A逆转座频率的调控中具有不同作用。尽管CbfA在体外与C模块结合,但该因子在体内既不调节C模块也不调节A模块启动子的活性。我们推测,CbfA通过抑制细胞转录后基因沉默机制中一个尚未鉴定的组分的表达来支持TRE5-A逆转座子的扩增。

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