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一个大型反转录转座子家族的成员是利什曼原虫转录后基因表达的决定因素。

Members of a large retroposon family are determinants of post-transcriptional gene expression in Leishmania.

作者信息

Bringaud Frédéric, Müller Michaela, Cerqueira Gustavo Coutinho, Smith Martin, Rochette Annie, El-Sayed Najib M A, Papadopoulou Barbara, Ghedin Elodie

机构信息

Laboratoire de Génomique Fonctionnelle des Trypanosomatides, Université Victor Segalen Bordeaux 2, Bordeaux, France.

出版信息

PLoS Pathog. 2007 Sep 7;3(9):1291-307. doi: 10.1371/journal.ppat.0030136.

DOI:10.1371/journal.ppat.0030136
PMID:17907803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2323293/
Abstract

Trypanosomatids are unicellular protists that include the human pathogens Leishmania spp. (leishmaniasis), Trypanosoma brucei (sleeping sickness), and Trypanosoma cruzi (Chagas disease). Analysis of their recently completed genomes confirmed the presence of non-long-terminal repeat retrotransposons, also called retroposons. Using the 79-bp signature sequence common to all trypanosomatid retroposons as bait, we identified in the Leishmania major genome two new large families of small elements--LmSIDER1 (785 copies) and LmSIDER2 (1,073 copies)--that fulfill all the characteristics of extinct trypanosomatid retroposons. LmSIDERs are approximately 70 times more abundant in L. major compared to T. brucei and are found almost exclusively within the 3'-untranslated regions (3'UTRs) of L. major mRNAs. We provide experimental evidence that LmSIDER2 act as mRNA instability elements and that LmSIDER2-containing mRNAs are generally expressed at lower levels compared to the non-LmSIDER2 mRNAs. The considerable expansion of LmSIDERs within 3'UTRs in an organism lacking transcriptional control and their role in regulating mRNA stability indicate that Leishmania have probably recycled these short retroposons to globally modulate the expression of a number of genes. To our knowledge, this is the first example in eukaryotes of the domestication and expansion of a family of mobile elements that have evolved to fulfill a critical cellular function.

摘要

锥虫是单细胞原生生物,包括人类病原体利什曼原虫属(引起利什曼病)、布氏锥虫(引起昏睡病)和克氏锥虫(引起恰加斯病)。对它们最近完成的基因组分析证实了非长末端重复逆转录转座子(也称为逆转座子)的存在。我们以所有锥虫逆转座子共有的79个碱基对的特征序列为诱饵,在硕大利什曼原虫基因组中鉴定出两个新的小元件大家族——LmSIDER1(785个拷贝)和LmSIDER2(1073个拷贝),它们具备已灭绝的锥虫逆转座子的所有特征。与布氏锥虫相比,LmSIDERs在硕大利什曼原虫中的丰度大约高70倍,并且几乎只存在于硕大利什曼原虫mRNA的3'非翻译区(3'UTR)。我们提供了实验证据,证明LmSIDER2作为mRNA不稳定元件,并且与不含LmSIDER2的mRNA相比,含有LmSIDER2的mRNA通常表达水平较低。在缺乏转录调控的生物体中,LmSIDERs在3'UTR内大量扩增及其在调节mRNA稳定性中的作用表明,利什曼原虫可能已重新利用这些短逆转座子来全局调节许多基因的表达。据我们所知,这是真核生物中一个移动元件家族被驯化并扩增以履行关键细胞功能的首个例子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/4a0f7133994b/ppat.0030136.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/bf5a2a38521a/ppat.0030136.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/7c35321e8a0a/ppat.0030136.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/615c3427d15c/ppat.0030136.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/ccd2b64793a7/ppat.0030136.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/9d92a89ad998/ppat.0030136.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/0b5a876bf008/ppat.0030136.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/31c14c642876/ppat.0030136.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/695108bd94d6/ppat.0030136.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/6b228a6ca665/ppat.0030136.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/0ecc19ba0c5c/ppat.0030136.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/4a0f7133994b/ppat.0030136.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/bf5a2a38521a/ppat.0030136.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/7c35321e8a0a/ppat.0030136.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/615c3427d15c/ppat.0030136.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/ccd2b64793a7/ppat.0030136.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/9d92a89ad998/ppat.0030136.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/0b5a876bf008/ppat.0030136.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/31c14c642876/ppat.0030136.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/695108bd94d6/ppat.0030136.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/6b228a6ca665/ppat.0030136.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/0ecc19ba0c5c/ppat.0030136.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3430/2323293/4a0f7133994b/ppat.0030136.g011.jpg

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