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布氏锥虫昆虫形态下VSG基因表达位点的控制

VSG gene expression site control in insect form Trypanosoma brucei.

作者信息

Rudenko G, Blundell P A, Taylor M C, Kieft R, Borst P

机构信息

The Netherlands Cancer Institute, Amsterdam.

出版信息

EMBO J. 1994 Nov 15;13(22):5470-82. doi: 10.1002/j.1460-2075.1994.tb06882.x.

DOI:10.1002/j.1460-2075.1994.tb06882.x
PMID:7957113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC395505/
Abstract

When the African trypanosome Trypanosoma brucei is taken up from mammals by a tse-tse fly, it replaces its variant surface glycoprotein (VSG) coat by a procyclin coat. Transcription of VSG genes stops in the fly, but transcription of sequences derived from the promoter area of the VSG expression site(s) remains high. Whether this is due to continuing high activity of one promoter or to low activity of many promoters was unclear. We have used the small differences between the sequences of different expression sites to show that multiple expression site promoters are active in insect form trypanosomes. This is confirmed by the low expression of single copy marker genes introduced into the transcribed area. However, if the expression site promoter is removed from the genomic location of the expression site and inserted in the non-transcribed spacer of the ribosomal DNA (rDNA), it is derepressed. Derepression of transcription can also be accomplished by replacing the promoter of an expression site by an rDNA promoter. We conclude that the down-regulation of VSG gene expression site promoters in insect form trypanosomes is affected by both the DNA sequence of the promoter and the genomic context in which it resides.

摘要

当非洲锥虫布氏锥虫被采采蝇从哺乳动物体内摄取后,它会用一种前环素外壳取代其可变表面糖蛋白(VSG)外壳。VSG基因的转录在采采蝇体内停止,但源自VSG表达位点启动子区域的序列转录仍保持高水平。这是由于一个启动子持续的高活性还是许多启动子的低活性尚不清楚。我们利用不同表达位点序列之间的微小差异表明,多个表达位点启动子在昆虫形态的锥虫中是活跃的。这通过导入转录区域的单拷贝标记基因的低表达得到证实。然而,如果将表达位点启动子从表达位点的基因组位置移除并插入核糖体DNA(rDNA)的非转录间隔区,它就会去抑制。转录的去抑制也可以通过用rDNA启动子取代表达位点的启动子来实现。我们得出结论,昆虫形态锥虫中VSG基因表达位点启动子的下调受启动子的DNA序列及其所在的基因组环境的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f9/395505/9ff46c5f0baa/emboj00070-0229-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f9/395505/9ff46c5f0baa/emboj00070-0229-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f9/395505/9ff46c5f0baa/emboj00070-0229-a.jpg

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Exposure of Trypanosoma brucei to an N-acetylglucosamine-binding lectin induces VSG switching and glycosylation defects resulting in reduced infectivity.布氏锥虫暴露于一种N-乙酰葡糖胺结合凝集素会诱导可变表面糖蛋白(VSG)转换和糖基化缺陷,从而导致感染力降低。
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