Temperature shift activates bloodstream VSG expression site promoters in Trypanosoma brucei

被引:4
作者
Kolev, Nikolay G. [1 ]
Ramsdell, Trisha K. [1 ]
Tschudi, Christian [1 ]
机构
[1] Yale Sch Publ Hlth, Dept Epidemiol Microbial Dis, Boyer Ctr Mol Med 135, 295 Congress Ave, New Haven, CT 06536 USA
基金
美国国家卫生研究院;
关键词
Trypanosoma brucei; Transcription; VSG; Expression site; Promoter; CLASS-I TRANSCRIPTION; RNA-POLYMERASE I; GENE-EXPRESSION; FORM; SEQUENCES;
D O I
10.1016/j.molbiopara.2018.10.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Trypanosome brucei relies on two types of variant surface glycoprotein (VSG) expression sites (ESs) for RNA polymerase I (Pol I) transcription of VSG pre-mRNA. Trypanosomes developing into infectious metacyclic cells in the tsetse vector use metacyclic VSG ESs (MESs) and proliferating parasites in the mammalian host deploy bloodstream VSG ESs (BESs). Unlike the monocistronic MESs, BESs are polycistronic and their highly conserved promoters differ considerably from the MES promoters. The significance of the divergent sequences of MES and BES promoters remains to be determined. We used a reporter system to specifically test the effect of temperature on the activity of MES and BES promoters in procyclic trypanosomes and our results demonstrate that transcription from the MES promoter is largely insensitive to changes in temperature. In contrast, the BES promoter drives rapid activation of transcription upon a change of temperature from 28 degrees C to 37 degrees C. Additionally, endogenous BESs respond similarly to the elevation of temperature and initiate increased production of BES premRNA and mRNA. Our results indicate that the sequence of the BES promoter is a specificity signal which triggers BES activation in vivo upon entry into the mammalian host.
引用
收藏
页码:20 / 23
页数:4
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