Temperature shift activates bloodstream VSG expression site promoters in Trypanosoma brucei
Autor: | Christian Tschudi, Trisha K. Ramsdell, Nikolay G. Kolev |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Transcription Genetic Trypanosoma brucei brucei Endogeny Trypanosoma brucei Article 03 medical and health sciences RNA Polymerase I Transcription (biology) parasitic diseases RNA polymerase I RNA Messenger Promoter Regions Genetic Molecular Biology chemistry.chemical_classification Messenger RNA Base Sequence Cell-Free System biology Temperature Promoter biology.organism_classification Cell biology 030104 developmental biology Gene Expression Regulation chemistry Parasitology Glycoprotein Variant Surface Glycoproteins Trypanosoma |
Zdroj: | Molecular and Biochemical Parasitology. 226:20-23 |
ISSN: | 0166-6851 |
DOI: | 10.1016/j.molbiopara.2018.10.003 |
Popis: | Trypanosoma 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 °C to 37 °C. Additionally, endogenous BESs respond similarly to the elevation of temperature and initiate increased production of BES pre-mRNA 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. |
Databáze: | OpenAIRE |
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