Developmentally regulated instability of the GPI-PLC mRNA is dependent on a short-lived protein factor.
Nucleic acids research
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Webb, H., Burns, R., Ellis, L., Kimblin, N., & Carrington, M. (2005). Developmentally regulated instability of the GPI-PLC mRNA is dependent on a short-lived protein factor.. Nucleic acids research, 33 (5), 1503-1512. https://doi.org/10.1093/nar/gki298
The expression of the vast majority of protein coding genes in trypanosomes is regulated exclusively at the post-transcriptional level. Developmentally regulated mRNAs that vary in levels of expression have provided an insight into one mechanism of regulation; a decrease in abundance is due to a shortened mRNA half-life. The decrease in half-life involves cis-acting elements in the 3' untranslated region of the mRNA. The trans-acting factors necessary for the increased rate of degradation remain uncharacterized. The GPI-PLC gene in Trypanosoma brucei encodes a phospholipase C expressed in mammalian bloodstream form, but not in the insect procyclic form. Here, it is reported that the differential expression of the GPI-PLC mRNA also results from a 10-fold difference in half-life. Second, the instability of the GPI-PLC mRNA in procyclic forms can be reversed by the inhibition of protein synthesis. Third, specifically blocking the translation of the GPI-PLC mRNA in procyclic forms by the inclusion of a hairpin in the 5' untranslated region does not result in stabilization of the mRNA. Thus, the effect of protein synthesis inhibitors in stabilizing the GPI-PLC mRNA operates in trans through a short-lived factor dependent on protein synthesis.
Animals, Trypanosoma brucei brucei, Phosphatidylinositol Diacylglycerol-Lyase, Protozoan Proteins, RNA, Messenger, RNA, Protozoan, Protein Synthesis Inhibitors, Gene Expression Regulation, Developmental, RNA Stability, Half-Life, Glycosylphosphatidylinositol Diacylglycerol-Lyase
Wellcome Trust (076935/Z/05/Z)
External DOI: https://doi.org/10.1093/nar/gki298
This record's URL: https://www.repository.cam.ac.uk/handle/1810/276243
Attribution 4.0 International
Licence URL: http://creativecommons.org/licenses/by/4.0/
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