ArticlePLoS pathogens2017
Expression of the RNA-binding protein RBP10 promotes the bloodstream-form differentiation state in Trypanosoma brucei.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 99 citations in OpenAlex.
- Five-layer systems analysis ofeLife · 2026Article
- Regulation of Leishmania surface coat proteins by the nuclear protein ESB1.Journal of cell science · 2026Article
- Specialized RNA decay fine-tunes monogenic antigen expression in Trypanosoma brucei.Nature microbiology · 2026Article
- Reversal of ATP synthase is a key attribute accompanying cellular differentiation of Trypanosoma brucei insect forms.Communications biology · 2026Article
- TblncRNA-23, a long non-coding RNA transcribed by RNA polymerase I, regulates developmental changes in Trypanosoma brucei.Nature communications · 2025Article
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- Differential regulatory role of AU-rich and GU-rich elements inFrontiers in microbiology · 2025Article
- Mechanisms of life cycle simplification in African trypanosomes.Nature communications · 2024Article
- Post-transcriptional reprogramming by thousands of mRNA untranslated regions in trypanosomes.Nature communications · 2024Article
- Life stage-specific poly(A) site selection regulated byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Translational control byRNA (New York, N.Y.) · 2023Article
- The RNA-binding protein RBP42 regulates cellular energy metabolism in mammalian-infectivemSphere · 2023Article
- Evolutionary, structural and functional insights in nuclear organisation and nucleocytoplasmic transport in trypanosomes.FEBS letters · 2023Review
- Chemical Inhibition of Bromodomain Proteins in Insect-Stage African Trypanosomes Perturbs Silencing of the Variant Surface Glycoprotein Repertoire and Results in Widespread Changes in the Transcriptome.Microbiology spectrum · 2023Article
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- Article
- Synthesis and characterization of I-BET151 derivatives for use in identifying protein targets in the African trypanosome.Current research in chemical biology · 2023Article
- Clinically relevant benzoxaboroles inhibit mRNA processing in Trypanosoma brucei.BMC research notes · 2022Article
- Sending the message: specialized RNA export mechanisms in trypanosomes.Trends in parasitology · 2022Review
- Sequences and proteins that influence mRNA processing in Trypanosoma brucei: Evolutionary conservation of SR-domain and PTB protein functions.PLoS neglected tropical diseases · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In nearly all eukaryotes, cellular differentiation is governed by changes in transcription, and stabilized by chromatin and DNA modification. Gene expression control in the pathogen Trypanosoma brucei, in contrast, relies almost exclusively on post-transcriptional mechanisms, so RNA binding proteins must assume the burden that is usually borne by transcription factors. T. brucei multiply in the blood of mammals as bloodstream forms, and in the midgut of Tsetse flies as procyclic forms. We show here that a single RNA-binding protein, RBP10, promotes the bloodstream-form trypanosome differentiation state. Depletion of RBP10 from bloodstream-form trypanosomes gives cells that can grow only as procyclic forms; conversely, expression of RBP10 in procyclic forms converts them to bloodstream forms. RBP10 binds to procyclic-specific mRNAs containing an UAUUUUUU motif, targeting them for translation repression and destruction. Products of RBP10 target mRNAs include not only the major procyclic surface protein and enzymes of energy metabolism, but also protein kinases and stage-specific RNA-binding proteins: this suggests that alterations in RBP10 trigger a regulatory cascade.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.