ArticlePLoS genetics2016
Base J and H3.V Regulate Transcriptional Termination in Trypanosoma brucei.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Transcription Start Regions in PTU-intergenic regions drive cell cycle-dependent transcriptional activation events inMicrobiology spectrum · 2026Article
- Genome-wide mapping of replication stress response factors reveals the management of polycistronic transcription, replication initiation, and responses to replication stress in Leishmania.Nucleic acids research · 2026Article
- Trypanosomatid histones: the building blocks of the epigenetic code of highly divergent eukaryotes.The Biochemical journal · 2025Review
- Mono-allelic epigenetic regulation of polycistronic transcription initiation by RNA polymerase II inmBio · 2025Article
- Protein phosphatase PP1 regulation of RNA polymerase II transcription termination and allelic exclusion of VSG genes in trypanosomes.Nucleic acids research · 2024Article
- Two DOT1 enzymes cooperatively mediate efficient ubiquitin-independent histone H3 lysine 76 tri-methylation in kinetoplastids.Nature communications · 2024Article
- Leishmania PNUTS discriminates between PP1 catalytic subunits through an RVxF-ΦΦ-F motif and polymorphisms in the PP1 C-tail and catalytic domain.The Journal of biological chemistry · 2023Article
- Histone divergence in trypanosomes results in unique alterations to nucleosome structure.Nucleic acids research · 2023Article
- Decoding the impact of nuclear organization on antigenic variation in parasites.Nature microbiology · 2023Review
- Identification of a small-molecule inhibitor that selectively blocks DNA-binding by Trypanosoma brucei replication protein A1.Nature communications · 2023Article
- Knockout of protein phosphatase 1 in Leishmania major reveals its role during RNA polymerase II transcription termination.Nucleic acids research · 2023Article
- How much (ATP) does it cost to build a trypanosome? A theoretical study on the quantity of ATP needed to maintain and duplicate a bloodstream-form Trypanosoma brucei cell.PLoS pathogens · 2023Article
- Behind Base J: The Roles of JBP1 and JBP2 on Trypanosomatids.Pathogens (Basel, Switzerland) · 2023Review
- The RNA-binding protein RBP33 dampens non-productive transcription in trypanosomes.Nucleic acids research · 2022Article
- The SPARC complex defines RNAPII promoters ineLife · 2022Article
- Trypanosoma brucei histones are heavily modified with combinatorial post-translational modifications and mark Pol II transcription start regions with hyperacetylated H2A.Nucleic acids research · 2022Article
- Localization of Epigenetic Markers inPathogens (Basel, Switzerland) · 2022Article
- A systematic analysis ofGenome research · 2021Article
- A nuclear enterprise: zooming in on nuclear organization and gene expression control in the African trypanosome.Parasitology · 2021Review
- Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Trypanosoma brucei is a protozoan parasite that lacks many transcription factors found in other eukaryotes, such as those whose binding demarcates enhancers. T. brucei retains histone variants and modifications, however, and it is hypothesized that it relies on epigenetic marks to define transcription-related boundaries. The histone H3 variant (H3.V) and an alternate nucleotide, base J (ß-D-glucosyl-hydroxymethyluracil), are two chromatin marks found at both transcription termination sites (TTSs) and telomeres. Here, we report that the absence of both base J and H3.V result in transcription readthrough and the appearance of antisense transcripts near TTSs. Additionally, we find that maintaining the transcriptional silencing of pol I-transcribed telomeric Variant Surface Glycoprotein (VSG) genes appears to be dependent on deposition of H3.V alone. Our study reveals that gene expression depends on different epigenetic cues depending on chromosomal location and on the transcribing polymerase. This work provides insight into how these signals may have evolved into the more nuanced and fine-tuned gene regulatory mechanisms observed in other model systems.
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Registered trials
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 OpenQuestion graph.