ArticleMolecular microbiology2014
Trypanosoma brucei histone H1 inhibits RNA polymerase I transcription and is important for parasite fitness in vivo.
Article in Molecular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- TelAP2 links TelAP1 to the telomere complex in Trypanosoma brucei.Scientific reports · 2024Article
- Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021Review
- Review
- Transcription Factor Analysis in Trypanosomatids.Methods in molecular biology (Clifton, N.J.) · 2020Article
- African trypanosomes expressing multiple VSGs are rapidly eliminated by the host immune system.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Transcriptomes of Trypanosoma brucei rhodesiense from sleeping sickness patients, rodents and culture: Effects of strain, growth conditions and RNA preparation methods.PLoS neglected tropical diseases · 2018Article
- Transcriptional Regulation of Telomeric Expression Sites and Antigenic Variation in Trypanosomes.Current genomics · 2018Review
- High-throughput Methods for Dissection of Trypanosome Gene Regulatory Networks.Current genomics · 2018Review
- Specialising the parasite nucleus: Pores, lamins, chromatin, and diversity.PLoS pathogens · 2017Review
- Well-positioned nucleosomes punctuate polycistronic pol II transcription units and flank silentEpigenetics & chromatin · 2017Article
- High-resolution analysis of multi-copy variant surface glycoprotein gene expression sites in African trypanosomes.BMC genomics · 2016Article
- Trypanosoma brucei Parasites Occupy and Functionally Adapt to the Adipose Tissue in Mice.Cell host & microbe · 2016Article
- Epigenetic Regulation of Virulence Gene Expression in Parasitic Protozoa.Cell host & microbe · 2016Review
- A transcription-independent epigenetic mechanism is associated with antigenic switching in Trypanosoma brucei.Nucleic acids research · 2016Article
- Purification of Messenger Ribonucleoprotein Particles via a Tagged Nascent Polypeptide.PloS one · 2016Article
- Histone H3 Variant Regulates RNA Polymerase II Transcription Termination and Dual Strand Transcription of siRNA Loci in Trypanosoma brucei.PLoS genetics · 2016Article
- DNA double-strand breaks and telomeres play important roles in trypanosoma brucei antigenic variation.Eukaryotic cell · 2015Review
- Review
- FACT plays a major role in histone dynamics affecting VSG expression site control in Trypanosoma brucei.Molecular microbiology · 2014Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma brucei is a unicellular parasite that causes sleeping sickness in humans. Most of its transcription is constitutive and driven by RNA polymerase II. RNA polymerase I (Pol I) transcribes not only ribosomal RNA genes, but also protein-encoding genes, including variant surface glycoproteins (VSGs) and procyclins. In T. brucei, histone H1 (H1) is required for VSG silencing and chromatin condensation. However, whether H1 has a genome-wide role in transcription is unknown. Here, using RNA sequencing we show that H1 depletion changes the expression of a specific cohort of genes. Interestingly, the predominant effect is partial loss of silencing of Pol I loci, such as VSG and procyclin genes. Labelling of nascent transcripts with 4-thiouridine showed that H1 depletion does not alter the level of labelled Pol II transcripts. In contrast, the levels of 4sU-labelled Pol I transcripts were increased by two- to sixfold, suggesting that H1 preferentially blocks transcription at Pol I loci. Finally, we observed that parasites depleted of H1 grow almost normally in culture but they have a reduced fitness in mice, suggesting that H1 is important for host-pathogen interactions.
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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 OpenQuestion graph.