ArticleThe EMBO journal1999
Trypanosoma brucei variant surface glycoprotein regulation involves coupled activation/inactivation and chromatin remodeling of expression sites.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 79 citations in OpenAlex.
- VEX1 Influences mVSG Expression During the Transition to Mammalian Infectivity inFrontiers in cell and developmental biology · 2022Article
- Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021Review
- Telomere and Subtelomere R-loops and Antigenic Variation in Trypanosomes.Journal of molecular biology · 2020Review
- Causes and Effects of Loss of Classical Nonhomologous End Joining Pathway in Parasitic Eukaryotes.mBio · 2019Article
- TelAP1 links telomere complexes with developmental expression site silencing in African trypanosomes.Nucleic acids research · 2018Article
- Transcriptional Regulation of Telomeric Expression Sites and Antigenic Variation in Trypanosomes.Current genomics · 2018Review
- A transcription-independent epigenetic mechanism is associated with antigenic switching in Trypanosoma brucei.Nucleic acids research · 2016Article
- Silencing subtelomeric VSGs by Trypanosoma brucei RAP1 at the insect stage involves chromatin structure changes.Nucleic acids research · 2013Article
- Histone H1 plays a role in heterochromatin formation and VSG expression site silencing in Trypanosoma brucei.PLoS pathogens · 2012Article
- The orthologue of Sjögren's syndrome nuclear autoantigen 1 (SSNA1) in Trypanosoma brucei is an immunogenic self-assembling molecule.PloS one · 2012Article
- NLP is a novel transcription regulator involved in VSG expression site control in Trypanosoma brucei.Nucleic acids research · 2011Article
- The FACT subunit TbSpt16 is involved in cell cycle specific control of VSG expression sites in Trypanosoma brucei.Molecular microbiology · 2010Article
- Active VSG expression sites in Trypanosoma brucei are depleted of nucleosomes.Eukaryotic cell · 2010Article
- A histone methyltransferase modulates antigenic variation in African trypanosomes.PLoS biology · 2008Article
- Histone acetylation and methylation at sites initiating divergent polycistronic transcription in Trypanosoma cruzi.The Journal of biological chemistry · 2008Article
- Acetylation of histone H4K4 is cell cycle regulated and mediated by HAT3 in Trypanosoma brucei.Molecular microbiology · 2008Article
- A novel ISWI is involved in VSG expression site downregulation in African trypanosomes.The EMBO journal · 2007Article
- Trypanosoma brucei ARF1 plays a central role in endocytosis and golgi-lysosome trafficking.Molecular biology of the cell · 2007Article
- Nuclear repositioning of the VSG promoter during developmental silencing in Trypanosoma brucei.The Journal of cell biology · 2007Article
- Expression site silencing and life-cycle progression appear normal in Argonaute1-deficient Trypanosoma brucei.Molecular and biochemical parasitology · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Trypanosoma brucei is an extracellular protozoan parasite that cycles between mammalian hosts and the tsetse vector. In bloodstream-form trypanosomes, only one variant surface glycoprotein gene (VSG) expression site (ES) is active at any time. Transcriptional switching between ESs results in antigenic variation. No VSG is transcribed in the insect procyclic stage. We have used bacteriophage T7 RNA polymerase (T7RNAP) to study the transcriptional accessibility of ES chromatin in vivo. We show that T7RNAP-mediated transcription from chromosomally integrated T7 promoters is repressed along the entire length of the ES in the procyclic form, but not in the bloodstream form, suggesting that the accessible chromatin of inactive bloodstream-form ESs is remodeled upon differentiation to yield a structure that is no longer permissive for T7RNAP-mediated transcription. In the bloodstream form, replacing the active ES promoter with a T7 promoter, which is incapable of sustaining high-level transcription of the entire ES, prompts an ES switch. These data suggest two distinct mechanisms for ES regulation: a chromatin-mediated developmental silencing of the ES in the procyclic form and a rapid coupled mechanism for ES activation and inactivation in the bloodstream form.
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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.