ArticleEukaryotic cell2002
Ex vivo and in vitro identification of a consensus promoter for VSG genes expressed by metacyclic-stage trypanosomes in the tsetse fly.
Article in Eukaryotic cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- De Novo Assembly of the Trypanosoma congolense Genome Reveals an Organization Influenced by Antigenic Variation but Distinct from Trypanosoma brucei.Genome biology and evolution · 2026Article
- Article
- Single-cell transcriptomics reveals expression profiles of Trypanosoma brucei sexual stages.PLoS pathogens · 2022Article
- Signatures of hybridization in Trypanosoma brucei.PLoS pathogens · 2022Article
- Shared Mechanisms for Mutually Exclusive Expression and Antigenic Variation by Protozoan Parasites.Frontiers in cell and developmental biology · 2022Review
- VEX1 Influences mVSG Expression During the Transition to Mammalian Infectivity inFrontiers in cell and developmental biology · 2022Article
- TbSAP is a novel chromatin protein repressing metacyclic variant surface glycoprotein expression sites in bloodstream form Trypanosoma brucei.Nucleic acids research · 2021Article
- Transcription Factor Analysis in Trypanosomatids.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Overview of the role of kinetoplastid surface carbohydrates in infection and host cell invasion: prospects for therapeutic intervention.Parasitology · 2019Review
- Temperature shift activates bloodstream VSG expression site promoters in Trypanosoma brucei.Molecular and biochemical parasitology · 2018Article
- A single-point mutation in the RNA-binding protein 6 generates Trypanosoma brucei metacyclics that are able to progress to bloodstream forms in vitro.Molecular and biochemical parasitology · 2018Article
- The proteome and transcriptome of the infectious metacyclic form of Trypanosoma brucei define quiescent cells primed for mammalian invasion.Molecular microbiology · 2017Article
- Metacyclic VSG expression site promoters are recognized by the same general transcription factor that is required for RNA polymerase I transcription of bloodstream expression sites.Molecular and biochemical parasitology · 2017Article
- Expression of the RNA-binding protein RBP10 promotes the bloodstream-form differentiation state in Trypanosoma brucei.PLoS pathogens · 2017Article
- Does DNA replication direct locus-specific recombination during host immune evasion by antigenic variation in the African trypanosome?Current genetics · 2017Review
- Transcriptome Profiling of Trypanosoma brucei Development in the Tsetse Fly Vector Glossina morsitans.PloS one · 2016Article
- Conserved Curvature of RNA Polymerase I Core Promoter Beyond rRNA Genes: The Case of the Tritryps.Genomics, proteomics & bioinformatics · 2015Article
- Review
- Trypanosoma brucei TIF2 suppresses VSG switching by maintaining subtelomere integrity.Cell research · 2014Article
- Silencing subtelomeric VSGs by Trypanosoma brucei RAP1 at the insect stage involves chromatin structure changes.Nucleic acids research · 2013Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The trypanosome variant surface glycoprotein (VSG) is first expressed during differentiation to the infective, metacyclic population in tsetse fly salivary glands. Unlike the VSG genes expressed by bloodstream form trypanosomes, metacyclic VSGs (MVSGs) have their own promoters. The scarcity of metacyclic cells has meant that only indirect approaches have been used to study these promoters, and not even their identities have been agreed on. Here, we isolated trypanosomes by dissection from salivary glands and used an approach involving 5' rapid amplification of cDNA ends to identify the transcription start site of three MVSGs. This shows that the authentic start site is that proposed for the MVAT series of MVSGs (K. S. Kim and J. E. Donelson, J. Biol. Chem. 272:24637-24645, 1997). In the more readily accessible procyclic trypanosome stage, where MVSGs are normally silent, we used reporter gene assays and linker scanning analysis to confirm that the 67 bp upstream of the start site is a promoter. This is confirmed further by accurate initiation in a homologous in vitro transcription system. We show also that MVSG promoters become derepressed when tested outwith their endogenous, subtelomeric loci. The MVSG promoters are only loosely conserved with bloodstream VSG promoters, and our detailed analysis of the 1.63 MVSG promoter reveals that its activity depends on the start site itself and sequences 26 to 49 bp and 56 to 60 bp upstream. These are longer than those necessary for the bloodstream promoter.
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