ArticleBMC biotechnology2005
Functional complementation of RNA interference mutants in trypanosomes.
Article in BMC biotechnology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Tetracycline-Inducible Functional Complementation Analysis in Trypanosoma Parasites.Methods in molecular biology (Clifton, N.J.) · 2026Article
- An independently tunable dual control system for RNAi complementation in Trypanosoma brucei.PloS one · 2025Article
- Deep mutational scanning of the RNase III-like domain inFrontiers in cellular and infection microbiology · 2024Article
- A DNA polymerization-independent role for mitochondrial DNA polymerase I-like protein C in African trypanosomes.Journal of cell science · 2020Article
- A Riboswitch-based Inducible Gene Expression System for Trypanosoma brucei.The Journal of eukaryotic microbiology · 2018Article
- Controlling transferrin receptor trafficking with GPI-valence in bloodstream stage African trypanosomes.PLoS pathogens · 2017Article
- CMF22 is a broadly conserved axonemal protein and is required for propulsive motility in Trypanosoma brucei.Eukaryotic cell · 2013Article
- Structure-function relationship of the Polo-like kinase in Trypanosoma brucei.Journal of cell science · 2012Article
- Flagellar motility of Trypanosoma cruzi epimastigotes.Journal of biomedicine & biotechnology · 2012Article
- Structure-function analysis of dynein light chain 1 identifies viable motility mutants in bloodstream-form Trypanosoma brucei.Eukaryotic cell · 2011Article
- Structural changes of the paraflagellar rod during flagellar beating in Trypanosoma cruzi.PloS one · 2010Article
- Mitochondrial localization of human frataxin is necessary but processing is not for rescuing frataxin deficiency in Trypanosoma brucei.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Stable silencing of SNAP-25 in PC12 cells by RNA interference.BMC neuroscience · 2006Article
- Silence of the transcripts: RNA interference in medicine.Journal of molecular medicine (Berlin, Germany) · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn many eukaryotic cells, double-stranded RNA (dsRNA) triggers RNA interference (RNAi), the specific degradation of RNA of homologous sequence. RNAi is now a major tool for reverse-genetics projects, including large-scale high-throughput screens. Recent reports have questioned the specificity of RNAi, raising problems in interpretation of RNAi-based experiments.
resultsUsing the protozoan Trypanosoma brucei as a model, we designed a functional complementation assay to ascertain that phenotypic effect(s) observed upon RNAi were due to specific silencing of the targeted gene. This was applied to a cytoskeletal gene encoding the paraflagellar rod protein 2 (TbPFR2), whose product is essential for flagellar motility. We demonstrate the complementation of TbPFR2, silenced via dsRNA targeting its UTRs, through the expression of a tagged RNAi-resistant TbPFR2 encoding a protein that could be immunolocalized in the flagellum. Next, we performed a functional complementation of TbPFR2, silenced via dsRNA targeting its coding sequence, through heterologous expression of the TbPFR2 orthologue gene from Trypanosoma cruzi: the flagellum regained its motility.
conclusionsThis work shows that functional complementation experiments can be readily performed in order to ascertain that phenotypic effects observed upon RNAi experiments are indeed due to the specific silencing of the targetted gene. Further, the results described here are of particular interest when reverse genetics studies cannot be easily achieved in organisms not amenable to RNAi. In addition, our strategy should constitute a firm basis to elaborate functional-dissection studies of genes from other organisms.
Indexed as
Identifiers
What OpenQuestion holds
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.