ArticlePLoS pathogens2017
Genome-wide RNAi selection identifies a regulator of transmission stage-enriched gene families and cell-type differentiation in Trypanosoma brucei.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Life stage-specific poly(A) site selection regulated byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Depolymerization of SUMO chains induces slender to stumpy differentiation in T. brucei bloodstream parasites.PLoS pathogens · 2024Article
- A conserved trypanosomatid differentiation regulator controls substrate attachment and morphological development in Trypanosoma congolense.PLoS pathogens · 2024Article
- Establishment of quantitative RNAi-based forward genetics in Entamoeba histolytica and identification of genes required for growth.PLoS pathogens · 2021Article
- Selective nuclear export of mRNAs is promoted by DRBD18 in Trypanosoma brucei.Molecular microbiology · 2021Article
- Right place, right time: Environmental sensing and signal transduction directs cellular differentiation and motility in Trypanosoma brucei.Molecular microbiology · 2021Review
- The Occurrence of Malignancy inFrontiers in microbiology · 2021Article
- Article
- Identification of clinically approved small molecules that inhibit growth and affect transcript levels of developmentally regulated genes in the African trypanosome.PLoS neglected tropical diseases · 2020Article
- Forward Genetics in African Trypanosomes.Methods in molecular biology (Clifton, N.J.) · 2020Article
- A post-transcriptional respiratome regulon in trypanosomes.Nucleic acids research · 2019Article
- Article
- Regulation of gene expression in trypanosomatids: living with polycistronic transcription.Open biology · 2019Article
- Glucose Signaling Is Important for Nutrient Adaptation during Differentiation of Pleomorphic African Trypanosomes.mSphere · 2018Article
- Dynamic regulation of the Trypanosoma brucei transferrin receptor in response to iron starvation is mediated via the 3'UTR.PloS one · 2018Article
- Expression of the RNA-binding protein RBP10 promotes the bloodstream-form differentiation state in Trypanosoma brucei.PLoS pathogens · 2017Article
- The Cytological Events and Molecular Control of Life Cycle Development of Trypanosoma brucei in the Mammalian Bloodstream.Pathogens (Basel, Switzerland) · 2017Review
- Characterisation of Casein Kinase 1.1 inBioMed research international · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Trypanosoma brucei, causing African sleeping-sickness, exploits quorum-sensing (QS) to generate the 'stumpy forms' necessary for the parasite's transmission to tsetse-flies. These quiescent cells are generated by differentiation in the bloodstream from proliferative slender forms. Using genome-wide RNAi selection we screened for repressors of transmission stage-enriched mRNAs in slender forms, using the stumpy-elevated ESAG9 transcript as a model. This identified REG9.1, whose RNAi-silencing alleviated ESAG9 repression in slender forms and tsetse-midgut procyclic forms. Interestingly, trypanosome surface protein Family 5 and Family 7 mRNAs were also elevated, which, like ESAG9, are T. brucei specific and stumpy-enriched. We suggest these contribute to the distinct transmission biology and vector tropism of T. brucei from other African trypanosome species. As well as surface family regulation, REG9.1-depletion generated QS-independent development to stumpy forms in vivo, whereas REG9.1 overexpression in bloodstream forms potentiated spontaneous differentiation to procyclic forms in the absence of an external signal. Combined, this identifies REG9.1 as a regulator of developmental cell fate, controlling the expression of Trypanosoma brucei-specific molecules elevated during transmission.
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.