ArticleNature2014
Genome-wide dissection of the quorum sensing signalling pathway in Trypanosoma brucei.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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Who cites it
131 citing papers in PubMed, 229 citations in OpenAlex.
- Voices of Eukaryotic Microbes: Chemical Communication Via Quorum Sensing.Microbial ecology · 2026Review
- Division of labor in trypanosome RNA processing and export through expanded Mex67 paralogs.Nucleic acids research · 2026Article
- An Auxin-Inducible Degron System for Trypanosomes.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Discovery of effectors for casein kinase signaling in the African trypanosome.Scientific reports · 2025Article
- Article
- Next generation genetic screens in kinetoplastids.Nucleic acids research · 2025Review
- Mechanisms of life cycle simplification in African trypanosomes.Nature communications · 2024Article
- Dose-dependent interaction of parasites with tiers of host defense predicts "wormholes" that prolong infection at intermediate inoculum sizes.PLoS computational biology · 2024Article
- Identification of immune feature genes and intercellular profiles in diabetic cardiomyopathy.World journal of diabetes · 2024Article
- Post-transcriptional reprogramming by thousands of mRNA untranslated regions in trypanosomes.Nature communications · 2024Article
- Differentiation granules, a dynamic regulator of T. brucei development.Nature communications · 2024Article
- Beyond the VSG layer: Exploring the role of intrinsic disorder in the invariant surface glycoproteins of African trypanosomes.PLoS pathogens · 2024Article
- Depolymerization of SUMO chains induces slender to stumpy differentiation in T. brucei bloodstream parasites.PLoS pathogens · 2024Article
- Purine nucleosides replace cAMP in allosteric regulation of PKA in trypanosomatid pathogens.eLife · 2024Article
- Pathogenicity and virulence of African trypanosomes: From laboratory models to clinically relevant hosts.Virulence · 2023Review
- The developmental hierarchy and scarcity of replicative slender trypanosomes in blood challenges their role in infection maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cell-cell communication in African trypanosomes.Microbiology (Reading, England) · 2023Review
- Two cold shock domain containing proteins trigger the development of infectious Trypanosoma brucei.PLoS pathogens · 2023Article
- Article
- In silico evolutionary and structural analysis of cAMP response proteins (CARPs) from Leishmania major.Archives of microbiology · 2023Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The protozoan parasites Trypanosoma brucei spp. cause important human and livestock diseases in sub-Saharan Africa. In mammalian blood, two developmental forms of the parasite exist: proliferative 'slender' forms and arrested 'stumpy' forms that are responsible for transmission to tsetse flies. The slender to stumpy differentiation is a density-dependent response that resembles quorum sensing in microbial systems and is crucial for the parasite life cycle, ensuring both infection chronicity and disease transmission. This response is triggered by an elusive 'stumpy induction factor' (SIF) whose intracellular signalling pathway is also uncharacterized. Laboratory-adapted (monomorphic) trypanosome strains respond inefficiently to SIF but can generate forms with stumpy characteristics when exposed to cell-permeable cAMP and AMP analogues. Exploiting this, we have used a genome-wide RNA interference library screen to identify the signalling components driving stumpy formation. In separate screens, monomorphic parasites were exposed to 8-(4-chlorophenylthio)-cAMP (pCPT-cAMP) or 8-pCPT-2'-O-methyl-5'-AMP to select cells that were unresponsive to these signals and hence remained proliferative. Genome-wide Ion Torrent based RNAi target sequencing identified cohorts of genes implicated in each step of the signalling pathway, from purine metabolism, through signal transducers (kinases, phosphatases) to gene expression regulators. Genes at each step were independently validated in cells naturally capable of stumpy formation, confirming their role in density sensing in vivo. The putative RNA-binding protein, RBP7, was required for normal quorum sensing and promoted cell-cycle arrest and transmission competence when overexpressed. This study reveals that quorum sensing signalling in trypanosomes shares similarities to fundamental quiescence pathways in eukaryotic cells, its components providing targets for quorum-sensing interference-based therapeutics.
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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.