Evidence map›Paper›PMID 30503212›Full record

ArticleCell2019

Oligopeptide Signaling through TbGPR89 Drives Trypanosome Quorum Sensing.

Federico Rojas, Eleanor Silvester, Julie Young, Rachel Milne, Mabel Tettey, Douglas R Houston, Malcolm D Walkinshaw, Irene Pérez-Pi, Manfred Auer, Helen Denton and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 166 citations in OpenAlex.

  1. Article
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  15. Drug-induced stress mediatesMicrobiology spectrum · 2024
    Article
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13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Federico RojasInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
Eleanor SilvesterInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
Julie YoungInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
Rachel MilneInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
Mabel TetteyInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
Douglas R HoustonInstitute of Quantitative Biology, Biochemistry and Biotechnology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Malcolm D WalkinshawInstitute of Quantitative Biology, Biochemistry and Biotechnology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Irene Pérez-PiInstitute of Quantitative Biology, Biochemistry and Biotechnology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Manfred AuerInstitute of Quantitative Biology, Biochemistry and Biotechnology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Helen DentonSchool of Biology, BSRC, University of St. Andrews, North Haugh, St. Andrews, Fife KY16 9ST, UK.
Terry K SmithSchool of Biology, BSRC, University of St. Andrews, North Haugh, St. Andrews, Fife KY16 9ST, UK.
Joanne ThompsonInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK. Electronic address: joanne.thompson@ed.ac.uk.
Keith R MatthewsInstitute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK. Electronic address: keith.matthews@ed.ac.uk.
University of Edinburgh · GBUniversity of St Andrews · GB

Funding

Medical Research Council J54359Medical Research Council MR/M020118/1Wellcome Trust 103740/Z/14/ZWellcome Trust 103740/Z14/ZWellcome Trust 202094/Z/16/Z
6 · The paper itself

Abstract

Trypanosome parasites control their virulence and spread by using quorum sensing (QS) to generate transmissible "stumpy forms" in their host bloodstream. However, the QS signal "stumpy induction factor" (SIF) and its reception mechanism are unknown. Although trypanosomes lack G protein-coupled receptor signaling, we have identified a surface GPR89-family protein that regulates stumpy formation. TbGPR89 is expressed on bloodstream "slender form" trypanosomes, which receive the SIF signal, and when ectopically expressed, TbGPR89 drives stumpy formation in a SIF-pathway-dependent process. Structural modeling of TbGPR89 predicts unexpected similarity to oligopeptide transporters (POT), and when expressed in bacteria, TbGPR89 transports oligopeptides. Conversely, expression of an E. coli POT in trypanosomes drives parasite differentiation, and oligopeptides promote stumpy formation in vitro. Furthermore, the expression of secreted trypanosome oligopeptidases generates a paracrine signal that accelerates stumpy formation in vivo. Peptidase-generated oligopeptide QS signals being received through TbGPR89 provides a mechanism for both trypanosome SIF production and reception.

Indexed as

Cell DifferentiationConserved SequenceGTP-Binding ProteinsMembrane Transport ProteinsOligopeptidesPhylogenyProtozoan ProteinsQuorum SensingSignal TransductionTrypanosomaTrypanosoma brucei bruceiTrypanosomiasis, AfricanVirulenceGTP-Binding ProteinsMembrane Transport ProteinsOligopeptidespeptide permeaseProtozoan ProteinsdifferentiationGPR89oligopeptideparasitequorum sensingsleeping sicknessstumpy induction factorTrypanosome brucei

Identifiers

PMID30503212
PMCPMC6333907
OpenAlexW2903103803

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.