Evidence map›Paper›PMID 24567306›Full record

ArticleGenome biology and evolution2014

The evolution of the GPCR signaling system in eukaryotes: modularity, conservation, and the transition to metazoan multicellularity.

Alex de Mendoza, Arnau Sebé-Pedrós, Iñaki Ruiz-Trillo

Open access · goldAbstract read
In one paragraph

Article in Genome biology and evolution, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

92 citing papers in PubMed, 199 citations in OpenAlex.

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32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Alex de MendozaInstitut de Biologia Evolutiva (CSIC-Universitat Pompeu Fabra) Passeig Marítim de la Barceloneta, Barcelona, Spain.
Arnau Sebé-Pedrós
Iñaki Ruiz-Trillo
Universitat Pompeu Fabra · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

European Research Council 206883
6 · The paper itself

Abstract

The G-protein-coupled receptor (GPCR) signaling system is one of the main signaling pathways in eukaryotes. Here, we analyze the evolutionary history of all its components, from receptors to regulators, to gain a broad picture of its system-level evolution. Using eukaryotic genomes covering most lineages sampled to date, we find that the various components of the GPCR signaling pathway evolved independently, highlighting the modular nature of this system. Our data show that some GPCR families, G proteins, and regulators of G proteins diversified through lineage-specific diversifications and recurrent domain shuffling. Moreover, most of the gene families involved in the GPCR signaling system were already present in the last common ancestor of eukaryotes. Furthermore, we show that the unicellular ancestor of Metazoa already had most of the cytoplasmic components of the GPCR signaling system, including, remarkably, all the G protein alpha subunits, which are typical of metazoans. Thus, we show how the transition to multicellularity involved conservation of the signaling transduction machinery, as well as a burst of receptor diversification to cope with the new multicellular necessities.

Indexed as

AnimalsArrestinEukaryotaEvolution, MolecularEye ProteinsGenomeG-Protein-Coupled Receptor KinasesGTP-Binding Protein RegulatorsMultigene FamilyPhosphoproteinsPhylogenyPrincipal Component AnalysisReceptors, G-Protein-CoupledSignal TransductionArrestinEye ProteinsG-Protein-Coupled Receptor KinasesGTP-Binding Protein RegulatorsphosducinPhosphoproteinsReceptors, G-Protein-CoupledarrestinGRKheterotrimeric G protein complexphosducinRic8

Identifiers

PMID24567306
PMCPMC3971589
OpenAlexW2143183867

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.