Evidence map›Paper›PMID 41174228›Full record

ArticleNature plants2025

Electrostatic changes enabled the diversification of an exocyst subunit via protein complex escape.

Juan Carlos De la Concepcion, Héloïse Duverge, Yoonwoo Kim, Jose Julian, Haonan D Xu, Matthew N Watt, Sara Ait Ikene, Anita Bianchi, Nenad Grujic, Ranjith K Papareddy and 6 more

Abstract read
In one paragraph

Article in Nature plants, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

16 authors.

Juan Carlos De la ConcepcionGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria. juan.concepcion@gmi.oeaw.ac.at.ORCID 0000-0002-7642-8375
Héloïse DuvergeGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.ORCID 0009-0008-2575-872X
Yoonwoo KimGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.
Jose JulianGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.ORCID 0000-0002-3078-0971
Haonan D XuDivision of Molecular Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dow Street, Dundee, UK.
Matthew N WattDivision of Molecular Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dow Street, Dundee, UK.
Sara Ait IkeneGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.
Anita BianchiGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.ORCID 0009-0007-0323-1399
Nenad GrujicGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.
Ranjith K PapareddyGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria.ORCID 0000-0002-4067-5999
Irina GrishkovskayaResearch Institute of Molecular Pathology, Vienna BioCenter, Vienna, Austria.ORCID 0000-0003-0164-9373
David HaselbachResearch Institute of Molecular Pathology, Vienna BioCenter, Vienna, Austria.ORCID 0000-0002-5276-5633
David H MurrayDivision of Molecular Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dow Street, Dundee, UK.
Marion ClavelMax-Planck-Institut für Molekulare Pflanzenphysiologie, Potsdam-Golm, Germany.ORCID 0000-0003-1322-7362
Nicholas A T IrwinGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria. nicholas.irwin@gmi.oeaw.ac.at.ORCID 0000-0002-2904-8214
Yasin DagdasGregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, Vienna, Austria. yasin.dagdas@cos.uni-heidelberg.de.ORCID 0000-0002-9502-355X

Funding

Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) I6760Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) P34944China Scholarship Council (CSC) 202008310117Deutsche Forschungsgemeinschaft (German Research Foundation) Heisenberg AwardEC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) 101043370EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) 847548Österreichischen Akademie der Wissenschaften (Austrian Academy of Sciences) SFB F79Royal Society RGS/R2/180284Vienna Science and Technology Fund (Wiener Wissenschafts-, Forschungs- und Technologiefonds) LS21-009Wellcome TrustWellcome Trust (Wellcome) 211193/Z/18/Z
6 · The paper itself

Abstract

Protein neofunctionalization is a key driver of cellular complexity. However, subunits of multimeric protein complexes are often thought to be evolutionarily constrained, limiting their capacity for functional divergence. This presents a paradox in plants, where the Exo70 subunit of the exocyst-an octameric complex essential for exocytosis-has undergone striking expansion and diversification. Here we show that electrostatic changes in the N-terminal helix of Exo70 facilitated its physical and functional dissociation from the exocyst, relieving constraints imposed by complex integration. Using Marchantia polymorpha and Arabidopsis thaliana, we demonstrate that this 'complex escape' enables Exo70 paralogues to acquire distinct localizations, interactomes and functions independent of canonical exocytosis. Ancestral reconstructions across land plants reveal that this electrostatic shift predates the extensive radiation of the plant Exo70 protein family, with some lineages later reassociating with the complex. Our findings reveal a reversible mechanism that enabled Exo70 to circumvent the evolutionary and biophysical constraints imposed by complex integration and diversify-a mechanism that could represent a generalizable route to protein neofunctionalization and cellular innovation.

Indexed as

ArabidopsisArabidopsis ProteinsMarchantiaPlant ProteinsVesicular Transport ProteinsEvolution, MolecularExocytosisProtein SubunitsStatic ElectricityArabidopsis ProteinsPlant ProteinsProtein SubunitsVesicular Transport Proteins

Identifiers

PMID41174228
PMCPMC12626893

What OpenQuestion holds

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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.