Evidence map›Paper›PMID 35076392›Full record

ArticleeLife2022

Evolution of host-microbe cell adherence by receptor domain shuffling.

EmilyClare P Baker, Ryan Sayegh, Kristin M Kohler, Wyatt Borman, Claire K Goodfellow, Eden R Brush, Matthew F Barber

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Evolution of CEACAM pathogen decoy receptors in primates.European journal of clinical investigation · 2024
    Article
  11. The role of CEACAMs in neutrophil function.European journal of clinical investigation · 2024
    Review
  12. Article
  13. Host-derived CEACAM-laden vesicles engage enterotoxigenicProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Host-derived CEACAM-laden vesicles engage enterotoxigenicbioRxiv : the preprint server for biology · 2024
    Article
  15. Article
  16. Review
  17. Interactions of pathogenicFrontiers in immunology · 2023
    Review
  18. 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

7 authors at 1 institution in 1 country.

EmilyClare P BakerInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.ORCID https://orcid.org/0000-0002-7875-2144
Ryan SayeghInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.
Kristin M KohlerInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.
Wyatt BormanInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.
Claire K GoodfellowInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.
Eden R BrushInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.
Matthew F BarberInstitute of Ecology and Evolution, University of Oregon, Eugene, United States.ORCID https://orcid.org/0000-0003-2008-2165
University of Oregon · US

Funding

Molecular mechanisms of evolution at the host-microbe interfaceR35GM133652 · NIGMS · UNIVERSITY OF OREGON · PI BARBER, MATTHEW FREDERICK · 2019 to 2023
$1.8M
Rapid evolution and bacterial evasion by a primate cell adhesion proteinF32AI147565 · NIAID · UNIVERSITY OF OREGON · PI BAKER, EMILYCLARE P · 2020 to 2022
$201k
NIAID NIH HHS F32 AI147565NIGMS NIH HHS R35 GM133652
6 · The paper itself

Abstract

Stable adherence to epithelial surfaces is required for colonization by diverse host-associated microbes. Successful attachment of pathogenic microbes to host cells via adhesin molecules is also the first step in many devastating infections. Despite the primacy of epithelial adherence in establishing host-microbe associations, the evolutionary processes that shape this crucial interface remain enigmatic. Carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) encompass a multifunctional family of vertebrate cell surface proteins which are recurrent targets of bacterial adhesins at epithelial barriers. Here, we show that multiple members of the primate CEACAM family exhibit evidence of repeated natural selection at protein surfaces targeted by bacteria, consistent with pathogen-driven evolution. Divergence of CEACAM proteins between even closely related great apes is sufficient to control molecular interactions with a range of bacterial adhesins. Phylogenetic analyses further reveal that repeated gene conversion of CEACAM extracellular domains during primate divergence plays a key role in limiting bacterial adhesin host tropism. Moreover, we demonstrate that gene conversion has continued to shape CEACAM diversity within human populations, with abundant human CEACAM1 variants mediating evasion of adhesins from pathogenic

Indexed as

PhylogenyAnimalsAntigens, CDBacterial AdhesionCell Adhesion MoleculesCloning, MolecularEscherichia coliHEK293 CellsHelicobacter pyloriHost Microbial InteractionsHumansPan paniscusProtein DomainsAntigens, CDCD66 antigensCell Adhesion Moleculesadhesinsevolutionary biologygene conversionhost-pathogen interactionsH. pylorihumaninfectious diseasemicrobiologynatural selectionNeisseria

Identifiers

PMID35076392
PMCPMC8860441
OpenAlexW4220681460

What OpenQuestion holds

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LicenceCC BY
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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.