Evidence map›Paper›PMID 35918345›Full record

ArticleNature communications2022

Ribosome impairment regulates intestinal stem cell identity via ZAKɑ activation.

Joana Silva, Ferhat Alkan, Sofia Ramalho, Goda Snieckute, Stefan Prekovic, Ana Krotenberg Garcia, Santiago Hernández-Pérez, Rob van der Kammen, Danielle Barnum, Liesbeth Hoekman and 5 more

Abstract read
In one paragraph

Article in Nature communications, 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
–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

18 citing papers in PubMed.

  1. NAR genomics and bioinformatics · 2026
    Article
  2. Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
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

15 authors.

Joana SilvaDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-5301-1799
Ferhat AlkanDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-6709-9605
Sofia RamalhoDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Goda SnieckuteCenter for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Stefan PrekovicDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-7051-9321
Ana Krotenberg GarciaInstitute of Byodynamics and Biocomplexity, Department of Biology, Faculty of Science, Utrecht University, Utrecht, The Netherlands.
Santiago Hernández-PérezDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Rob van der KammenDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Danielle BarnumDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Liesbeth HoekmanProteomics Facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Maarten AltelaarProteomics Facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Wilbert ZwartDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-9823-7289
Saskia Jacoba Elisabeth SuijkerbuijkInstitute of Byodynamics and Biocomplexity, Department of Biology, Faculty of Science, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-3197-1307
Simon Bekker-JensenCenter for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-7308-4597
William James FallerDivision of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands. w.faller@nki.nl.ORCID 0000-0002-0738-2254

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small intestine is a rapidly proliferating organ that is maintained by a small population of Lgr5-expressing intestinal stem cells (ISCs). However, several Lgr5-negative ISC populations have been identified, and this remarkable plasticity allows the intestine to rapidly respond to both the local environment and to damage. However, the mediators of such plasticity are still largely unknown. Using intestinal organoids and mouse models, we show that upon ribosome impairment (driven by Rptor deletion, amino acid starvation, or low dose cyclohexamide treatment) ISCs gain an Lgr5-negative, fetal-like identity. This is accompanied by a rewiring of metabolism. Our findings suggest that the ribosome can act as a sensor of nutrient availability, allowing ISCs to respond to the local nutrient environment. Mechanistically, we show that this phenotype requires the activation of ZAKɑ, which in turn activates YAP, via SRC. Together, our data reveals a central role for ribosome dynamics in intestinal stem cells, and identify the activation of ZAKɑ as a critical mediator of stem cell identity.

Indexed as

Intestinal MucosaStem CellsAnimalsIntestinesIntestine, SmallMiceReceptors, G-Protein-CoupledRibosomesReceptors, G-Protein-Coupled

Identifiers

PMID35918345
PMCPMC9345940

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.