Evidence map›Paper›PMID 36879119›Full record

ArticleNature metabolism2023

Primary cilia sense glutamine availability and respond via asparagine synthetase.

Maria Elena Steidl, Elisa A Nigro, Anne Kallehauge Nielsen, Roberto Pagliarini, Laura Cassina, Matteo Lampis, Christine Podrini, Marco Chiaravalli, Valeria Mannella, Gianfranco Distefano and 6 more

Open access · hybridFull text read
In one paragraph

Article in Nature metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
14.4field-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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025
    Review
  19. NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. 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 at 4 institutions in 5 countries.

Maria Elena Steidl *Molecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Elisa A Nigro *Molecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Anne Kallehauge NielsenMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Roberto PagliariniMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Laura CassinaMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Matteo LampisMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Christine PodriniMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0002-5391-3378
Marco ChiaravalliMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Valeria MannellaCenter for Omics Sciences, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Gianfranco DistefanoMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.
Ming YangMRC, Cancer Unit Cambridge, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, UK.
Mariam AslanyanDepartment of Human Genetics and Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Giovanna MuscoBiomolecular Nuclear Magnetic Resonance Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0002-0469-2994
Ronald RoepmanDepartment of Human Genetics and Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Christian FrezzaMRC, Cancer Unit Cambridge, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-3293-7397
Alessandra BolettaMolecular Basis of Cystic Kidney Disorders Unit, Division of Genetics and Cell Biology, IRCCS, San Raffaele Scientific Institute, Milan, Italy. boletta.alessandra@hsr.it.ORCID http://orcid.org/0000-0002-4704-4006
Vita-Salute San Raffaele University · ITRadboud University Nijmegen · NLUniversity of Cambridge · GBIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depriving cells of nutrients triggers an energetic crisis, which is resolved by metabolic rewiring and organelle reorganization. Primary cilia are microtubule-based organelles at the cell surface, capable of integrating multiple metabolic and signalling cues, but their precise sensory function is not fully understood. Here we show that primary cilia respond to nutrient availability and adjust their length via glutamine-mediated anaplerosis facilitated by asparagine synthetase (ASNS). Nutrient deprivation causes cilia elongation, mediated by reduced mitochondrial function, ATP availability and AMPK activation independently of mTORC1. Of note, glutamine removal and replenishment is necessary and sufficient to induce ciliary elongation or retraction, respectively, under nutrient stress conditions both in vivo and in vitro by restoring mitochondrial anaplerosis via ASNS-dependent glutamate generation. Ift88-mutant cells lacking cilia show reduced glutamine-dependent mitochondrial anaplerosis during metabolic stress, due to reduced expression and activity of ASNS at the base of cilia. Our data indicate a role for cilia in responding to, and possibly sensing, cellular glutamine levels via ASNS during metabolic stress.

Indexed as

Aspartate-Ammonia LigaseGlutamineCiliaSignal TransductionAspartate-Ammonia LigaseGlutamine

Identifiers

PMID36879119
PMCPMC10042734
OpenAlexW4323310020

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read139
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.