Evidence map›Paper›PMID 41476940›Full record

ArticleiScience2025

Growth factor-independent mTORC1 signaling promotes primary cilia length via suppression of autophagy.

Jong Shin, Khaled Tighanimine, Yann Cormerais, Dean M Rosenthal, Pratima Niroula, Samuel C Lapp, Krystle C Kalafut, Madi Y Cisse, Sandra Schrötter, Brendan D Manning

Abstract read
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Jong ShinDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Khaled TighanimineDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Yann CormeraisDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Dean M RosenthalDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Pratima NiroulaDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Samuel C LappDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Krystle C KalafutDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Madi Y CisseDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Sandra SchrötterDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Brendan D ManningDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Decoding and Targeting the PI3K-mTOR Signaling Network in CancerR35CA197459 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI BRENDAN D. MANNING · 2015 to 2026
$10.8M
Training Program in Molecular MetabolismT32DK128781 · NIDDK · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Sudha B Biddinger, GOKHAN S HOTAMISLIGIL · 2021 to 2026
$1.1M
Neurodevelopmental Function of TBC1D7: A Core Component of the TSC ComplexR21NS126952 · NINDS · HARVARD SCHOOL OF PUBLIC HEALTH · PI MANNING, BRENDAN D. · 2022 to 2022
$439k
Defining Mechanisms of Dynamic mTORC1 Regulation in the Liver with Fasting and FeedingF31DK128873 · NIDDK · HARVARD SCHOOL OF PUBLIC HEALTH · PI KALAFUT, KRYSTLE · 2022 to 2023
$71k
NCI NIH HHS P01 CA120964NCI NIH HHS R35 CA197459NIDDK NIH HHS F31 DK128873NIDDK NIH HHS T32 DK128781NINDS NIH HHS R21 NS126952
6 · The paper itself

Abstract

The mechanistic target of rapamycin (mTOR) complex 1 (mTORC1), a sensor of growth signals that control cell growth, has been studied mainly in proliferating cells. Primary cilia are sensory organelles present on most quiescent cells and are essential for receiving environmental and developmental signals. Given that ciliated cells are non-proliferative, we investigated whether mTORC1 signaling influences primary cilia growth. Here, we show that mTORC1 promotes cilia elongation without affecting ciliogenesis by suppressing autophagy. Inhibiting mTORC1 through pharmacological, nutritional, or genetic interventions shortened primary cilia, whereas activation of the pathway elongated them. Furthermore, pharmacological or genetic inhibition of autophagy-a key downstream process blocked by mTORC1-elongated primary cilia and rendered them resistant to mTORC1 inhibition. These mTORC1-mediated effects extend to mouse neurons

Indexed as

Cell biologyMolecular physiology

Identifiers

PMID41476940
PMCPMC12752765

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.