Evidence map›Paper›PMID 39571580›Full record

ArticleMolecular cell2024

Nutrient control of growth and metabolism through mTORC1 regulation of mRNA splicing.

Takafumi Ogawa, Meltem Isik, Ziyun Wu, Kiran Kurmi, Jin Meng, Sungyun Cho, Gina Lee, L Paulette Fernandez-Cardenas, Masaki Mizunuma, John Blenis and 2 more

Abstract read
In one paragraph

Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Vitamin BNature communications · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Vitamin BResearch square · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. 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

12 authors.

Takafumi OgawaResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Unit of Biotechnology, Graduate School of Integrated Sciences for Life, Hiroshima University, Higashi-Hiroshima, Japan; Hiroshima Research Center for Healthy Aging (HiHA), Hiroshima University, Higashi-Hiroshima, Japan.
Meltem IsikResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
Ziyun WuResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Department of Food Science and Engineering, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Kiran KurmiDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center, Harvard Medical School, Boston, MA 02115, USA.
Jin MengResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
Sungyun ChoMeyer Cancer Center and Department of Pharmacology, Weill Cornell Medicine, New York, NY 10021, USA.
Gina LeeMeyer Cancer Center and Department of Pharmacology, Weill Cornell Medicine, New York, NY 10021, USA; Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine, Irvine, CA 92617, USA.
L Paulette Fernandez-CardenasResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
Masaki MizunumaUnit of Biotechnology, Graduate School of Integrated Sciences for Life, Hiroshima University, Higashi-Hiroshima, Japan; Hiroshima Research Center for Healthy Aging (HiHA), Hiroshima University, Higashi-Hiroshima, Japan.
John BlenisMeyer Cancer Center and Department of Pharmacology, Weill Cornell Medicine, New York, NY 10021, USA.
Marcia C HaigisDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center, Harvard Medical School, Boston, MA 02115, USA.
T Keith BlackwellResearch Division, Joslin Diabetes Center, Boston, MA 02215, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Electronic address: keith.blackwell@joslin.harvard.edu.

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
SIGNAL TRANSDUCTION TO PP70 S6KR01GM051405 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLENIS, JOHN · 1995 to 2023
$14.0M
Signaling mechanisms that detect stress and maintain homeostasis - Research Supplement to Promote Diversity in Health-Related ResearchR35GM122610 · NIGMS · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2017 to 2025
$4.7M
Progenitor cell states contributing to aging and lung cancerU01CA267827 · NCI · HARVARD MEDICAL SCHOOL · PI HAIGIS, MARCIA, KIM, CARLA F. · 2021 to 2025
$2.2M
Elucidating the regulation of RNA methylation by mTOR signaling in cancerK22CA234399 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LEE, GINA · 2022 to 2023
$440k
NCI NIH HHS K22 CA234399NCI NIH HHS U01 CA267827NIDDK NIH HHS P30 DK036836NIGMS NIH HHS R01 GM051405NIGMS NIH HHS R35 GM122610
6 · The paper itself

Abstract

Cellular growth and organismal development are remarkably complex processes that require the nutrient-responsive kinase mechanistic target of rapamycin complex 1 (mTORC1). Anticipating that important mTORC1 functions remained to be identified, we employed genetic and bioinformatic screening in C. elegans to uncover mechanisms of mTORC1 action. Here, we show that during larval growth, nutrients induce an extensive reprogramming of gene expression and alternative mRNA splicing by acting through mTORC1. mTORC1 regulates mRNA splicing and the production of protein-coding mRNA isoforms largely independently of its target p70 S6 kinase (S6K) by increasing the activity of the serine/arginine-rich (SR) protein RSP-6 (SRSF3/7) and other splicing factors. mTORC1-mediated mRNA splicing regulation is critical for growth; mediates nutrient control of mechanisms that include energy, nucleotide, amino acid, and other metabolic pathways; and may be conserved in humans. Although mTORC1 inhibition delays aging, mTORC1-induced mRNA splicing promotes longevity, suggesting that when mTORC1 is inhibited, enhancement of this splicing might provide additional anti-aging benefits.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsMechanistic Target of Rapamycin Complex 1RNA, MessengerAlternative SplicingAnimalsHumansLongevityMultiprotein ComplexesNutrientsRibosomal Protein S6 Kinases, 70-kDaRNA SplicingSignal TransductionTOR Serine-Threonine KinasesCaenorhabditis elegans ProteinsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNutrientsRibosomal Protein S6 Kinases, 70-kDaRNA, MessengerTOR Serine-Threonine KinasesC. elegansdevelopmentgene expressiongrowthhuman cell growthlongevitymetabolismmRNA splicingmTORC1nutrient responseSR proteins

Identifiers

PMID39571580
PMCPMC12455899

What OpenQuestion holds

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Registered trials

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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.