Evidence map›Paper›PMID 32561715›Full record

ArticleNature communications2020

Leucine regulates autophagy via acetylation of the mTORC1 component raptor.

Sung Min Son, So Jung Park, Eleanna Stamatakou, Mariella Vicinanza, Fiona M Menzies, David C Rubinsztein

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
10.0field-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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
    Review
  4. Article
  5. Leucine regulates the mTOR pathway to improve growth and enhance immune responses inAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
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  14. Article
  15. Review
  16. Article
  17. Review
  18. Tspo Depletion Exacerbates Steatosis Through Fatty Acid Uptake.Journal of cellular and molecular medicine · 2025
    Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 2 countries.

Sung Min SonDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK.
So Jung ParkDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK.
Eleanna StamatakouDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK.
Mariella VicinanzaDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK.
Fiona M MenziesDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK.
David C RubinszteinDepartment of Medical Genetics, Cambridge Institute for Medical Research (CIMR), University of Cambridge, Cambridge, UK. dcr1000@cam.ac.uk.ORCID http://orcid.org/0000-0001-5002-5263
University of Cambridge · GB

Funding

Department of HealthMedical Research Council UKDRI-2002
6 · The paper itself

Abstract

Macroautophagy ("autophagy") is the main lysosomal catabolic process that becomes activated under nutrient-depleted conditions, like amino acid (AA) starvation. The mechanistic target of rapamycin complex 1 (mTORC1) is a well-conserved negative regulator of autophagy. While leucine (Leu) is a critical mTORC1 regulator under AA-starved conditions, how Leu regulates autophagy is poorly understood. Here, we describe that in most cell types, including neurons, Leu negatively regulates autophagosome biogenesis via its metabolite, acetyl-coenzyme A (AcCoA). AcCoA inhibits autophagy by enhancing EP300-dependent acetylation of the mTORC1 component raptor, with consequent activation of mTORC1. Interestingly, in Leu deprivation conditions, the dominant effects on autophagy are mediated by decreased raptor acetylation causing mTORC1 inhibition, rather than by altered acetylation of other autophagy regulators. Thus, in most cell types we examined, Leu regulates autophagy via the impact of its metabolite AcCoA on mTORC1, suggesting that AcCoA and EP300 play pivotal roles in cell anabolism and catabolism.

Indexed as

AcetylationAcetyl Coenzyme AAnimalsAutophagosomesAutophagyCell LineE1A-Associated p300 ProteinHumansLeucineMechanistic Target of Rapamycin Complex 1MicePrimary Cell CultureRegulatory-Associated Protein of mTORStarvationAcetyl Coenzyme AE1A-Associated p300 ProteinEP300 protein, humanLeucineMechanistic Target of Rapamycin Complex 1Regulatory-Associated Protein of mTOR

Identifiers

PMID32561715
PMCPMC7305105
OpenAlexW3035769304

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.