Evidence map›Paper›PMID 38316984›Full record

ArticleNature cell biology2024

A metabolite sensor subunit of the Atg1/ULK complex regulates selective autophagy.

A S Gross, R Ghillebert, M Schuetter, E Reinartz, A Rowland, B C Bishop, M Stumpe, J Dengjel, M Graef

Open access · hybridAbstract read
In one paragraph

Article in Nature cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Core principles of autophagy initiation mechanisms.Nature structural & molecular biology · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 4 countries.

A S GrossMax Planck Research Group of Autophagy and Cellular Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany.
R GhillebertMax Planck Research Group of Autophagy and Cellular Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany.
M SchuetterMax Planck Research Metabolomics Core Facility, Max Planck Institute for Biology of Ageing, Cologne, Germany.
E ReinartzMax Planck Research Group of Autophagy and Cellular Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany.
A RowlandMax Planck Research Group of Autophagy and Cellular Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany.
B C BishopDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA.
M StumpeDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
J DengjelDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0002-9453-4614
M GraefMax Planck Research Group of Autophagy and Cellular Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany. Martin.Graef@cornell.edu.ORCID 0000-0002-6820-1533
Max Planck Institute for Biology of Ageing · DECornell University · USUniversity of Fribourg · CHGregor Mendel Institute of Molecular Plant Biology · AT

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 269925409
6 · The paper itself

Abstract

Cells convert complex metabolic information into stress-adapted autophagy responses. Canonically, multilayered protein kinase networks converge on the conserved Atg1/ULK kinase complex (AKC) to induce non-selective and selective forms of autophagy in response to metabolic changes. Here we show that, upon phosphate starvation, the metabolite sensor Pho81 interacts with the adaptor subunit Atg11 at the AKC via an Atg11/FIP200 interaction motif to modulate pexophagy by virtue of its conserved phospho-metabolite sensing SPX domain. Notably, core AKC components Atg13 and Atg17 are dispensable for phosphate starvation-induced autophagy revealing significant compositional and functional plasticity of the AKC. Our data indicate that, instead of functioning as a selective autophagy receptor, Pho81 compensates for partially inactive Atg13 by promoting Atg11 phosphorylation by Atg1 critical for pexophagy during phosphate starvation. Our work shows Atg11/FIP200 adaptor subunits bind not only selective autophagy receptors but also modulator subunits that convey metabolic information directly to the AKC for autophagy regulation.

Indexed as

Adaptor Proteins, Signal TransducingMacroautophagyAutophagyAutophagy-Related ProteinsCarrier ProteinsPhagosomesPhosphatesTranscription FactorsAdaptor Proteins, Signal TransducingAutophagy-Related ProteinsCarrier ProteinsPhosphatesTranscription Factors

Identifiers

PMID38316984
PMCPMC10940145
OpenAlexW4391539753

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.