Evidence map›Paper›PMID 36888706›Full record

ArticleScience advances2023

The TORC1 activates Rpd3L complex to deacetylate Ino80 and H2A.Z and repress autophagy.

Xin Li, Qianyun Mei, Qi Yu, Min Wang, Fei He, Duncheng Xiao, Huan Liu, Feng Ge, Xilan Yu, Shanshan Li

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Review
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  9. NADCells · 2025
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  11. Menthone lowers H3K27ac levels to inhibitFrontiers in microbiology · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. 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

10 authors at 2 institutions in 1 country.

Xin LiState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.ORCID 0000-0003-3251-5722
Qianyun MeiState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Qi YuState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Min WangKey Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei 430072, China.
Fei HeState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Duncheng XiaoState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Huan LiuState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.
Feng GeKey Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei 430072, China.ORCID 0000-0002-1032-280X
Xilan YuState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.ORCID 0000-0002-7550-7012
Shanshan LiState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei 430062, China.ORCID 0000-0002-0359-2369
Hubei University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a critical process to maintain homeostasis, differentiation, and development. How autophagy is tightly regulated by nutritional changes is poorly understood. Here, we identify chromatin remodeling protein Ino80 and histone variant H2A.Z as the deacetylation targets for histone deacetylase Rpd3L complex and uncover how they regulate autophagy in response to nutrient availability. Mechanistically, Rpd3L deacetylates Ino80 K929, which protects Ino80 from being degraded by autophagy. The stabilized Ino80 promotes H2A.Z eviction from autophagy-related genes, leading to their transcriptional repression. Meanwhile, Rpd3L deacetylates H2A.Z, which further blocks its deposition into chromatin to repress the transcription of autophagy-related genes. Rpd3-mediated deacetylation of Ino80 K929 and H2A.Z is enhanced by the target of rapamycin complex 1 (TORC1). Inactivation of TORC1 by nitrogen starvation or rapamycin inhibits Rpd3L, leading to induction of autophagy. Our work provides a mechanism for chromatin remodelers and histone variants in modulating autophagy in response to nutrient availability.

Indexed as

HistonesSaccharomyces cerevisiae ProteinsChromatinHistone DeacetylasesMechanistic Target of Rapamycin Complex 1NucleosomesChromatinHistone DeacetylasesHistonesMechanistic Target of Rapamycin Complex 1NucleosomesSaccharomyces cerevisiae Proteins

Identifiers

PMID36888706
PMCPMC9995077
OpenAlexW4323636989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.