Evidence map›Paper›PMID 32460019›Full record

ArticleCell reports2020

Regulation of Expression of Autophagy Genes by Atg8a-Interacting Partners Sequoia, YL-1, and Sir2 in Drosophila.

Anne-Claire Jacomin, Stavroula Petridi, Marisa Di Monaco, Zambarlal Bhujabal, Ashish Jain, Nitha C Mulakkal, Anthimi Palara, Emma L Powell, Bonita Chung, Cleidiane Zampronio and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Review
  14. Restoration of Sleep and Circadian Behavior by Autophagy Modulation in Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  15. Article
  16. Protein modification regulated autophagy inFrontiers in physiology · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 2 institutions in 2 countries.

Anne-Claire JacominSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Stavroula PetridiSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Marisa Di MonacoSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Zambarlal BhujabalMolecular Cancer Research Group, Institute of Medical Biology, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway.
Ashish JainMolecular Cancer Research Group, Institute of Medical Biology, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway; Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello, 0379 Oslo, Norway; Centre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Montebello, 0379 Oslo, Norway.
Nitha C MulakkalSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Anthimi PalaraSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK; Molecular Cancer Research Group, Institute of Medical Biology, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway.
Emma L PowellSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Bonita ChungSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Cleidiane ZampronioSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Alexandra JonesSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Alexander CameronSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK.
Terje JohansenMolecular Cancer Research Group, Institute of Medical Biology, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway.
Ioannis P NezisSchool of Life Sciences, University of Warwick, CV4 7AL Coventry, UK. Electronic address: i.nezis@warwick.ac.uk.
University of Warwick · GBUiT The Arctic University of Norway · NO

Funding

Biotechnology and Biological Sciences Research Council BB/P007856/1
6 · The paper itself

Abstract

Autophagy is the degradation of cytoplasmic material through the lysosomal pathway. One of the most studied autophagy-related proteins is LC3. Despite growing evidence that LC3 is enriched in the nucleus, its nuclear role is poorly understood. Here, we show that Drosophila Atg8a protein, homologous to mammalian LC3, interacts with the transcription factor Sequoia in a LIR motif-dependent manner. We show that Sequoia depletion induces autophagy in nutrient-rich conditions through the enhanced expression of autophagy genes. We show that Atg8a interacts with YL-1, a component of a nuclear acetyltransferase complex, and that it is acetylated in nutrient-rich conditions. We also show that Atg8a interacts with the deacetylase Sir2, which deacetylates Atg8a during starvation to activate autophagy. Our results suggest a mechanism of regulation of the expression of autophagy genes by Atg8a, which is linked to its acetylation status and its interaction with Sequoia, YL-1, and Sir2.

Indexed as

AnimalsAutophagy-Related Protein 8 FamilyDrosophilaDrosophila ProteinsHistone ChaperonesHistone DeacetylasesSequoiaSirtuinsAutophagy-Related Protein 8 FamilyDrosophila ProteinsHistone ChaperonesHistone DeacetylasesSirt2 protein, DrosophilaSirtuinsYL-1 protein, DrosophilaacetylationautophagyLC3/Atg8LIR motifnucleustranscription

Identifiers

PMID32460019
PMCPMC7262597
OpenAlexW3032479665

What OpenQuestion holds

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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.