Evidence map›Paper›PMID 35771772›Full record

ArticlePLoS genetics2022

PACSIN1 is indispensable for amphisome-lysosome fusion during basal autophagy and subsets of selective autophagy.

Yukako Oe, Keita Kakuda, Shin-Ichiro Yoshimura, Naohiro Hara, Junya Hasegawa, Seigo Terawaki, Yasuyoshi Kimura, Kensuke Ikenaka, Shiro Suetsugu, Hideki Mochizuki and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2022. 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
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Integrative MRI and Genomics Analyses PrioritizeAnimals : an open access journal from MDPI · 2026
    Article
  2. SNX-3 confers lysosomal fusion-competence to sustain basal autophagy.Cellular and molecular life sciences : CMLS · 2026
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  13. Life science alliance · 2023
    Article
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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 at 4 institutions in 1 country.

Yukako OeLaboratory of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Keita KakudaDepartment of Neurology, Graduate School of Medicine, Osaka University, Osaka, Japan.ORCID 0000-0003-2563-5443
Shin-Ichiro YoshimuraDepartment of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan.ORCID 0000-0003-3632-0674
Naohiro HaraDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Junya HasegawaDepartment of Biochemical Pathophysiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.ORCID 0000-0003-1216-7468
Seigo TerawakiDepartment of Molecular and Genetic Medicine, Kawasaki Medical School, Okayama, Japan.ORCID 0000-0001-6019-1628
Yasuyoshi KimuraDepartment of Neurology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Kensuke IkenakaDepartment of Neurology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shiro SuetsuguDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, Ikoma, Japan.ORCID 0000-0002-4612-0628
Hideki MochizukiDepartment of Neurology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tamotsu YoshimoriLaboratory of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Shuhei NakamuraLaboratory of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.ORCID 0000-0002-1488-8317
The University of Osaka · JPKawasaki Medical School · JPNara Institute of Science and Technology · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an indispensable process that degrades cytoplasmic materials to maintain cellular homeostasis. During autophagy, double-membrane autophagosomes surround cytoplasmic materials and either fuse with endosomes (called amphisomes) and then lysosomes, or directly fuse with lysosomes, in both cases generating autolysosomes that degrade their contents by lysosomal hydrolases. However, it remains unclear if there are specific mechanisms and/or conditions which distinguish these alternate routes. Here, we identified PACSIN1 as a novel autophagy regulator. PACSIN1 deletion markedly decreased autophagic activity under basal nutrient-rich conditions but not starvation conditions, and led to amphisome accumulation as demonstrated by electron microscopic and co-localization analysis, indicating inhibition of lysosome fusion. PACSIN1 interacted with SNAP29, an autophagic SNARE, and was required for proper assembly of the STX17 and YKT6 complexes. Moreover, PACSIN1 was required for lysophagy, aggrephagy but not mitophagy, suggesting cargo-specific fusion mechanisms. In C. elegans, deletion of sdpn-1, a homolog of PACSINs, inhibited basal autophagy and impaired clearance of aggregated protein, implying a conserved role of PACSIN1. Taken together, our results demonstrate the amphisome-lysosome fusion process is preferentially regulated in response to nutrient state and stress, and PACSIN1 is a key to specificity during autophagy.

Indexed as

Caenorhabditis elegansMacroautophagyAnimalsAutophagosomesAutophagyLysosomesSNARE ProteinsSNARE Proteins

Identifiers

PMID35771772
PMCPMC9246181
OpenAlexW4283733605

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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.