Evidence map›Paper›PMID 26353861›Full record

ArticleBiology open2015

Atg9 is required for intraluminal vesicles in amphisomes and autolysosomes.

C A Bader, T Shandala, Y S Ng, I R D Johnson, D A Brooks

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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  12. The role of extracellular vesicles in podocyte autophagy in kidney disease.Journal of cell communication and signaling · 2021
    Review
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  16. The Messenger Apps of the cell: Extracellular Vesicles as Regulatory Messengers of Microglial Function in the CNS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
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  20. Autophagy and Exosomes Relationship in Cancer: Friends or Foes?Frontiers in cell and developmental biology · 2020
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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

5 authors at 1 institution in 1 country.

C A BaderMechanisms in Cell Biology and Diseases Research Group, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia 5001, Australia.
T ShandalaMechanisms in Cell Biology and Diseases Research Group, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia 5001, Australia.
Y S NgMechanisms in Cell Biology and Diseases Research Group, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia 5001, Australia.
I R D JohnsonMechanisms in Cell Biology and Diseases Research Group, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia 5001, Australia.
D A BrooksMechanisms in Cell Biology and Diseases Research Group, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia 5001, Australia Doug.Brooks@unisa.edu.au.
University of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an intracellular recycling and degradation process, which is important for energy metabolism, lipid metabolism, physiological stress response and organism development. During Drosophila development, autophagy is up-regulated in fat body and midgut cells, to control metabolic function and to enable tissue remodelling. Atg9 is the only transmembrane protein involved in the core autophagy machinery and is thought to have a role in autophagosome formation. During Drosophila development, Atg9 co-located with Atg8 autophagosomes, Rab11 endosomes and Lamp1 endosomes-lysosomes. RNAi silencing of Atg9 reduced both the number and the size of autophagosomes during development and caused morphological changes to amphisomes/autolysosomes. In control cells there was compartmentalised acidification corresponding to intraluminal Rab11/Lamp-1 vesicles, but in Atg9 depleted cells there were no intraluminal vesicles and the acidification was not compartmentalised. We concluded that Atg9 is required to form intraluminal vesicles and for localised acidification within amphisomes/autolysosomes, and consequently when depleted, reduced the capacity to degrade and remodel gut tissue during development.

Indexed as

AmphisomeAtg9AutolysosomeAutophagosomeAutophagyIntraluminal vesiclesLysosomeMultivesicular endosome

Identifiers

PMID26353861
PMCPMC4728360
OpenAlexW2178245835

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.