Evidence map›Paper›PMID 18474623›Full record

ArticleThe Journal of cell biology2008

The class III PI(3)K Vps34 promotes autophagy and endocytosis but not TOR signaling in Drosophila.

Gábor Juhász, Jahda H Hill, Ying Yan, Miklós Sass, Eric H Baehrecke, Jonathan M Backer, Thomas P Neufeld

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 2 pooled it
17.7field-weighted citation impact, top 1% 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

190 citing papers in PubMed, 2 syntheses or guidelines pooled it, 301 citations in OpenAlex.

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  19. Adaptation to hypoxia inAutophagy · 2022
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130 more citing papers are in PubMed but not listed here.

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

7 authors at 5 institutions in 2 countries.

Gábor JuhászDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.
Jahda H Hill
Ying Yan
Miklós Sass
Eric H Baehrecke
Jonathan M Backer
Thomas P Neufeld
Biotechnology Institute · USUniversity of Minnesota · USAlbert Einstein College of Medicine · USEötvös Loránd University · HUYeshiva University · US

Funding

Regulation of TOR Signaling and Autophagy in DrosophilaR01GM062509 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NEUFELD, THOMAS P. · 2001 to 2013
$3.8M
STEROID REGULATION OF DROSOPHILA PROGRAMMED CELL DEATHR01GM059136 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BAEHRECKE, ERIC H · 1999 to 2007
$1.8M
Regulation and Function of hVps34 in Insulin SignalingR01DK070679 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BACKER, JONATHAN M. · 2006 to 2010
$1.2M
Steroid Regulation of Drosophila Programmed Cell DeathR56GM059136 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BAEHRECKE, ERIC H · 2009 to 2009
$328k
NIDDK NIH HHS DK070679NIDDK NIH HHS R01 DK070679NIGMS NIH HHS GM59136NIGMS NIH HHS GM62509NIGMS NIH HHS R01 GM059136NIGMS NIH HHS R01 GM062509NIGMS NIH HHS R56 GM059136
6 · The paper itself

Abstract

Degradation of cytoplasmic components by autophagy requires the class III phosphatidylinositol 3 (PI(3))-kinase Vps34, but the mechanisms by which this kinase and its lipid product PI(3) phosphate (PI(3)P) promote autophagy are unclear. In mammalian cells, Vps34, with the proautophagic tumor suppressors Beclin1/Atg6, Bif-1, and UVRAG, forms a multiprotein complex that initiates autophagosome formation. Distinct Vps34 complexes also regulate endocytic processes that are critical for late-stage autophagosome-lysosome fusion. In contrast, Vps34 may also transduce activating nutrient signals to mammalian target of rapamycin (TOR), a negative regulator of autophagy. To determine potential in vivo functions of Vps34, we generated mutations in the single Drosophila melanogaster Vps34 orthologue, causing cell-autonomous disruption of autophagosome/autolysosome formation in larval fat body cells. Endocytosis is also disrupted in Vps34(-/-) animals, but we demonstrate that this does not account for their autophagy defect. Unexpectedly, TOR signaling is unaffected in Vps34 mutants, indicating that Vps34 does not act upstream of TOR in this system. Instead, we show that TOR/Atg1 signaling regulates the starvation-induced recruitment of PI(3)P to nascent autophagosomes. Our results suggest that Vps34 is regulated by TOR-dependent nutrient signals directly at sites of autophagosome formation.

Indexed as

AutophagyEndocytosisSignal TransductionAnimalsAutophagy-Related Protein-1 HomologDrosophila melanogasterDrosophila ProteinsEndosomesFat BodyFoodFood DeprivationIntracellular MembranesLarvaMutationPhagosomesPhosphatidylinositol 3-KinasesAtg1 protein, DrosophilaAutophagy-Related Protein-1 HomologDrosophila Proteinsphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesProtein Serine-Threonine KinasesReceptor Protein-Tyrosine Kinasestor protein, Drosophila

Identifiers

PMID18474623
PMCPMC2386105
OpenAlexW2093882277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.