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The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Deletion of PIK3C3/Vps34 in sensory neurons causes rapid neurodegeneration by disrupting the endosomal but not the autophagic pathway

Zhou, Xiang, Wang, Liangli, Hasegawa, Hiroshi, Amin, Priyanka, Han, Bao-Xia, Kaneko, Shinjiro, He, Youwen, Wang, Fan·2010·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0914725107
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Abstract

The lipid kinase PIK3C3 (also called Vps34) regulates both the endosomal and autophagic pathways. However, the effect of inactivating PIK3C3 on neuronal endosomal versus autophagic processes in vivo has not been studied. We generated mice in which Pik3c3 was conditionally deleted in differentiated sensory neurons. Within a few days after Pik3c3 deletion, mutant large-diameter myelinated neurons accumulated numerous enlarged vacuoles and ubiquitin-positive aggregates and underwent rapid degeneration. By contrast, Pik3c3 -deficient small-diameter unmyelinated neurons accumulated excessive numbers of lysosome-like organelles and degenerated more slowly. These differential degenerative phenotypes are unlikely caused by a disruption in the autophagy pathway, because inhibiting autophagy alone by conditional deletion of Atg7 results in a completely distinct phenotype in all sensory neurons (i.e., formation of very large intracellular inclusion bodies and slow degeneration over a period of several months). More surprisingly, a noncanonical PIK3C3-independent LC3-positive autophagosome formation pathway was activated in Pik3c3 -deficient small-diameter neurons. Analyses of Pik3c3/Atg7 double mutant neurons revealed that this unconventional initiation pathway still depends on ATG7. Our studies represent in vivo characterization of PIK3C3 functions in mammals and provide insights into the complexity of neuronal endo-lysosomal and autophagic pathways.

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  • Chronic defects in PI(3)P synthesis are linked to reductions in dendritic spine density, reactive gliosis, and progressive neurodegeneration.

    “Chronic defects in PI(3)P synthesis are linked to reductions in dendritic spine density, reactive gliosis, and progressive neurodegeneration”

    From PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity (2025) · cites this paper as Zhou et al., 2010

    The Results report that Pik3c3 deletion depleted PI3P and caused progressive degeneration of sensory neurons, but describe that degeneration as rapid, occurring within days. The paper does not report reduced dendritic spine density. Its observation of activated astrocytes and microglia concerns aged Atg7-deficient mice, not the Pik3c3-deficient mice used to study PI3P depletion. (LLM, conf=0.90)

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Research works printed but not linked: 41

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Metadata

Authors
Zhou, X., Wang, L., Hasegawa, H., Amin, P., Han, B.-X., Kaneko, S., He, Y., & Wang, F.
Affiliations
  • Department of Cell Biology, Duke University Medical Center, Durham, NC 27710;
  • Department of Orthopaedic Surgery, Keio University School of Medicine, 160-8582 Tokyo, Japan;
  • Department of Immunology, Duke University Medical Center, Durham, NC 27710
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2010-05-03
Volume
107
Issue
20
Pages
9424-9429
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.0914725107
Cited by
247
References
8
Language
en

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