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. 2011 Apr;7(4):445-7.
doi: 10.4161/auto.7.4.14682. Epub 2011 Apr 1.

Uncovering the role of Snapin in regulating autophagy-lysosomal function

Qian Cai  1 , Zu-Hang Sheng
Affiliations

Uncovering the role of Snapin in regulating autophagy-lysosomal function

Qian Cai et al. Autophagy. 2011 Apr.

Abstract

The autophagy-lysosomal system is the major degradation pathway essential for the maintenance and survival of neurons. This process requires efficient late endocytic transport from distal processes to the soma, in which lysosomes are predominantly localized. However, it is not clear how late endocytic transport has an impact upon neuronal autophagy-lysosomal function. We recently revealed that Snapin acts as a dynein motor adaptor and coordinates retrograde transport and late endosomal-lysosomal trafficking, thus maintaining efficient autophagy-lysosomal function in neurons. Snapin(-/-) neurons display impaired retrograde transport and clustering of late endosomes along neuronal processes, aberrant accumulation of immature lysosomes, and impaired clearance of autolysosomes. Snapin deficiency leads to reduced neuron viability, neurodegeneration, and developmental defects in the central nervous system. Reintroducing the snapin transgene rescues these phenotypes by enhancing the delivery of endosomal cargos to lysosomes and by facilitating autophagy-lysosomal function. Our study suggests that Snapin is a candidate molecular target for autophagy-lysosomal regulation.

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Figures

Figure 1
Figure 1
The model of Snapin in coordinating late endosomal transport and autophagy-lysosomal function in neurons. (A) Snapin serves as an adaptor of the dynein motor by interacting with dynein DIC and attaching to late endosomes (LE). (B) Snapin-dynein-mediated long-distance delivery of endocytosed proteins and target materials from distal processes to the soma, where lysosomes (lyso) are predominantly localized. Such a mechanism enables neurons to maintain efficient degradative capacities via the lysosomal system. (C) Snapin deletion impairs retrograde transport of late endosomes, resulting in late endosome clustering along processes, aberrant accumulation of immature lysosomes and autolysosomes in the soma, and reduced degradative capacity in the autophagy-lysosomal system. (Modified with permission from Cai Q, Lu L, Tian JT, Zhu YB, Qiao H, Sheng ZH. Snapin-regulated late endosomal transport is critical for efficient autophagy-lysosomal function in neurons, Neuron 2010; 68:73–86).
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References

    1. Neuron. 2010 Oct 6;68(1):73-86 - PubMed

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