Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease

Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease

Mitochondria-lysosome contact sites mediate cross-talk between the two organelles. Here, the authors show mitochondria-lysosome contacts are prolonged and defective in heterozygous mutant GBA1 neurons, which is caused by defective modulation of TBC1D15 due to decreased GBA1 activity.

Bibliographic Details
Main Authors: Soojin Kim, Yvette C. Wong, Fanding Gao, Dimitri Krainc
Format: Article
Language:English
Published: Nature Publishing Group 2021-03-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-021-22113-3
Description
Summary:Mitochondria-lysosome contact sites mediate cross-talk between the two organelles. Here, the authors show mitochondria-lysosome contacts are prolonged and defective in heterozygous mutant GBA1 neurons, which is caused by defective modulation of TBC1D15 due to decreased GBA1 activity.
ISSN:2041-1723

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