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

Soojin Kim; Yvette C. Wong; Fanding Gao; Dimitri Krainc

doi:10.1038/s41467-021-22113-3

Nature Communications (Mar 2021)

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

Soojin Kim,
Yvette C. Wong,
Fanding Gao,
Dimitri Krainc

Affiliations

Soojin Kim: Department of Neurology, Northwestern University Feinberg School of Medicine
Yvette C. Wong: Department of Neurology, Northwestern University Feinberg School of Medicine
Fanding Gao: Department of Neurology, Northwestern University Feinberg School of Medicine
Dimitri Krainc: Department of Neurology, Northwestern University Feinberg School of Medicine

DOI: https://doi.org/10.1038/s41467-021-22113-3
Journal volume & issue: Vol. 12, no. 1
pp. 1 – 14

Abstract

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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.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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