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
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spelling doaj-40982e38dcd44c1f9dff1e73b1f33d9a2021-03-28T11:11:33ZengNature Publishing GroupNature Communications2041-17232021-03-0112111410.1038/s41467-021-22113-3Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s diseaseSoojin Kim0Yvette C. Wong1Fanding Gao2Dimitri Krainc3Department of Neurology, Northwestern University Feinberg School of MedicineDepartment of Neurology, Northwestern University Feinberg School of MedicineDepartment of Neurology, Northwestern University Feinberg School of MedicineDepartment of Neurology, Northwestern University Feinberg School of MedicineMitochondria-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.https://doi.org/10.1038/s41467-021-22113-3
collection DOAJ
language English
format Article
sources DOAJ
author Soojin Kim
Yvette C. Wong
Fanding Gao
Dimitri Krainc
spellingShingle Soojin Kim
Yvette C. Wong
Fanding Gao
Dimitri Krainc
Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
Nature Communications
author_facet Soojin Kim
Yvette C. Wong
Fanding Gao
Dimitri Krainc
author_sort Soojin Kim
title Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
title_short Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
title_full Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
title_fullStr Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
title_full_unstemmed Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson’s disease
title_sort dysregulation of mitochondria-lysosome contacts by gba1 dysfunction in dopaminergic neuronal models of parkinson’s disease
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2021-03-01
description 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.
url https://doi.org/10.1038/s41467-021-22113-3
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AT yvettecwong dysregulationofmitochondrialysosomecontactsbygba1dysfunctionindopaminergicneuronalmodelsofparkinsonsdisease
AT fandinggao dysregulationofmitochondrialysosomecontactsbygba1dysfunctionindopaminergicneuronalmodelsofparkinsonsdisease
AT dimitrikrainc dysregulationofmitochondrialysosomecontactsbygba1dysfunctionindopaminergicneuronalmodelsofparkinsonsdisease
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