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1. The Ca2+/Mn2+ ion-pump PMR1 links elevation of cytosolic Ca2+ levels to α-synuclein toxicity in Parkinson’s disease models

Author

Büttner, S, primary, Faes, L, additional, Reichelt, W N, additional, Broeskamp, F, additional, Habernig, L, additional, Benke, S, additional, Kourtis, N, additional, Ruli, D, additional, Carmona-Gutierrez, D, additional, Eisenberg, T, additional, D'hooge, P, additional, Ghillebert, R, additional, Franssens, V, additional, Harger, A, additional, Pieber, T R, additional, Freudenberger, P, additional, Kroemer, G, additional, Sigrist, S J, additional, Winderickx, J, additional, Callewaert, G, additional, Tavernarakis, N, additional, and Madeo, F, additional

Published
2012
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2. The Ca2+/Mn2+ ion-pump PMR1 links elevation of cytosolic Ca2+ levels to α-synuclein toxicity in Parkinson's disease models.

Author

Büttner, S, Faes, L, Reichelt, W N, Broeskamp, F, Habernig, L, Benke, S, Kourtis, N, Ruli, D, Carmona-Gutierrez, D, Eisenberg, T, D'hooge, P, Ghillebert, R, Franssens, V, Harger, A, Pieber, T R, Freudenberger, P, Kroemer, G, Sigrist, S J, Winderickx, J, and Callewaert, G

Subjects
PARKINSON'S disease, DOPAMINERGIC neurons, SYNUCLEINS, GENE expression, DOPAMINERGIC mechanisms, PHYSIOLOGICAL control systems, EDIBLE fungi
Abstract

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons, which arises from a yet elusive concurrence between genetic and environmental factors. The protein α-synuclein (αSyn), the principle toxic effector in PD, has been shown to interfere with neuronal Ca2+ fluxes, arguing for an involvement of deregulated Ca2+ homeostasis in this neuronal demise. Here, we identify the Golgi-resident Ca2+/Mn2+ ATPase PMR1 (plasma membrane-related Ca2+-ATPase 1) as a phylogenetically conserved mediator of αSyn-driven changes in Ca2+ homeostasis and cytotoxicity. Expression of αSyn in yeast resulted in elevated cytosolic Ca2+ levels and increased cell death, both of which could be inhibited by deletion of PMR1. Accordingly, absence of PMR1 prevented αSyn-induced loss of dopaminergic neurons in nematodes and flies. In addition, αSyn failed to compromise locomotion and survival of flies when PMR1 was absent. In conclusion, the αSyn-driven rise of cytosolic Ca2+ levels is pivotal for its cytotoxicity and requires PMR1. [ABSTRACT FROM AUTHOR]

Published
2013
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3. The Ca2+/Mn2+ ion-pump PMR1 links elevation of cytosolic Ca(2+) levels to α-synuclein toxicity in Parkinson's disease models.

Author

Büttner S, Faes L, Reichelt WN, Broeskamp F, Habernig L, Benke S, Kourtis N, Ruli D, Carmona-Gutierrez D, Eisenberg T, D'hooge P, Ghillebert R, Franssens V, Harger A, Pieber TR, Freudenberger P, Kroemer G, Sigrist SJ, Winderickx J, Callewaert G, Tavernarakis N, and Madeo F

Subjects
Acetylcysteine pharmacology, Animals, Apoptosis, Caenorhabditis elegans metabolism, Caenorhabditis elegans Proteins genetics, Caenorhabditis elegans Proteins metabolism, Calcium-Transporting ATPases deficiency, Calcium-Transporting ATPases genetics, Humans, Manganese metabolism, Molecular Chaperones, Oxidative Stress, Parkinson Disease metabolism, Parkinson Disease pathology, Phosphorylation, Promoter Regions, Genetic, RNA Interference, RNA, Small Interfering metabolism, Saccharomyces cerevisiae drug effects, Saccharomyces cerevisiae metabolism, Saccharomyces cerevisiae Proteins genetics, alpha-Synuclein genetics, alpha-Synuclein toxicity, Calcium metabolism, Calcium-Transporting ATPases metabolism, Models, Biological, Saccharomyces cerevisiae Proteins metabolism, alpha-Synuclein metabolism
Abstract

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons, which arises from a yet elusive concurrence between genetic and environmental factors. The protein α-synuclein (αSyn), the principle toxic effector in PD, has been shown to interfere with neuronal Ca(2+) fluxes, arguing for an involvement of deregulated Ca(2+) homeostasis in this neuronal demise. Here, we identify the Golgi-resident Ca(2+)/Mn(2+) ATPase PMR1 (plasma membrane-related Ca(2+)-ATPase 1) as a phylogenetically conserved mediator of αSyn-driven changes in Ca(2+) homeostasis and cytotoxicity. Expression of αSyn in yeast resulted in elevated cytosolic Ca(2+) levels and increased cell death, both of which could be inhibited by deletion of PMR1. Accordingly, absence of PMR1 prevented αSyn-induced loss of dopaminergic neurons in nematodes and flies. In addition, αSyn failed to compromise locomotion and survival of flies when PMR1 was absent. In conclusion, the αSyn-driven rise of cytosolic Ca(2+) levels is pivotal for its cytotoxicity and requires PMR1.

Published
2013
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