Altered ER-mitochondria contact impacts mitochondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models.

ABSTRACT: Calcium (Ca²⁺) homeostasis is essential for neuronal function and survival. Altered Ca²⁺ homeostasis has been consistently observed in neurological diseases. How Ca²⁺ homeostasis is achieved in various cellular compartments of disease-relevant cell types is not well understood. Here we show in Drosophila Parkinson's disease (PD) models that Ca²⁺ transport from the endoplasmic reticulum (ER) to mitochondria through the ER-mitochondria contact site (ERMCS) critically regulates mitochondrial Ca²⁺ (mito-Ca²⁺) homeostasis in dopaminergic (DA) neurons, and that the PD-associated PINK1 protein modulates this process. In PINK1 mutant DA neurons, the ERMCS is strengthened and mito-Ca²⁺ level is elevated, resu

SUBMITTER: Lee KS 

PROVIDER: S-EPMC6156612 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature