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Proteomic and functional data sets on synaptic mitochondria from rats with genetic ablation of Parkin.

ABSTRACT: In this paper, we provide proteomic and functional data for synaptic mitochondria from the striatum of rats with Parkin ablation. The quantitative proteomic data was obtained using SWATH-MS methodology and mitochondrial function was assessed through measurement of oxygen consumption rate using the Seahorse XF Analyzer. This data facilitates comparisons with previous proteomic and functional data obtained using the exact same methods. A complete set of proteomic data is contained in Supplementary Table 1.

SUBMITTER: Villeneuve LM

PROVIDER: S-EPMC6126403 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Proteomic and functional data sets on synaptic mitochondria from rats with genetic ablation of <i>Parkin</i>.

Villeneuve Lance M LM Stauch Kelly L KL Purnell Phillip S PS Fox Howard S HS

Data in brief 20180828

In this paper, we provide proteomic and functional data for synaptic mitochondria from the striatum of rats with <i>Parkin</i> ablation. The quantitative proteomic data was obtained using SWATH-MS methodology and mitochondrial function was assessed through measurement of oxygen consumption rate using the Seahorse XF Analyzer. This data facilitates comparisons with previous proteomic and functional data obtained using the exact same methods. A complete set of proteomic data is contained in Supple ...[more]

PMID: 30197913

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Project description:BackgroundNeurons are highly polarized cells consisting of three distinct functional domains: the cell body (and associated dendrites), the axon and the synapse. Previously, it was believed that the clinical phenotypes of neurodegenerative diseases were caused by the loss of entire neurons, however it has recently become apparent that these neuronal sub-compartments can degenerate independently, with synapses being particularly vulnerable to a broad range of stimuli. Whilst the properties governing the differential degenerative mechanisms remain unknown, mitochondria consistently appear in the literature, suggesting these somewhat promiscuous organelles may play a role in affecting synaptic stability. Synaptic and non-synaptic mitochondrial subpools are known to have different enzymatic properties (first demonstrated by Lai et al., 1977). However, the molecular basis underpinning these alterations, and their effects on morphology, has not been well documented.MethodsThe current study has employed electron microscopy, label-free proteomics and in silico analyses to characterize the morphological and biochemical properties of discrete sub-populations of mitochondria. The physiological relevance of these findings was confirmed in-vivo using a molecular genetic approach at the Drosophila neuromuscular junction.ResultsHere, we demonstrate that mitochondria at the synaptic terminal are indeed morphologically different to non-synaptic mitochondria, in both rodents and human patients. Furthermore, generation of proteomic profiles reveals distinct molecular fingerprints - highlighting that the properties of complex I may represent an important specialisation of synaptic mitochondria. Evidence also suggests that at least 30% of the mitochondrial enzymatic activity differences previously reported can be accounted for by protein abundance. Finally, we demonstrate that the molecular differences between discrete mitochondrial sub-populations are capable of selectively influencing synaptic morphology in-vivo. We offer several novel mitochondrial candidates that have the propensity to significantly alter the synaptic architecture in-vivo.ConclusionsOur study demonstrates discrete proteomic profiles exist dependent upon mitochondrial subcellular localization and selective alteration of intrinsic mitochondrial proteins alters synaptic morphology in-vivo.

Dataset Information

Proteomic and functional data sets on synaptic mitochondria from rats with genetic ablation of Parkin.

Publications

Proteomic and functional data sets on synaptic mitochondria from rats with genetic ablation of <i>Parkin</i>.

Similar Datasets

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