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Analysis of neuronal phosphoproteome reveals PINK1 regulation of BAD function and cell death

ABSTRACT: We interrogated whether there existed a broader effect of PINK1-dependent phosphorylation after mitochondrial damage by utilizing primary cultured neurons from WT and Pink1 KO mice. Because persistent depolarization leads to mitochondrial damage {}, we treated cultured neurons with the protonophore carbonyl cyanide m-chlorophenyl hydrazine (CCCP) and blotted for PINK1. Consistent with previous studies, CCCP treatment results in an upregulation of endogenous PINK1 in WT neurons. Endogenous PINK1 is undetectable in Pink1 KO neurons with CCCP treatment.Overall, our phosphoproteome analysis of biological duplicates experiments quantified 10930 and 7207 phosphorylation sites, respectively, from the early (designated as 15-45 min) and late (designated as 2-6 hr) treatment time points

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Lujian Liao

PROVIDER: MSV000080923 | MassIVE | Fri Apr 14 05:43:00 BST 2017

SECONDARY ACCESSION(S): PXD006304

REPOSITORIES: MassIVE

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Analysis of phosphoproteome reveals PINK1 regulation of BAD function and cell death

Project description:We interrogated whether there existed a broader effect of PINK1-dependent phosphorylation after mitochondrial damage by utilizing primary cultured neurons from WT and Pink1 KO mice. Because persistent depolarization leads to mitochondrial damage, we treated cultured neurons with the protonophore carbonyl cyanide m-chlorophenyl hydrazine (CCCP) and blotted for PINK1. Overall, our phosphoproteome analysis of biological duplicates experiments quantified 10930 and 7207 phosphorylation sites, respectively, from the early (designated as 15-45 min) and late (designated as 2-6 hr) treatment time points.

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