FBXO7 and Parkin-Dependent Mitophagy

This repository contains scripts and analysis files related to the study:

FBXO7/PARK15 is dispensable for canonical mitophagy
Kraus et al., EMBO Reports (2023)
📄 Published paper
📝 Preprint (bioRxiv)
🧪 Experimental protocol

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🔬 Abstract

The protein kinase PINK1 and ubiquitin ligase Parkin promote removal of damaged mitochondria via a feed‐forward mechanism involving ubiquitin phosphorylation (pUb), Parkin activation, and ubiquitylation of mitochondrial outer membrane proteins. FBXO7/PARK15, a substrate receptor mutated in early-onset parkinsonian–pyramidal syndrome, was proposed to support Parkin-dependent mitophagy. Using HeLa and induced neuron (iN) models, we find that FBXO7 knockout cells show no measurable defects in pUb kinetics, Parkin recruitment, mitophagic flux, or mitochondrial clearance. Proteomic profiling during neurogenesis in FBXO7−/− cells also reveals no clear alterations in mitochondria or other organelles. These results suggest FBXO7 is not generally required for canonical Parkin-mediated mitophagy.

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📁 Repository structure

• GFP-Parkin eval/: ImageJ and CellProfiler pipelines for Parkin translocation
• mtDNA/, p62eval/, pUb-mito coloc/: Quantification of mitophagy markers
• iN morphology/: Neuronal morphology quantification
• Imaris-FBXO7pUbHSP60evals.rtfd/: Imaris snapshots and processed figure panels

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