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PARKIN is not required to sustain OXPHOS function in adult mammalian tissues

GSE263057 Mus musculus (mouse) RNA-seq (gene expression) 142 samples Submitted 2024/04/03 Platform GPL17021
At a glance

RNA-seq (gene expression) · mouse · 142 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
142 samples: 30 conditions, mostly with about 5 replicates eachGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
PARKIN is not required to sustain OXPHOS function in adult mammalian tissuesNPJ Parkinson's disease · 2024
Summary (written by the submitters)
Loss-of-function variants in the PRKN gene encoding the ubiquitin E3 ligase PARKIN cause autosomal recessive early-onset Parkinson’s disease (PD). Extensive in vitro and in vivo studies have reported that PARKIN is involved in multiple pathways of mitochondrial quality control, including mitochondrial degradation and biogenesis. However, these findings are surrounded by substantial controversy due to conflicting experimental data.
Read the full summary ↓
In addition, the existing PARKIN-deficient mouse models have failed to faithfully recapitulate PD phenotypes. Therefore, we have investigated the mitochondrial role of PARKIN during ageing and in response to stress by employing a series of conditional Parkin knockout mice. We report that PARKIN loss does not affect oxidative phosphorylation (OXPHOS) capacity and mitochondrial DNA (mtDNA) levels in the brain, heart, and skeletal muscle of aged mice. We also demonstrate that PARKIN deficiency does not exacerbate the brain defects and the pro-inflammatory phenotype observed in mice carrying high levels of mtDNA mutations. To rule out compensatory mechanisms activated during embryonic development of Parkin-deficient mice, we generated a mouse model where loss of PARKIN was induced in adult dopaminergic (DA) neurons. Surprisingly, also these mice did not show motor impairment or neurodegeneration, and no major transcriptional changes were found in isolated midbrain DA neurons. Finally, we report a patient with compound heterozygous PRKN pathogenic variants that lacks PARKIN and has developed PD. The PARKIN deficiency did not impair OXPHOS activities or induce mitochondrial pathology in skeletal muscle from the patient. Altogether, our results argue that PARKIN is dispensable for OXPHOS function in adult mammalian tissues.
Published in
PARKIN is not required to sustain OXPHOS function in adult mammalian tissues
Filograna R, Gerlach J, Choi HN et al. · NPJ Parkinson's disease 2024 · PMID 38684669 · doi:10.1038/s41531-024-00707-0
This dataset
Open GSE263057 in finder → Find more mouse RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE263057_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1095524 and SRA study SRP499396. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38684669) ↗
Study design
30 conditions, mostly with about 5 replicates each
DA neurons, Control_1609_P ×8 DA neurons, Control_B553_P ×8 DA neurons, Control_B548_P ×7 DA neurons, Control_1472_P ×6 DA neurons, Control_1474_P ×6 DA neurons, Parkin_1601_P ×6 DA neurons, Parkin_1608_P ×6 DA neurons, Parkin_1639_P ×6 +23 more

Supports a between-group comparison across 141 samples.

How we read this: 30 replicated groups read from 142 sample titles; they account for 141 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 102 more — browse all 142 samples with per-sample file links →

Datasets on a similar topic

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