ArticleNature communications2022
Maintenance of mitochondrial integrity in midbrain dopaminergic neurons governed by a conserved developmental transcription factor.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Intrinsic and non-cell-autonomous roles for the neurodevelopmental syndrome-linked transcription factor UNC-3/EBF.Nature communications · 2026Article
- Transcription Factor Evolution Associated with Social Transitions in Blattodea.Journal of molecular evolution · 2026Article
- Intrinsic and non-cell autonomous roles for a neurodevelopmental syndrome-linked transcription factor.bioRxiv : the preprint server for biology · 2025Article
- Lysosomal TFEB-TRPML1 Axis in Astrocytes Modulates Depressive-like Behaviors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The lncRNA lnc_AABR07044470.1 promotes the mitochondrial-damaged inflammatory response to neuronal injury via miR-214-3p/PERM1 axis in acute ischemic stroke.Molecular biology reports · 2024Article
- Article
- Circadian clock disruption promotes the degeneration of dopaminergic neurons in male Drosophila.Nature communications · 2023Article
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive degeneration of dopaminergic (DA) neurons in the substantia nigra is a hallmark of Parkinson's disease (PD). Dysregulation of developmental transcription factors is implicated in dopaminergic neurodegeneration, but the underlying molecular mechanisms remain largely unknown. Drosophila Fer2 is a prime example of a developmental transcription factor required for the birth and maintenance of midbrain DA neurons. Using an approach combining ChIP-seq, RNA-seq, and genetic epistasis experiments with PD-linked genes, here we demonstrate that Fer2 controls a transcriptional network to maintain mitochondrial structure and function, and thus confers dopaminergic neuroprotection against genetic and oxidative insults. We further show that conditional ablation of Nato3, a mouse homolog of Fer2, in differentiated DA neurons causes mitochondrial abnormalities and locomotor impairments in aged mice. Our results reveal the essential and conserved role of Fer2 homologs in the mitochondrial maintenance of midbrain DA neurons, opening new perspectives for modeling and treating PD.
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