ArticleMolecular biology of the cell2013
Ndufaf5 deficiency in the Dictyostelium model: new roles in autophagy and development.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- Genome-wide association study identifies genetic variants associated with single-parity reproductive loss in three commercial pig breeds.BMC genomics · 2025Article
- Targeting lncRNA16 by GalNAc-siRNA conjugates facilitates chemotherapeutic sensibilization via the HBB/NDUFAF5/ROS pathway.Science China. Life sciences · 2024Article
- Plate-Based Assays for the Characterization of Mitochondrial and Cellular Phenotypes.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Methylarginine efflux in nutrient-deprived yeast mitigates disruption of nitric oxide synthesis.Amino acids · 2023Article
- A Leigh syndrome caused by compound heterozygous mutations on NDUFAF5 induce early infant death: A case report.Molecular genetics & genomic medicine · 2022Article
- Blackout in the powerhouse: clinical phenotypes associated with defects in the assembly of OXPHOS complexes and the mitoribosome.The Biochemical journal · 2020Review
- Comparative transcriptome analysis in the hepatopancreas of Helice tientsinensis exposed to the toxic metal cadmium.Genes & genomics · 2019Article
- Methods to Monitor and Quantify Autophagy in the Social Amoeba Dictyostelium discoideum.Cells · 2017Review
- Autophagy in Dictyostelium: Mechanisms, regulation and disease in a simple biomedical model.Autophagy · 2017Review
- NDUFAF5 Hydroxylates NDUFS7 at an Early Stage in the Assembly of Human Complex I.The Journal of biological chemistry · 2016Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Ndufaf5 (also known as C20orf7) is a mitochondrial complex I (CI) assembly factor whose mutations lead to human mitochondrial disease. Little is known about the function of the protein and the cytopathological consequences of the mutations. Disruption of Dictyostelium Ndufaf5 leads to CI deficiency and defects in growth and development. The predicted sequence of Ndufaf5 contains a putative methyltransferase domain. Site-directed mutagenesis indicates that the methyltransferase motif is essential for its function. Pathological mutations were recreated in the Dictyostelium protein and expressed in the mutant background. These proteins were unable to complement the phenotypes, which further validates Dictyostelium as a model of the disease. Chronic activation of AMP-activated protein kinase (AMPK) has been proposed to play a role in Dictyostelium and human cytopathology in mitochondrial diseases. However, inhibition of the expression of AMPK gene in the Ndufaf5-null mutant does not rescue the phenotypes associated with the lack of Ndufaf5, suggesting that novel AMPK-independent pathways are responsible for Ndufaf5 cytopathology. Of interest, the Ndufaf5-deficient strain shows an increase in autophagy. This phenomenon was also observed in a Dictyostelium mutant lacking MidA (C2orf56/PRO1853/Ndufaf7), another CI assembly factor, suggesting that autophagy activation might be a common feature in mitochondrial CI dysfunction.
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