ArticlePLoS genetics2018
Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in zebrafish.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- In and out of the mitochondrial intermembrane space.Protein science : a publication of the Protein Society · 2026Review
- Secreted novel AID/APOBEC-like deaminase 1 (SNAD1) - a new important player in fish immunology.Frontiers in immunology · 2024Review
- Article
- Profiling subcellular localization of nuclear-encoded mitochondrial gene products in zebrafish.Life science alliance · 2023Article
- Transgenic fluorescent zebrafish lines that have revolutionized biomedical research.Laboratory animal research · 2021Review
- CHCHD4 (MIA40) and the mitochondrial disulfide relay system.Biochemical Society transactions · 2021Review
- Early sarcomere and metabolic defects in a zebrafishProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Correction: Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in zebrafish.PLoS genetics · 2019Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development and function of tissues and organs are powered by the activity of mitochondria. In humans, inherited genetic mutations that lead to progressive mitochondrial pathology often manifest during infancy and can lead to death, reflecting the indispensable nature of mitochondrial biogenesis and function. Here, we describe a zebrafish mutant for the gene mia40a (chchd4a), the life-essential homologue of the evolutionarily conserved Mia40 oxidoreductase which drives the biogenesis of cysteine-rich mitochondrial proteins. We report that mia40a mutant animals undergo progressive cellular respiration defects and develop enlarged mitochondria in skeletal muscles before their ultimate death at the larval stage. We generated a deep transcriptomic and proteomic resource that allowed us to identify abnormalities in the development and physiology of endodermal organs, in particular the liver and pancreas. We identify the acinar cells of the exocrine pancreas to be severely affected by mutations in the MIA pathway. Our data contribute to a better understanding of the molecular, cellular and organismal effects of mitochondrial deficiency, important for the accurate diagnosis and future treatment strategies of mitochondrial diseases.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.