ArticleCell death and differentiation2016
Loss of Drosophila i-AAA protease, dYME1L, causes abnormal mitochondria and apoptotic degeneration.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Mitochondrial proteases maintain cellular protein homeostasis and tissue integrity.Cell & bioscience · 2026Article
- Mitochondrial proteases and their roles in mitophagy in plants, animals, and yeast.Plant & cell physiology · 2025Review
- NADH:ubiquinone oxidoreductase core subunit S8 expression and functional significance in non-small cell lung cancer.Cell death & disease · 2025Article
- Mitochondrial AAAFrontiers in cell and developmental biology · 2025Article
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024Review
- Review
- Association Between L-OPA1 Cleavage and Cardiac Dysfunction During Ischemia-Reperfusion Injury in Rats.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020Article
- Inactivation of the mitochondrial protease Afg3l2 results in severely diminished respiratory chain activity and widespread defects in mitochondrial gene expression.PLoS genetics · 2020Article
- Article
- Inactivation of Lon protease reveals a link between mitochondrial unfolded protein stress and mitochondrial translation inhibition.Cell death & disease · 2018Article
- Article
- Article
- Review
- Mutations of mitochondrial DNA are not major contributors to aging of fruit flies.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Overexpression of antimicrobial peptides contributes to aging through cytotoxic effects in Drosophila tissues.Archives of insect biochemistry and physiology · 2018Article
- Thin is required for cell death in the Drosophila abdominal muscles by targeting DIAP1.Cell death & disease · 2018Article
- Loss of the Drosophila m-AAA mitochondrial protease paraplegin results in mitochondrial dysfunction, shortened lifespan, and neuronal and muscular degeneration.Cell death & disease · 2018Article
- Lon protease inactivation inCell death discovery · 2018Article
- Coordinating Mitochondrial Biology Through the Stress-Responsive Regulation of Mitochondrial Proteases.International review of cell and molecular biology · 2018Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondrial AAA (ATPases Associated with diverse cellular Activities) proteases i-AAA (intermembrane space-AAA) and m-AAA (matrix-AAA) are closely related and have major roles in inner membrane protein homeostasis. Mutations of m-AAA proteases are associated with neuromuscular disorders in humans. However, the role of i-AAA in metazoans is poorly understood. We generated a deletion affecting Drosophila i-AAA, dYME1L (dYME1L(del)). Mutant flies exhibited premature aging, progressive locomotor deficiency and neurodegeneration that resemble some key features of m-AAA diseases. dYME1L(del) flies displayed elevated mitochondrial unfolded protein stress and irregular cristae. Aged dYME1L(del) flies had reduced complex I (NADH/ubiquinone oxidoreductase) activity, increased level of reactive oxygen species (ROS), severely disorganized mitochondrial membranes and increased apoptosis. Furthermore, inhibiting apoptosis by targeting dOmi (Drosophila Htra2/Omi) or DIAP1, or reducing ROS accumulation suppressed retinal degeneration. Our results suggest that i-AAA is essential for removing unfolded proteins and maintaining mitochondrial membrane architecture. Loss of i-AAA leads to the accumulation of oxidative damage and progressive deterioration of membrane integrity, which might contribute to apoptosis upon the release of proapoptotic molecules such as dOmi. Containing ROS level could be a potential strategy to manage mitochondrial AAA protease deficiency.
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Registered trials
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