ArticleEukaryotic cell2009
Downregulation of mitochondrial porin inhibits cell growth and alters respiratory phenotype in Trypanosoma brucei.
Article in Eukaryotic cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Down the membrane hole: Ion channels in protozoan parasites.PLoS pathogens · 2022Review
- Intracellular CaInternational journal of molecular sciences · 2021Review
- Novel IM-associated protein Tim54 plays a role in the mitochondrial import of internal signal-containing proteins in Trypanosoma brucei.Biology of the cell · 2021Article
- Isolation and Characterization of Acidocalcisomes from Trypanosomatids.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Article
- Divergent Small Tim Homologues Are Associated with TbTim17 and Critical for the Biogenesis of TbTim17 Protein Complexes inmSphere · 2018Article
- RNA-Seq analysis validates the use of culture-derived Trypanosoma brucei and provides new markers for mammalian and insect life-cycle stages.BMC genomics · 2018Article
- Acidocalcisome-Mitochondrion Membrane Contact Sites in Trypanosoma brucei.Pathogens (Basel, Switzerland) · 2018Article
- The divergent N-terminal domain of Tim17 is critical for its assembly in the TIM complex in Trypanosoma brucei.Molecular and biochemical parasitology · 2017Article
- HJournal of bioenergetics and biomembranes · 2017Article
- CRISPR/Cas9-mediated endogenous C-terminal Tagging of Trypanosoma cruzi Genes Reveals the Acidocalcisome Localization of the Inositol 1,4,5-Trisphosphate Receptor.The Journal of biological chemistry · 2016Article
- Tim62, a Novel Mitochondrial Protein in Trypanosoma brucei, Is Essential for Assembly and Stability of the TbTim17 Protein Complex.The Journal of biological chemistry · 2015Article
- Functional complementation analyses reveal that the single PRAT family protein of trypanosoma brucei is a divergent homolog of Tim17 in saccharomyces cerevisiae.Eukaryotic cell · 2015Article
- Trypanosome alternative oxidase possesses both an N-terminal and internal mitochondrial targeting signal.Eukaryotic cell · 2014Article
- Tim50 in Trypanosoma brucei possesses a dual specificity phosphatase activity and is critical for mitochondrial protein import.The Journal of biological chemistry · 2013Article
- Identification of two voltage-dependent anion channel-like protein sequences conserved in Kinetoplastida.Biology letters · 2012Article
- Protein translocase of mitochondrial inner membrane in Trypanosoma brucei.The Journal of biological chemistry · 2012Article
- Trypanosomes and the solution to a 50-year mitochondrial calcium mystery.Trends in parasitology · 2012Review
- (-)-Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle.The Journal of physiology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Porin is the most abundant outer membrane (OM) protein of mitochondria. It forms the aqueous channel on the mitochondrial OM and mediates major metabolite flux between mitochondria and cytosol. Mitochondrial porin in Trypanosoma brucei, a unicellular parasitic protozoan and the causative agent of African trypanosomiasis, possesses a beta-barrel structure similar to the bacterial OM porin OmpA. T. brucei porin (TbPorin) is present as a monomer as well as an oligomer on the mitochondrial OM, and its expression is developmentally regulated. In spite of its distinct structure, the TbPorin function is similar to those of other eukaryotic porins. TbPorin RNA interference (RNAi) reduced cell growth in both procyclic and bloodstream forms. The depletion of TbPorin decreased ATP production by inhibiting metabolite flux through the OM. Additionally, the level of trypanosome alternative oxidase (TAO) decreased, whereas the levels of cytochrome-dependent respiratory complexes III and IV increased in TbPorin-depleted mitochondria. Furthermore, the depletion of TbPorin reduced cellular respiration via TAO, which is not coupled with oxidative phosphorylation, but increased the capacity for cyanide-sensitive respiration. Together, these data reveal that TbPorin knockdown reduced the mitochondrial ATP level, which in turn increased the capacity of the cytochrome-dependent respiratory pathway (CP), in an attempt to compensate for the mitochondrial energy crisis. However, a simultaneous decrease in the substrate-level phosphorylation due to TbPorin RNAi caused growth inhibition in the procyclic form. We also found that the expressions of TAO and CP proteins are coordinately regulated in T. brucei according to mitochondrial energy demand.
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