ArticleProceedings of the National Academy of Sciences of the United States of America2008
Mitochondrial localization of human frataxin is necessary but processing is not for rescuing frataxin deficiency in Trypanosoma brucei.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 39 citations in OpenAlex.
- Protoporphyrin IX Binds to Iron(II)-Loaded and to Zinc-Loaded Human Frataxin.Life (Basel, Switzerland) · 2023Article
- Article
- Determinism and contingencies shaped the evolution of mitochondrial protein import.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Branched late-steps of the cytosolic iron-sulphur cluster assembly machinery of Trypanosoma brucei.PLoS pathogens · 2018Article
- Impact ofInternational journal of molecular sciences · 2018Review
- Fe-S cluster assembly in the supergroup Excavata.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018Review
- Trypanosomal mitochondrial intermediate peptidase does not behave as a classical mitochondrial processing peptidase.PloS one · 2018Article
- Development of a toolbox to dissect host-endosymbiont interactions and protein trafficking in the trypanosomatid Angomonas deanei.BMC evolutionary biology · 2016Article
- Mitochondrial protein import receptors in Kinetoplastids reveal convergent evolution over large phylogenetic distances.Nature communications · 2015Article
- Mitochondrial and nucleolar localization of cysteine desulfurase Nfs and the scaffold protein Isu in Trypanosoma brucei.Eukaryotic cell · 2014Article
- IRONy OF FATE: role of iron-mediated ROS in Leishmania differentiation.Trends in parasitology · 2013Review
- An Advanced System of the Mitochondrial Processing Peptidase and Core Protein Family in Trypanosoma brucei and Multiple Origins of the Core I Subunit in Eukaryotes.Genome biology and evolution · 2013Article
- Euglena gracilis and Trypanosomatids possess common patterns in predicted mitochondrial targeting presequences.Journal of molecular evolution · 2012Article
- Evolution of Fe/S cluster biogenesis in the anaerobic parasite Blastocystis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Trypanosomes and the solution to a 50-year mitochondrial calcium mystery.Trends in parasitology · 2012Review
- Article
- Friedreich's ataxia variants I154F and W155R diminish frataxin-based activation of the iron-sulfur cluster assembly complex.Biochemistry · 2011Article
- Normal and Friedreich ataxia cells express different isoforms of frataxin with complementary roles in iron-sulfur cluster assembly.The Journal of biological chemistry · 2010Article
- The Trypanosoma brucei MitoCarta and its regulation and splicing pattern during development.Nucleic acids research · 2010Article
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4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma brucei, the agent of human sleeping sickness and ruminant nagana, is the most genetically tractable representative of the domain Excavata. It is evolutionarily very distant from humans, with a last common ancestor over 1 billion years ago. Frataxin, a highly conserved small protein involved in iron-sulfur cluster synthesis, is present in both organisms, and its deficiency is responsible for Friedreich's ataxia in humans. We have found that T. brucei growth-inhibition phenotype caused by down-regulated frataxin is rescued by means of human frataxin. The rescue is fully dependent on the human frataxin being imported into the trypanosome mitochondrion. Processing of the imported protein by mitochondrial processing peptidase can be blocked by mutations in the signal peptide, as in human cells. Although in human cells frataxin must be processed to execute its function, the same protein in the T. brucei mitochondrion is functional even in the absence of processing. Our results illuminate remarkable conservation of the mechanisms of mitochondrial protein import and processing.
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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.