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  • 1
    Electronic Resource
    Electronic Resource
    Mechanism of resistance of African trypanosomes to cytotoxic human HDL (1997)
    [s.l.] : Nature Publishing Group
    Nature 385 (1997), S. 823-826 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The human and animal diseases caused by subspecies of African trypanosomes are biochemically and morphologically indistinguishable14. Resistance to normal human serum is an unstable phenotype in T. b. rhodesiense because trypanosomes susceptible to lysis by human serum rapidly accumulate upon ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/385823a0
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of Hydroxyurea on Crithidia fasciculata (1979)
    Oxford, UK : Blackwell Publishing Ltd
    The @journal of eukaryotic microbiology 26 (1979), S. 0 
    Details
    ISSN: 1550-7408
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: SYNOPSIS Hydroxyurea (HU) inhibits increase in cell number in cultures of Crithidia fasciculata. Complete inhibition is produced by 8 mM and higher concentrations. If HU is not removed, population growth resumes in 45–50 h: if HU is removed, partially synchronous growth occurs through 2 cycles. During HU inhibition, the rate of DNA synthesis is reduced to 1% of that in exponentially growing cultures; protein and RNA syntheses continue at slightly reduced rates. Mean cell size and protein and RNA contents per cell increase; rate of oxygen consumption per mg cell protein remains constant. The behavior of a culture upon addition of HU and upon its removal agrees with predictions based on the hypothesis that the only direct effect of HU is to block DNA synthesis. The synchrony produced by HU is judged satisfactory for investigations of kinetoplast and nuclear replication but not for biochemical characterization of other aspects of the cell cycle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1550-7408.1979.tb04212.x
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  • 3
    Electronic Resource
    Electronic Resource
    Developmental regulation of mitochondrial biogenesis inTrypanosoma brucei (1994)
    Springer
    Journal of bioenergetics and biomembranes 26 (1994), S. 179-191 
    Details
    ISSN: 1573-6881
    Keywords: Kinetoplastid ; organelle ; cytochrome ; assembly
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract The metabolism ofTrypanosoma brucei undergoes a significant change as the parasite differentiates from the mammalian bloodstream form to the form found in the tse-tse fly vector. Because the mitochondria of bloodstream form cells lack cytochromes and several key citric acid cycle enzymes, the metabolism of these cells is mostly limited to glycolysis. The reducing equivalents generated by this process are passed to oxygen by a plantlike alternative oxidase. As cells differentiate to the insect form, they begin to oxidatively metabolize proline. The mitochondria of insect form cells contain functional, cytochromemediated electron transport chains and have complete complements of citric acid cycle enzymes. Although the characterization is far from complete, the nuclear and mitochondrial genes involved in the expression of these mitochondrial functions appear to be developmentally regulated at posttranscriptional and posttranslational levels. This review outlines some of the molecular processes that are associated with the developmental regulation of mitochondrial biogenesis and suggests some possible mechanisms of regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00763067
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  • 4
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    Light and electron microscopical observations of the effects of high-density lipoprotein on growth of Plasmodium falciparum in vitro (2005)
    Cambridge University Press
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © Cambridge University Press, 2004. This article is posted here by permission of Cambridge University Press for personal use, not for redistribution. The definitive version was published in Parasitology 128 (2004): 577-584, doi:10.1017/S0031182004005025.
    Description: Human serum high-density lipoprotein (HDL) is necessary and sufficient for the short-term maintenance of Plasmodium falciparum in in vitro culture. However, at high concentrations it is toxic to the parasite. A heat-labile component is apparently responsible for the stage-specific toxicity to parasites within infected erythrocytes 12–42 h after invasion, i.e. during trophozoite maturation. The effects of HDL on parasite metabolism (as determined by nucleic acid synthesis) are evident at about 30 h after invasion. Parasites treated with HDL show gross abnormalities by light and electron microscopy.
    Description: Professor Hajduk was supported by NIH. Professor Day was supported by a Research Leave Fellowship from The Wellcome Trust. Dr Imrie and Ms Carter were supported by Programme Grant funding awarded to Professor Day from The Wellcome Trust. Dr Ferguson was supported by an equipment grant from The Wellcome Trust.
    Keywords: Plasmodium falciparum ; High density lipoprotein
    Repository Name: Woods Hole Open Access Server
    Type: Article
    Format: 179037 bytes
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  • 5
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    Sequence motif within trypanosome precursor tRNAs influences abundance and mitochondrial localization (2005)
    American Society for Microbiology
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © American Society for Microbiology, 2003. This article is posted here by permission of American Society for Microbiology for personal use, not for redistribution. The definitive version was published in Molecular and Cellular Biology 23 (2003): 9061-9072, doi:10.1128/MCB.23.24.9061-9072.2003.
    Description: Trypanosoma brucei lacks mitochondrial genes encoding tRNAs and must import nuclearly encoded tRNAs from the cytosol. The mechanism and specificity of this process remain unclear. We have identified a unique sequence motif, YGG(C/A)RRC, upstream of the genes encoding mitochondrially localized tRNAs in T. brucei. Both in vitro import studies and in vivo transfection studies indicate that deletion of the YGG(C/A)RRC sequence alters mitochondrial localization of tRNALeu, and in vivo studies also show a decrease in the cellular abundance of tRNALeu. These studies provide direct evidence for cis-acting RNA motifs within precursor tRNAs that facilitate the selection of tRNAs for mitochondrial import in trypanosomes. Furthermore, we found that mutations to the YGG(C/A)RRC sequence also altered the intracellular distribution of other endogenous tRNAs, suggesting a general role for this sequence in tRNA trafficking in trypanosomes.
    Description: This work was supported by the National Institutes of Health grant AI21401 (to S.L.H.).
    Keywords: Trypanosoma brucei ; Mitochondrial localization
    Repository Name: Woods Hole Open Access Server
    Type: Article
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  • 6
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    Serum resistance-associated protein blocks lysosomal targeting of trypanosome lytic factor in Trypanosoma brucei (2006)
    American Society for Microbiology
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © American Society for Microbiology, 2006. This article is posted here by permission of American Society for Microbiology for personal use, not for redistribution. The definitive version was published in Eukaryotic Cell 5 (2006): 132-139, doi:10.1128/EC.5.1.132-139.2006.
    Description: Trypanosoma brucei brucei is the causative agent of nagana in cattle and can infect a wide range of mammals but is unable to infect humans because it is susceptible to the innate cytotoxic activity of normal human serum. A minor subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I (apoA-I), apolipoprotein L-I (apoL-I), and haptoglobin-related protein (Hpr) provides this innate protection against T. b. brucei infection. This HDL subfraction, called trypanosome lytic factor (TLF), kills T. b. brucei following receptor binding, endocytosis, and lysosomal localization. Trypanosoma brucei rhodesiense, which is morphologically and physiologically indistinguishable from T. b. brucei, is resistant to TLF-mediated killing and causes human African sleeping sickness. Human infectivity by T. b. rhodesiense correlates with the evolution of a resistance-associated protein (SRA) that is able to ablate TLF killing. To examine the mechanism of TLF resistance, we transfected T. b. brucei with an epitope-tagged SRA gene. Transfected T. b. brucei expressed SRA mRNA at levels comparable to those in T. b. rhodesiense and was highly resistant to TLF. In the SRA-transfected cells, intracellular trafficking of TLF was altered, with TLF being mainly localized to a subset of SRA-containing cytoplasmic vesicles but not to the lysosome. These results indicate that the cellular distribution of TLF is influenced by SRA expression and may directly determine the organism's susceptibility to TLF.
    Description: This research was supported by a grant from the NIH (AI39033) and support from the Ellison Medical Foundation.
    Repository Name: Woods Hole Open Access Server
    Type: Article
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  • 7
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    Human high density lipoproteins are platforms for the assembly of multi-component innate immune complexes (2009)
    American Society for Biochemistry and Molecular Biology
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © American Society for Biochemistry and Molecular Biology, 2005. This article is posted here by permission of American Society for Biochemistry and Molecular Biology for personal use, not for redistribution. The definitive version was published in Journal of Biological Chemistry 280 (2005): 32578-3258, doi:10.1074/jbc.M503510200.
    Description: Human innate immunity to non-pathogenic species of African trypanosomes is provided by human high density lipoprotein (HDL) particles. Here we show that native human HDLs containing haptoglobin-related protein (Hpr), apolipoprotein L-I (apoL-I) and apolipoprotein A-I (apoA-I) are the principle antimicrobial molecules providing protection from trypanosome infection. Other HDL subclasses containing either apoA-I and apoL-I or apoA-I and Hpr have reduced trypanolytic activity, whereas HDL subclasses lacking apoL-I and Hpr are non-toxic to trypanosomes. Highly purified, lipid-free Hpr and apoL-I were both toxic to Trypanosoma brucei brucei but with specific activities at least 500-fold less than those of native HDLs, suggesting that association of these apolipoproteins within the HDL particle was necessary for optimal cytotoxicity. These studies show that HDLs can serve as platforms for the assembly of multiple synergistic proteins and that these assemblies may play a critical role in the evolution of primate-specific innate immunity to trypanosome infection.
    Description: These studies were supported by National Institutes of Health Grants AI39033 and AI054496 and a grant from the Ellison Medical Foundation. Mass spectrometry was carried out at the University of Alabama at Birmingham Mass Spectrometry Shared Facility and was supported in part by NCI, National Institutes of Health Core Research Support Grant P30 CA 1314 to the University of Alabama at Birmingham Comprehensive Cancer Center.
    Repository Name: Woods Hole Open Access Server
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  • 8
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    In vitro generation of human high-density-lipoprotein-resistant Trypanosoma brucei brucei (2009)
    American Society for Microbiology
    Details
    Publication Date: 2022-05-26
    Description: Author Posting. © American Society for Microbiology, 2006. This article is posted here by permission of American Society for Microbiology for personal use, not for redistribution. The definitive version was published in Eukaryotic Cell 5 (2006): 1276-1286, doi:10.1128/EC.00116-06.
    Description: The host range of African trypanosomes is influenced by innate protective molecules in the blood of primates. A subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I, apolipoprotein L-I, and haptoglobin-related protein is toxic to Trypanosoma brucei brucei but not the human sleeping sickness parasite Trypanosoma brucei rhodesiense. It is thought that T. b. rhodesiense evolved from a T. b. brucei-like ancestor and expresses a defense protein that ablates the antitrypanosomal activity of human HDL. To directly investigate this possibility, we developed an in vitro selection to generate human HDL-resistant T. b. brucei. Here we show that conversion of T. b. brucei from human HDL sensitive to resistant correlates with changes in the expression of the variant surface glycoprotein (VSG) and abolished uptake of the cytotoxic human HDLs. Complete transcriptome analysis of the HDL-susceptible and -resistant trypanosomes confirmed that VSG switching had occurred but failed to reveal the expression of other genes specifically associated with human HDL resistance, including the serum resistance-associated gene (SRA) of T. b. rhodesiense. In addition, we found that while the original active expression site was still utilized, expression of three expression site-associated genes (ESAG) was altered in the HDL-resistant trypanosomes. These findings demonstrate that resistance to human HDLs can be acquired by T. b. brucei.
    Description: These studies were supported by grants AI39033 and AI054596 from the National Institutes of Health and the Ellison Medical Foundation. Mass spectrometry was supported by NIH P20 RR17695 from the Institutional Development Award (IDeA) Program of the National Center for Research Resources. Computational resources were provided by the Josephine Bay Paul Center for Comparative Molecular Biology and Evolution (MBL) through funds provided by the W. M. Keck Foundation and the G. Unger Vetlesen Foundation.
    Repository Name: Woods Hole Open Access Server
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  • 9
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    Trypanosome resistance to human innate immunity: targeting Achilles’ heel (2012)
    Cell Press
    Details
    Publication Date: 2012-12-01
    Print ISSN: 1471-4922
    Electronic ISSN: 1471-5007
    Topics: Biology , Medicine
    Published by Cell Press
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  • 10
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    RNA Editing–Associated Protein 1 Is an RNA Binding Protein with Specificity for Preedited mRNA (2001)
    Cell Press
    Details
    Publication Date: 2001-04-01
    Print ISSN: 1097-2765
    Electronic ISSN: 1097-4164
    Topics: Biology , Medicine
    Published by Cell Press
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