Relevant bibliographies by topics / Kinetoplasts

Academic literature on the topic 'Kinetoplasts'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Kinetoplasts"

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Sinha, Krishna Murari, Jane C. Hines, and Dan S. Ray. "Cell Cycle-Dependent Localization and Properties of a Second Mitochondrial DNA Ligase in Crithidia fasciculata." Eukaryotic Cell 5, no. 1 (January 2006): 54–61. http://dx.doi.org/10.1128/ec.5.1.54-61.2006.

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ABSTRACT The mitochondrial DNA in kinetoplastid protozoa is contained in a single highly condensed structure consisting of thousands of minicircles and approximately 25 maxicircles. The disk-shaped structure is termed kinetoplast DNA (kDNA) and is located in the mitochondrial matrix near the basal body. We have previously identified a mitochondrial DNA ligase (LIG kβ) in the trypanosomatid Crithidia fasciculata that localizes to antipodal sites flanking the kDNA disk where several other replication proteins are localized. We describe here a second mitochondrial DNA ligase (LIG kα). LIG kα localizes to the kinetoplast primarily in cells that have completed mitosis and contain either a dividing kinetoplast or two newly divided kinetoplasts. Essentially all dividing or newly divided kinetoplasts show localization of LIG kα. The ligase is present on both faces of the kDNA disk and at a high level in the kinetoflagellar zone of the mitochondrial matrix. Cells containing a single nucleus show localization of the LIG kα to the kDNA but at a much lower frequency. The mRNA level of LIG kα varies during the cell cycle out of phase with that of LIG kβ. LIG kα transcript levels are maximal during the phase when cells contain two nuclei, whereas LIG kβ transcript levels are maximal during S phase. The LIG kα protein decays with a half-life of 100 min in the absence of protein synthesis. The periodic expression of the LIG kα transcript and the instability of the LIG kα protein suggest a possible role of the ligase in regulating minicircle replication.
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Klotz, Alexander R., Beatrice W. Soh, and Patrick S. Doyle. "Equilibrium structure and deformation response of 2D kinetoplast sheets." Proceedings of the National Academy of Sciences 117, no. 1 (December 6, 2019): 121–27. http://dx.doi.org/10.1073/pnas.1911088116.

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The considerable interest in two-dimensional (2D) materials and complex molecular topologies calls for a robust experimental system for single-molecule studies. In this work, we study the equilibrium properties and deformation response of a complex DNA structure called a kinetoplast, a 2D network of thousands of linked rings akin to molecular chainmail. Examined in good solvent conditions, kinetoplasts appear as a wrinkled hemispherical sheet. The conformation of each kinetoplast is dictated by its network topology, giving it a unique shape, which undergoes small-amplitude thermal fluctuations at subsecond timescales, with a wide separation between fluctuation and diffusion timescales. They deform elastically when weakly confined and swell to their equilibrium dimensions when the confinement is released. We hope that, in the same way that linear DNA became a canonical model system on the first investigations of its polymer-like behavior, kinetoplasts can serve that role for 2D and catenated polymer systems.
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Simpson, Alastair G. B., Julius Lukeš, and Andrew J. Roger. "The Evolutionary History of Kinetoplastids and Their Kinetoplasts." Molecular Biology and Evolution 19, no. 12 (December 1, 2002): 2071–83. http://dx.doi.org/10.1093/oxfordjournals.molbev.a004032.

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Marande, William, Julius Lukeš, and Gertraud Burger. "Unique Mitochondrial Genome Structure in Diplonemids, the Sister Group of Kinetoplastids." Eukaryotic Cell 4, no. 6 (June 2005): 1137–46. http://dx.doi.org/10.1128/ec.4.6.1137-1146.2005.

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ABSTRACT Kinetoplastid flagellates are characterized by uniquely massed mitochondrial DNAs (mtDNAs), the kinetoplasts. Kinetoplastids of the trypanosomatid group possess two types of mtDNA molecules: maxicircles bearing protein and mitoribosomal genes and minicircles specifying guide RNAs, which mediate uridine insertion/deletion RNA editing. These circles are interlocked with one another to form dense networks. Whether these peculiar mtDNA features are restricted to kinetoplastids or prevail throughout Euglenozoa (euglenids, diplonemids, and kinetoplastids) is unknown. Here, we describe the mitochondrial genome and the mitochondrial ultrastructure of Diplonema papillatum, a member of the diplonemid flagellates, the sister group of kinetoplastids. Fluorescence and electron microscopy show a single mitochondrion per cell with an ultrastructure atypical for Euglenozoa. In addition, DNA is evenly distributed throughout the organelle rather than compacted. Molecular and electron microscopy studies distinguish numerous 6- and 7-kbp-sized mitochondrial chromosomes of monomeric circular topology and relaxed conformation in vivo. Remarkably, the cox1 gene (and probably other mitochondrial genes) is fragmented, with separate gene pieces encoded on different chromosomes. Generation of the contiguous cox1 mRNA requires trans-splicing, the precise mechanism of which remains to be determined. Taken together, the mitochondrial gene/genome structure of Diplonema is not only different from that of kinetoplastids but unique among eukaryotes as a whole.
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Beck, Kirsten, Nathalie Acestor, Anjelique Schulfer, Atashi Anupama, Jason Carnes, Aswini K. Panigrahi, and Ken Stuart. "Trypanosoma brucei Tb927.2.6100 Is an Essential Protein Associated with Kinetoplast DNA." Eukaryotic Cell 12, no. 7 (May 6, 2013): 970–78. http://dx.doi.org/10.1128/ec.00352-12.

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ABSTRACT The mitochondrial DNA of trypanosomatid protozoa consists of a complex, intercatenated network of tens of maxicircles and thousands of minicircles. This structure, called kinetoplast DNA (kDNA), requires numerous proteins and multiprotein complexes for replication, segregation, and transcription. In this study, we used a proteomic approach to identify proteins that are associated with the kDNA network. We identified a novel protein encoded by Tb927.2.6100 that was present in a fraction enriched for kDNA and colocalized the protein with kDNA by fluorescence microscopy. RNA interference (RNAi) knockdown of its expression resulted in a growth defect and changes in the proportion of kinetoplasts and nuclei in the cell population. RNAi also resulted in shrinkage and loss of the kinetoplasts, loss of maxicircle and minicircle components of kDNA at similar rates, and (perhaps secondarily) loss of edited and pre-edited mRNA. These results indicate that the Tb927.2.6100 protein is essential for the maintenance of kDNA.
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Tu, Xiaoming, and Ching C. Wang. "The Involvement of Two cdc2-related Kinases (CRKs) inTrypanosoma bruceiCell Cycle Regulation and the Distinctive Stage-specific Phenotypes Caused by CRK3 Depletion." Journal of Biological Chemistry 279, no. 19 (March 8, 2004): 20519–28. http://dx.doi.org/10.1074/jbc.m312862200.

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Cyclin-dependent protein kinases are among the key regulators of eukaryotic cell cycle progression. Potential functions of the five cdc2-related kinases (CRK) inTrypanosoma bruceiwere analyzed using the RNA interference (RNAi) technique. In both the procyclic and bloodstream forms ofT. brucei, CRK1 is apparently involved in controlling the G1/S transition, whereas CRK3 plays an important role in catalyzing cells across the G2/M junction. A knockdown of CRK1 caused accumulation of cells in the G1phase without apparent phenotypic change, whereas depletion of CRK3 enriched cells of both forms in the G2/M phase. However, two distinctive phenotypes were observed between the CRK3-deficient procyclic and bloodstream forms. The procyclic form has a majority of the cells containing a single enlarged nucleus plus one kinetoplast. There is also an enhanced population of anucleated cells, each containing a single kinetoplast known as the zoids (0N1K). The CRK3-depleted bloodstream form has an increased number of one nucleus-two kinetoplast cells (1N2K) and a small population containing aggregated multiple nuclei and multiple kinetoplasts. Apparently, these two forms have different mechanisms in cell cycle regulation. Although the procyclic form can be driven into cytokinesis and cell division by kinetoplast segregation without a completed mitosis, the bloodstream form cannot enter cytokinesis under the same condition. Instead, it keeps going through another G1phase and enters a new S phase resulting in an aggregate of multiple nuclei and multiple kinetoplasts in an undivided cell. The different leakiness in cell cycle regulation between two stage-specific forms of an organism provides an interesting and useful model for further understanding the evolution of cell cycle control among the eukaryotes.
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Robinson, D. R., T. Sherwin, A. Ploubidou, E. H. Byard, and K. Gull. "Microtubule polarity and dynamics in the control of organelle positioning, segregation, and cytokinesis in the trypanosome cell cycle." Journal of Cell Biology 128, no. 6 (March 15, 1995): 1163–72. http://dx.doi.org/10.1083/jcb.128.6.1163.

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Trypanosoma brucei has a precisely ordered microtubule cytoskeleton whose morphogenesis is central to cell cycle events such as organelle positioning, segregation, mitosis, and cytokinesis. We have defined microtubule polarity and show the + ends of the cortical microtubules to be at the posterior end of the cell. Measurements of organelle positions through the cell cycle reveal a high degree of coordinate movement and a relationship with overall cell extension. Quantitative analysis of the segregation of the replicated mitochondrial genome (the kinetoplast) by the flagellar basal bodies identifies a new G2 cell cycle event marker. The subsequent mitosis then positions one "daughter" nucleus into the gap between the segregated basal bodies/kinetoplasts. The anterior daughter nucleus maintains its position relative to the anterior of the cell, suggesting an effective yet cryptic nuclear positioning mechanism. Inhibition of microtubule dynamics by rhizoxin results in a phenomenon whereby cells, which have segregated their kinetoplasts yet are compromised in mitosis, cleave into a nucleated portion and a flagellated, anucleate, cytoplast. We term these cytoplasts "zoids" and show that they contain the posterior (new) flagellum and associated basal-body/kinetoplast complex. Examination of zoids suggests a role for the flagellum attachment zone (FAZ) in defining the position for the axis of cleavage in trypanosomes. Progression through cytokinesis, (zoid formation) while mitosis is compromised, suggests that the dependency relationships leading to the classical cell cycle check points may be altered in trypanosomes, to take account of the need to segregate two unit genomes (nuclear and mitochondrial) in this cell.
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Ebiloma, Godwin U., Nahandoo Ichoron, Weam Siheri, David G. Watson, John O. Igoli, and Harry P. De Koning. "The Strong Anti-Kinetoplastid Properties of Bee Propolis: Composition and Identification of the Active Agents and Their Biochemical Targets." Molecules 25, no. 21 (November 5, 2020): 5155. http://dx.doi.org/10.3390/molecules25215155.

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The kinetoplastids are protozoa characterized by the presence of a distinctive organelle, called the kinetoplast, which contains a large amount of DNA (kinetoplast DNA (kDNA)) inside their single mitochondrion. Kinetoplastids of medical and veterinary importance include Trypanosoma spp. (the causative agents of human and animal African Trypanosomiasis and of Chagas disease) and Leishmania spp. (the causative agents of the various forms of leishmaniasis). These neglected diseases affect millions of people across the globe, but drug treatment is hampered by the challenges of toxicity and drug resistance, among others. Propolis (a natural product made by bees) and compounds isolated from it are now being investigated as novel treatments of kinetoplastid infections. The anti-kinetoplastid efficacy of propolis is probably a consequence of its reported activity against kinetoplastid parasites of bees. This article presents a review of the reported anti-kinetoplastid potential of propolis, highlighting its anti-kinetoplastid activity in vitro and in vivo regardless of geographical origin. The mode of action of propolis depends on the organism it is acting on and includes growth inhibition, immunomodulation, macrophage activation, perturbation of the cell membrane architecture, phospholipid disturbances, and mitochondrial targets. This gives ample scope for further investigations toward the rational development of sustainable anti-kinetoplastid drugs.
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Sullenberger, Catherine, Benjamin Hoffman, Justin Wiedeman, Gaurav Kumar, and Kojo Mensa-Wilmot. "Casein kinase TbCK1.2 regulates division of kinetoplast DNA, and movement of basal bodies in the African trypanosome." PLOS ONE 16, no. 4 (April 16, 2021): e0249908. http://dx.doi.org/10.1371/journal.pone.0249908.

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The single mitochondrial nucleoid (kinetoplast) ofTrypanosoma bruceiis found proximal to a basal body (mature (mBB)/probasal body (pBB) pair). Kinetoplast inheritance requires synthesis of, and scission of kinetoplast DNA (kDNA) generating two kinetoplasts that segregate with basal bodies into daughter cells. Molecular details of kinetoplast scission and the extent to which basal body separation influences the process are unavailable. To address this topic, we followed basal body movements in bloodstream trypanosomes following depletion of protein kinase TbCK1.2 which promotes kinetoplast division. In control cells we found that pBBs are positioned 0.4 um from mBBs in G1, and they mature after separating from mBBs by at least 0.8 um: mBB separation reaches ~2.2 um. These data indicate that current models of basal body biogenesis in which pBBs mature in close proximity to mBBs may need to be revisited. Knockdown of TbCK1.2 produced trypanosomes containing one kinetoplast and two nuclei (1K2N), increased the percentage of cells with uncleaved kDNA 400%, decreased mBB spacing by 15%, and inhibited cytokinesis 300%. We conclude that (a) separation of mBBs beyond a threshold of 1.8 um correlates with division of kDNA, and (b) TbCK1.2 regulates kDNA scission. We propose a Kinetoplast Division Factor hypothesis that integrates these data into a pathway for biogenesis of two daughter mitochondrial nucleoids.
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Ferguson, M. L., A. F. Torri, D. Pérez-Morga, D. C. Ward, and P. T. Englund. "Kinetoplast DNA replication: mechanistic differences between Trypanosoma brucei and Crithidia fasciculata." Journal of Cell Biology 126, no. 3 (August 1, 1994): 631–39. http://dx.doi.org/10.1083/jcb.126.3.631.

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Kinetoplast DNA, the mitochondrial DNA of trypanosomatid parasites, is a network containing several thousand minicircles and a few dozen maxicircles. We compared kinetoplast DNA replication in Trypanosoma brucei and Crithidia fasciculata using fluorescence in situ hybridization and electron microscopy of isolated networks. One difference is in the location of maxicircles in situ. In C. fasciculata, maxicircles are concentrated in discrete foci embedded in the kinetoplast disk; during replication the foci increase in number but remain scattered throughout the disk. In contrast, T. brucei maxicircles generally fill the entire disk. Unlike those in C. fasciculata, T. brucei maxicircles become highly concentrated in the central region of the kinetoplast after replication; then during segregation they redistribute throughout the daughter kinetoplasts. T. brucei and C. fasciculata also differ in the pattern of attachment of newly synthesized minicircles to the network. In C. fasciculata it was known that minicircles are attached at two antipodal sites but subsequently are found uniformly distributed around the network periphery, possibly due to a relative movement of the kinetoplast disk and two protein complexes responsible for minicircle synthesis and attachment. In T. brucei, minicircles appear to be attached at two antipodal sites but then remain concentrated in these two regions. Therefore, the relative movement of the kinetoplast and the two protein complexes may not occur in T. brucei.
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Dissertations / Theses on the topic "Kinetoplasts"

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Dewar, Caroline E. "What do kinetoplastids need a kinetoplast for? : life cycle progression of Trypanosoma brucei in the presence and absence of mitochondrial DNA." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/17943.

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The parasitic protist Trypanosoma brucei is the causative agent of human African trypanosomiasis. The parasite undergoes a complex life cycle involving stages within the mammalian bloodstream and its tsetse fly vector. The fundamental differences between energy metabolism in the procyclic insect form (PCF) and long slender bloodstream form (BSF) T. brucei involve a switch in the directionality of the F1Fo- ATPase. In PCF, the need for oxidative phosphorylation in low glucose conditions requires the enzyme to generate ATP. In the slender BSF, the enzyme uses ATP from glycolysis to drive proton pumping to maintain the essential mitochondrial membrane potential. Fo-ATPase subunit 6 (A6) is critical for proton translocation in either direction and is encoded in the mitochondrial DNA (kDNA). The parasite’s kDNA is therefore essential in the slender BSF, and also in PCF where it encodes multiple subunits of the respiratory chain complexes that constitute the oxidative phosphorylation pathway. Specific point mutations in the nuclearly encoded γ subunit of the mitochondrial F1Fo-ATPase allow survival in the absence of kDNA in the slender BSF T. brucei (Dean et al., 2013). These mutations, even in the heterozygous genotype, cause an increase in resistance to multiple drugs in vitro (Gould and Schnaufer, 2014). This thesis investigates two questions: (1) What is the molecular mechanism of compensation for kDNA loss? (2) Are kDNA and a functional FoF1-ATPase required for life cycle progression? Slender BSF T. brucei were generated expressing ATPase L262Pγ. The effects of this γ mutation and kDNA loss, respectively, on structure/function of the F1Fo- ATPase were probed. Cells expressing L262Pγ show decreased sensitivity to Fo inhibitor oligomycin compared to WT cells, suggesting that the L262Pγ mutation functionally uncouples the enzyme. The impact of the L262Pγ mutation on the structure of the enzyme was probed by high resolution clear native electrophoresis. This shows there are dramatic consequences to F1Fo structure in the presence of the L262Pγ mutation. The apparent selection for cells that no longer express intact F1Fo suggests that L262Pγ uncouples the enzyme, resulting in a lethal proton leak. Pleomorphic T. brucei with and without kDNA were also generated by expressing mutant γ in strain AnTat1.1 90:13. Differentiation studies demonstrate kDNA0 cells can differentiate to insect-transmissible stumpy forms. These cells show a decreased lifespan, suggesting a critical role for a kDNA-encoded product in the stumpy form. Tsetse fly infections show kDNA is indispensable for progression to the PCF. Unexpectedly, parasites homozygous for L262Pγ can establish a midgut infection, while they do not infect the salivary glands. Heterozygous parasites, on the other hand, can form animal-transmissible metacyclics in the salivary glands, providing a potential mechanism for spreading decreased sensitivity to multiple drugs.
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Alkhaldi, Abdulsalam Abdulhadi. "Drug development against kinetoplastid parasites." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3637/.

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Human African trypanosomiasis and leishmaniasis are caused by parasites belonging to the genera Trypanosoma and Leishmania, respectively. Significant numbers of people are affected by these diseases worldwide, which are fatal if untreated. Animals can also be infected, posing agricultural and economic hindrances, especially in poor countries. Although chemotherapy can be used for treatment, many problems are associated with it, including drug toxicity, resistance, lack of guaranteed supply, and high treatment cost. Therefore, there is an urgent need for new treatment approaches. Here, we aim to examine the in vitro efficacy of curcumin and phosphonium compounds against these parasites, assay their toxicity to human kidney cells in vitro, and investigate the mechanism of antiparasite activity of curcumin. The Alamar blue assay was used to test 158 curcumin analogues against Leishmania major promastigotes and Leishmania mexicana promastigotes and axenic amastigotes to obtain in vitro EC50 values. Many curcumin compounds such as AS-HK122 and AS-HK126 exhibited anti-leishmanial activities similar to or better than the current clinical drug pentamidine. Similarly, EC50 values of 83 phosphonium compounds against Trypanosoma brucei brucei bloodstream forms were determined. More than 20% of the tested compounds were found to be more active than the standard veterinary drug diminazene aceturate. Multi-drug resistant strains were used to determine that there is no cross-resistance between the tested compounds and the diamidine or melaminophenyl arsenical classes of trypanocides. Structure activity relationship (SAR) analysis revealed that mono-O-demethylated curcumin compounds showed 10-fold higher activity against the parasites than curcumin. The addition of one or two pentyl pyridinium (C10H15N) groups on specific positions of the aromatic ring also increased the activity of these compounds. Furthermore, curcumin compounds with an isoxazole ring instead of the diketo motif showed higher activity and the lowest EC50 values. Similarly, pentyl bromide (OC5H10Br) substitutions on the phenyl rings improved the antiparasitic activity. Curcuminoids with trienone linkers showed increased antiparasitic activity against all parasites tested. Eighty-three phosphonium analogues were tested against T. brucei brucei. SAR analysis indicated that the bulky substituents surrounding the bisphosphonium cations led to strong antiparasitic activity while the nature of the linker had less effect on the activity. Some monophosphonium analogues registered the lowest EC50 values of all the phosphonium compounds. The toxicity of the curcumin and phosphonium analogues to HEK cells was analysed in vitro. All curcumin and phosphonium compounds demonstrated lower toxicity to HEK cells than to the parasites. Of the 83 phosphonium compounds, 60 displayed >200-fold in vitro selectivity index (SI). We also investigated the mode of antiparasitic activity of curcumin compounds. Preliminary toxicity tests had revealed that AS-HK014 caused rapid depletion of glutathione content in rat hepatocytes. Therefore, we tested AS-HK014 activity in the presence of different concentrations of L-glutathione, and AS-HK014 activity was found to decrease with increased L-glutathione concentrations, strongly suggesting that glutathione reacted with the active compound. Indeed, a chemical adduct was observed between the two compounds and identified through mass spectrometry. A trypanosome cell line (TA014) adapted to AS-HK014 was produced. TA014 and wild-type T. brucei brucei were treated with AS-HK014 and compared with each other and with untreated controls. The glutathione and trypanothione levels were lower in the treated WT cells than in the untreated cells. However, there was no change in the glutamate, ornithine, or spermidine levels, providing no evidence for the inhibition of trypanothione synthesis, suggesting that the effect is probably not metabolic but chemical. AS-HK014 did not significantly affect thiol levels in TA014; this might reflect a higher level of trypanothione synthesis through increased glutathione synthetase (GS) and/or γ-glutamylcysteine synthetase (γ-GCS) expression. Therefore, we analysed the protein levels using western blotting, and sequenced the encoding genes in both WT and TA014 to identify any mutations in the open reading frames (ORFs). However, we found no changes in the GS and γ-GCS protein levels in resistant trypanosomes and no mutations were found in the GS and γ-GCS ORFs. It is clear that the resistance is to the reactive enone motif of AS-HK014 rather than to curcumin and curcuminoids in general, since TA014 only displayed resistance to AS-HK014 analogues bearing the enone motif while sensitivity to curcumin remained unchanged, confirming that this motif is responsible for the higher activity of AS-HK014 compared to curcumin. The effects of bisphosphonium analogues on T. brucei brucei bloodstream forms were investigated to identify the target. All tested analogues rapidly reduced the T. brucei brucei mitochondrial membrane potential Ψm and decreased the intracellular ATP level after one hour of incubation, suggesting that the compounds may be targeting the mitochondria. The intracellular Ca2+ levels increased gradually after eight hours, suggesting that the damaged mitochondria are unable to retain the stored Ca2+ as their membrane potential dissipates. We also studied the trypanosome cell cycle after incubating the parasites with bisphosphonium compounds. The cell cycle defects became apparent after eight hours of incubation: DNA synthesis could not be initiated, leading to a dramatic reduction of cells in the S phase. This result was also confirmed by fluorescence microscopic assessment of DNA configuration. After eight hours of incubation with the bisphosphonium compound CD38, the number of 2K1N cells significantly decreased as compared with the control. There may be a causal relationship between mitochondrial damage and cell cycle defects. Transmission electron microscopy images of the cells obtained after 12 h of exposure to CD38 also revealed the presence of mitochondrial damage. We tested whether bisphosphonium compounds can induce programmed cell death in trypanosomes. A TUNEL assay was used to detecting DNA fragmentation; the results showed increased DNA fragmentation after 24-h treatment with two different bisphosphonium compounds, CD38 and EFpI7. This result indicates is consistent with apoptosis occurring in treated cells but there was no evidence suggesting that bisphosophonium-induced cell death in trypanosomes is dependent on new protein synthesis. In conclusion, curcumin and phosphonium analogues exhibit promising antiparasitic activity, and some analogues could be optimised for in vivo evaluation. Further investigations on the site of action of phosphonium compounds in the mitochondrion are in progress.
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Brewster, S. "Analysis of the kinetoplast DNA of Leishmania panamensis." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596899.

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An in-depth study of the kinetoplast DNA of the human-infecting parasite Leishmania panamensis was conducted with the following objectives: • To find out how many minicircle sequence classes are present in the kinetoplast, and the relative abundance of each class; • To use this information to develop and test a kDNA-based diagnostic test specific for this species of parasite; • To investigate whether minicircle sequence data can be meaningfully used to infer phylogenetic relationships between Leishmania species; • To also investigate RNA editing in this parasite and compare it with previous results in a lizard-infecting Leishmania. Kinetoplast DNA from L. panamensis was cloned and investigated in detail by restriction enzyme typing and sequence analysis, and three other species of the braziliensis complex of New World Leishmania were analysed in a similar way. It was found that the minicircle component of the kinetoplast DNA is highly complex, and is comprised of at least 35 classes of minicircle per kinetoplast, with each class having a varying level of abundance. A kDNA probe and primers specific for L. panamensis were designed from an abundant minicircle class, and were subsequently field-tested in Medellin, Colombia. The sequence data generated during this study was used to infer phylogenetic relationships between the species of New World Leishmania. A variety of different approaches were used, and the suitability of this type of sequence data for phylogenetic analysis is discussed. The sequence data was also screened for potential guide RNA genes, and a total of 26 possible genes were identified. Comparison of the maxicircle gene sequence for the ATPase subunit 6 gene between L. panamensis and L. tarentolae (lizard-infecting) together with an analysis of previous work revealed that the RNA editing process is remarkably similar between Leishmania species. This study extends the little known about the organisation and function of minicircle DNA in pathogenic Leishmania species.
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Timm, Jennifer. "Structure-function studies of kinetoplastid proteins." Thesis, University of York, 2014. http://etheses.whiterose.ac.uk/7454/.

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The class kinetoplastida include parasites responsible for devastating diseases like African sleeping sickness, Chagas’s disease and Leishmaniases, mainly effecting people in the developing world. Current treatments are highly toxic and inefficient, leading to an urgent need of novel anti-parasitic compounds. This thesis focuses on the structural characterisation of potential drug targets against these parasites, namely adenosine kinase from Trypanosoma brucei (TbAK), thymidine kinases from T. brucei (TbTK) and Leishmania major (LmTK) and the leucyl aminopeptidases from T. brucei (TbLAP-A), T. cruzi (TcLAP-A) and L. major (LmLAP-A). Structures of TbAK were solved in two conformations, open (apo) and closed (in complex with adenosine and ADP), both to 2.6 Å. Comprised of a big α/β-domain and a small lid domain, the structures confirm the large conformational change of the lid domain upon substrate binding. The structures of C-terminally truncated versions of LmTK and TbTK were determined as ligand-bound complexes with resolutions up to 2.4 Å and 2.2 Å, respectively. They show high similarity to structures of homologues in the PDB. The structures solved in this thesis give valuable information about ligand binding and aid rational drug design. Leucyl aminopeptidase (LAP-A) was evaluated as a potential drug target in T. brucei parasites. It is not essential for T. brucei parasites grown in vitro, shown by generation and analysis of LAP-A-depleted parasites. Although this does not support LAP-A as a drug target in T. brucei, no conclusions can be drawn about the potential in T. cruzi and L. major. Several structures of the LAP-As were solved, the highest resolution ones to 2.3 Å, 2.3 Å and 2.5 Å for TbLAP-A, TcLAP-A and LmLAP-A, respectively. These enzymes are hexameric and show the typical two-domain architecture of M17 LAPs. Although the physiological function remains elusive, the work in this thesis provides a firm basis for future studies.
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Rodriguez, Noris Marcela. "PCR diagnosis of Leishmania using nuclear and kinetoplast primers." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627544.

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Tiesen, K. L. "Studies on monogenetic kinetoplastid flagellates of hemiptera." Thesis, University of Salford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376881.

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Ali, Juma Ahmed Mohmed. "Pyrimidine salvage and metabolism in kinetoplastid parasites." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4664/.

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Pyrimidine uptake has previously been investigated in Trypanosoma brucei procyclics and partly investigated in promastigotes of Leishmania major; however, no such study has been performed using bloodstream forms of Trypanosoma or promastigotes of Leishmania. Here we report a comprehensive study of pyrimidine salvage and metabolism in bloodstream forms of Trypanosoma and promastigotes of Leishmania species. In T. b. brucei bloodstream forms, the uptake of 3H-uracil and 3H-tymidine each appeared to be mediated by a single transporter, designated TbU3 and TbT1, respectively. The procyclic uracil transporter,TbU1, has a high affinity for uracil, with a Km value of 0.46 ± 0.09 μM and Vmax of 0.65 ± 0.008 pmol (107cell)-1 s-1. These values were similar for TbU3 (Km = 0.54 ± 0.11 µM; Vmax = 0.14 ± 0.03), but the main differences between TbU1 and TbU3 are their sensitivity to uridine and 4-thiouracil. Thymidine uptake is detectable at 10 μM over a period from 5 to 30 minutes. This uptake was not inhibited by uracil which indicates that TbT1 is a novel thymidine transporter. The uptake of other pyrimidines, including uridine and 2’-deoxyuridine, by BSF are investigated here but these substrates were also transported by TbU3, and no additional pyrimidine transport activities were found. In L. mexicana and L. major, the uptake of 3H-uracil and 3H-uridine was mediated by separate transporters, designated as follows; for uracil uptake LmexU1, LmajU1; and for uridine uptake LmexNT1, LmajNT1 and LmajNT2, respectively. LmexU1 is a uracil transporter with high affinity to uridine and 2’deoxyuridine, and the LmexNT1 is a nucleoside transporter with broad specificity for purine and pyrimidine nucleosides. L. major uracil transporter (LmajU1) has already been reported by others; and here we report that there are also two distinct uridine transporters expressed in L. major. LmajNT1 is a high affinity uridine transporter which is also inhibited by uracil, inosine and adenine; LmajNT2 is low affinity uridine transporter, with very poor affinity for uracil, inosine and adenine. However, both transporters are inhibited by 2’-deoxyuridine, thymidine and adenosine. Several fluorinated pyrimidine analogues were assessed against kinetoplastid cells, the most effective compounds, which displayed EC50 values at micromolar level, are 5-FU, 5F-2’dUrd, 5-FOA (only against T. brucei BSF) and 5F-Urd (only against L. major). We induced resistance to 5-FU, 5-F2’dUrd and 5-FOA by in vitro exposure of Tbb-BSF and promastigotes of L. mexicana and L. major. The resistance was performed by stepwise increase concentration of the drugs. For T. b. brucei BSF, the resistance factors of clonal lines were 131, 825, and 83-fold, respectively. For L. mexicana and L. major, the resistance factor for 5-FU were 147 and 17-fold, and for 5F-2’dUrd were >3500 and 381-fold, respectively. We also measured 3H–pyrimidine uptake in these cell lines; the resistant bloodstream form strains showed no changes in pyrimidine uptake, with one exception, which is a 76% reduction in 5-FU uptake. In contrast, each resistant strain of Leishmania spp had lost its natural pyrimidine transporter. For example, Leishmania cells resistant to 5-FU had lost uracil transport activity, and cells that were resistant to 5F-2’dUrd had lost uridine transport activity. In addition, we identified kinetoplastid genes that appeared to be associated with resistance to fluorinated pyrimidines. Based on these findings, metabolomic analysis of fluorinated pyrimidines in T. b. brucei resistant cell lines was performed in comparison with parental wild-type; for Leishmania species we only investigated the metabolism of fluorinated pyrimidine in wild type cells, as the fluorinated analogues were simply not taken up in the resistant clones. The metabolomic analysis data showed that, in T. b. brucei, 5-fluorouracil and 5-fluoro orotate are incorporated into a large number of metabolites, but likely act through incorporation into RNA. 5F-2’dUrd and 5F-2’dCtd are not incorporated into nucleic acids but act as prodrugs by inhibiting thymidylate synthase after conversion to 5F-dUMP. Cells treated with 5-fluoro-2’deoxyuridine showed an increase of dUMP, which suggest a block in thymidylate synthase or possibly thymidylate kinase. We also present the most complete model of pyrimidine salvage in T. brucei to date, supported by genome-wide profiling of the predicted pyrimidine biosynthesis and conversion enzymes. The effect of fluorinated pyrimidine analogues in the two Leishmania species was almost identical. Each of the tested drugs (5-FU, 5F-2’dUrd and 5F-Urd) produced a limited number of fluorinated metabolites, and their common mode of action was inhibition in thymidylate synthase by 5F-dUMP and thymidine kinase by 5F-2’dUrd. Interestingly, we found that the cause of L. mexicana resistance to 5F-Urd was due to the absence of the 5F-2’dUrd metabolite, as a result of the rapid conversion of 5F-2’dUrd to 5F-dUMP; also we suggest that, in L. mexicana, but not in L. major the high affinity salvage of thymidine is sufficient to provide the cells with thymidine deoxynucleotides. It has been found that pyrimidine salvage is not an essential function for Leishmania cells in vitro conditions. However, it is not known whether either, pyrimidine salvage or biosynthesis, or both of these systems are essential to the trypanosomes in vitro and in vivo study. As T. b. brucei bloodstream forms grew unimpeded in vitro in the complete absence of pyrimidines, uptake is clearly not essential. Disruption of the pyrimidine biosynthesis pathway by deletion of the OMPDCase/OPRTase gene resulted in pyrimidine auxotrophic trypanosomes that were unable to grow in the absence of added pyrimidines. The phenotype was rescued by addition of uracil, and to a lesser extent by some pyrimidine nucleosides. Pyrimidine starvation led rapidly to DNA fragmentation. Adaptations to low pyrimidine availability included upregulation of uracil transport capacity and of uridine phosphorylase expression. However, pyrimidine auxotrophic T. brucei were able to establish a high parasitemia in mice. We therefore conclude that pyrimidine salvage was not an essential function for bloodstream T. b. brucei. However, trypanosomes lacking de novo pyrimidine biosynthesis are completely dependent on an extracellular pyrimidine source, strongly preferring uracil, and display reduced infectivity and strongly increased sensitivity to fluorinated pyrimidines. As T. brucei are able to salvage sufficient pyrimidines from the host environment, the pyrimidine biosynthesis pathway is not a viable drug target, although any interruption of pyrimidine supply was lethal.
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8

Hitchcock, Robert Arthur. "Epigenetic control of the kinetoplastid spliced leader RNA." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1998392041&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Blom, Daniël. "Mechanism and evolution of RNA editing in kinetoplastids." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/83225.

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Gaston, Kirk W. "Editing and Modification of Threonyl-tRNAs in Kinetoplastids." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1248965851.

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Books on the topic "Kinetoplasts"

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Majumder, Hemanta K., ed. Drug Targets in Kinetoplastid Parasites. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77570-8.

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Tieszen, Kenneth L. Studies on monogenetic kinetoplastid flagellates of hemiptera. Salford: University of Salford, 1986.

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Yurchenko, Vyacheslav, and Dmitri Maslov. Kinetoplastid Phylogenomics and Evolution. Mdpi AG, 2022.

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Kinetoplastid Genomics and Beyond. MDPI, 2021. http://dx.doi.org/10.3390/books978-3-0365-1581-6.

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Kinetoplastid Phylogenomics and Evolution. MDPI, 2022. http://dx.doi.org/10.3390/books978-3-0365-3052-9.

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K, Majumder Hemanta, ed. Drug targets in kinetoplastid parasites. New York: Springer Science+Business Media, 2008.

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Majumder, Hemanta K. Drug Targets in Kinetoplastid Parasites. Springer, 2010.

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Molecular Biology of Kinetoplastid Parasites. Caister Academic Press, 2018. http://dx.doi.org/10.21775/9781910190715.

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Majumder, Hemanta K. Drug Targets in Kinetoplastid Parasites. Springer London, Limited, 2008.

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Kreir, Julius. Taxonomy, Kinetoplastids, and Flagellates of Fish. Elsevier Science & Technology Books, 2012.

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Book chapters on the topic "Kinetoplasts"

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Trager, William. "The Kinetoplast and Kinetoplast DNA." In Living Together, 185–99. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9465-9_11.

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Gibson, Wendy. "Kinetoplastea." In Handbook of the Protists, 1089–138. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28149-0_7.

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Gibson, Wendy. "Kinetoplastea." In Handbook of the Protists, 1–50. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32669-6_7-1.

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von Geldern, Tomas, Michael Oscar Harhay, Ivan Scandale, and Robert Don. "Kinetoplastid Parasites." In Topics in Medicinal Chemistry, 181–241. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/7355_2011_17.

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Müller, Ingrid, and Pascale Kropf. "Kinetoplastids: Leishmania." In Immunity to Parasitic Infection, 153–64. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118393321.ch7.

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Sternberg, Jeremy. "Kinetoplastids: Trypanosomes." In Immunity to Parasitic Infection, 165–77. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118393321.ch8.

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Lobanov, Alexei V., and Vadim N. Gladyshev. "Selenoproteome of Kinetoplastids." In Trypanosomatid Diseases, 237–42. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527670383.ch12.

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Bachmaier, Sabine, and Michael Boshart. "Kinetoplastid AGC Kinases." In Protein Phosphorylation in Parasites, 99–122. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527675401.ch05.

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Mehlhorn, Heinz. "Kinetoplastid RNA (kRNA)." In Encyclopedia of Parasitology, 1399. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3980.

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Mehlhorn, Heinz. "Kinetoplastid RNA (kRNA)." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3980-1.

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Conference papers on the topic "Kinetoplasts"

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Ebiloma, Godwin, John Igoli, David Watson, and Harry de Koning. "Propolis and its bioactive chemical constituents offer a novel and sustainable treatment option for kinetoplastid infections." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11499.

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Nué Martinez, Jorge Jonathan, Cinthia Millan, Godwin Ebiloma, Harry De Koning, Lourdes Campos, and Christophe Dardonville. "pKa modulation of a bis(2-aminoimidazoline) DNA minor groove binder that targets the kinetoplast of Trypanosoma brucei." In 4th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2018. http://dx.doi.org/10.3390/ecmc-4-05626.

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Matić, Sanja, Snežana Stanić, Nevena Tomašević, Rino Ragno, and Milan Mladenović. "DISCLOSING THE TRUE NATURE OF HESPERETIN’S ANTIGENOTOXICITY „IN VIVO“ WITHIN THE „DROSOPHILA MELANOGASTER“ SOMATIC CELLS THROUGH THE EXTENSIVE GENOTOXICAL AND STRUCTURE-BASED STUDIES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.427m.

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Abstract:
Previously unreported genotoxic and antigenotoxic potentials of hesperetin (Hes) were revealed by treating the Drosophila melanogaster (dm) whose DNA has been altered by means of O6-ethylguanine (dmGO6-Et) and O4-ethylthymine (dmTO4-Et) lesions appearance, caused by ethyl methanesulfonate (EMS), a proven alkylating agent and mutagen. Therefore, Hes potencies were determined by means of the comet assay on somatic cells level, where compound exerted no genotoxic effects but acted genotoxically as a Topoisomerase IIα (dmTopIIα) catalytic inhibitor by invading the Binding and Cleavage Domain and stabilizing the noncovalent dmTopIIα-plasmid DNA (dmPDNA) complex, as verified by the kinetoplast DNA (dmK-DNA) decatenation assays. Hes’s structure-based alignment caused compound’s A and C rings to occupy the area normally invaded by EMS, thus making a spatial barrier for the dmGO6-Et or dmTO4-Et lesions formation: the A ring C7-OH group formed hydrogen bonds (HBs) with either dmGO6 (dHB = 2.576 Å) or guanine’s N7 nitrogen (dmGN7, dHB = 2.737 Å), whereas the A ring C5-OH group formed an HB with dmTO4 (dHB = 3.548 Å). Furthermore, Hes likewise acted as a mixed-type competitive inhibitor of dmATPase, as verified by the catalytic, FRET, and structure-based studies where it affected the dmATPase dimerization and the hydrolysis of ATP, denying the metabolic energy for the catenation of ethylated G-dmDNA segment, the formation of dmTO4-Et-G-dmDNA phosphotyrosine intermediate (dmTO4-Et-G- dmDNA-PTyr785I), and the passage of ethylated T-dmDNA segment through the temporarily broken dmTO4-Et-G-dmDNA-PTyr785I, processes seen as comets. Conclusively, Hes may be used in anticancer therapy controlling the effects of alkylating agents.
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