Influence of DNA Complexing Compounds on the Kinetoplast of Trypanosomatids

Hajduk, Stephen L.

doi:10.1007/978-3-642-66856-2_4

Cited by 25 publications

(10 citation statements)

References 145 publications

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“…Nevertheless, pararosaniline was able to induce mutation in the kDNA of the kinetoplastid thereby producing akinetoplastic forms in agreement with the results of Inoki et al (1962). Other dyes (e.g., acriflavine, ethidium bromide) and antitrypanosomal drugs (e.g., berenil, samorin) have likewise been shown to exert the same effect on other trypanosomes (Hajduk, 1978;Shapiro and Englund, 1990). Notwithstanding, it is also possible that pararosaniline could have produced the concavities.…”

Section: Resultsmentioning

confidence: 99%

Trypanosoma evansi: Unique Concavities on the Surface Membrane of Pararosaniline-induced Akinetoplastic Clones as Revealed by Scanning Electron Microscopy.

Silva-Tahat

Ichinose

Uemura

et al. 1995

Jap. J. Trop. Med. Hyg.

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Abstract:Pararosaniline-induced akinetoplastic clones of Trypanosoma evansi which lack DAPI-stainable kDNA network were characterized by scanning electron microscopy. Independent batches of akinetoplastic parasites from two passages in mice were observed to have similarities with parental kinetoplastic strain with respect to shape, form, and pleomorphism.The marked difference in surface topography was noted between the wildtype and the mutant as unique concavities on the cell surface of the latter. These concavities are variable in size, number and extent and may be inheritable. In addition, akinetoplastic cells were found to undergo active longitudinal binary fission and filopodia formation as reported by others. These observations suggest that the kDNA-deficient mutants of T evansi have maintained their basic functions of cell division and infectivity and, therefore, the concavities on their surface are not detrimental to their existence.

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Section: Resultsmentioning

confidence: 99%

Trypanosoma evansi: Unique Concavities on the Surface Membrane of Pararosaniline-induced Akinetoplastic Clones as Revealed by Scanning Electron Microscopy.

Silva-Tahat

Ichinose

Uemura

et al. 1995

Jap. J. Trop. Med. Hyg.

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“…The last group consists of a series of dyskinetoplasmic strains in which no trace of nüni-circles or maxi-circles has been found by electron microscopy or hybridization analysis. A confusing point that has only been recently clarified is that the dyskinetoplastic strains still contain a satellite DNA that bands at the density of T. brucei kDNA in CsCl (Riou & Pautrizel, 1977;Hajduk, 1978). This satellite has no sequence homology with kDNA (Frasch et al 1980) and recent experiments have shown that it is located in the nucleus and that it is also present in K+ Stocks (Borst et al 1980c).…”

Section: Replication and Segregation Of Kdna Networkmentioning

confidence: 99%

“…Whether some dyskinetoplastic strains may still contain some DNA in their mitochondria is not yet clear. Support for the presence of DNA comes from the patchy staining throughout the cytoplasm with the DNA-specific fluorescent dye DAPI and from the observation in thin sections of remaining electron-dense, DNA-like material in the mitochondria (see Hajduk, 1978). It is possible that such a strain may represent transition states between I~ strains with kDNA networks and without kDNA at all.…”

Section: Replication and Segregation Of Kdna Networkmentioning

confidence: 99%

Workshop no. 6. Structure, function and evolution of kinetoplast DNA

1981

Parasitology

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The kinetoplast DNA (kDNA) of kinetoplastidae was the first mitochondrial DNA (mtDNA) to be discovered, and with its unusual network structure, consisting of more than 104catenated DNA circles, it is without equal in nature. Analysis of networks from various genera (reviewed by Borst & Hoeijmakers (1979a) and Englund (1980)) has shown that they always consist of two components: mini-circles and maxi-circles (see Table 1). The mini-circles are the major component and deterraine the size and sliape of networks. They vary in size between 1 and 3 kilo-base pairs (kb = 1000 base pairs (bp)), they are heterogeneous in sequence, their sequence evolves rapidly and their function is not yet known. The maxi-circles, on the other hand, are homogeneous in sequence, their sequence is conserved and they probably represent the counterpart of mtDNA in other organisms.

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“…Available evidence points to kDNA being essential for PCF viability and fly transmissibility [90]. RNAi knockdown of genes required for kDNA replication and division was lethal in PCF in vitro [69, [91][92][93], and chemically induced kDNA 0 PCF cells were also non-viable in vitro [68,94]. Similarly, from a mixed population of kDNA + and kDNA 0 parasites (the latter were obtained by treatment of kDNA + parasites with acriflavine), only kDNA + cells were able to establish a tsetse midgut infection [95].…”

Section: Introductionmentioning

confidence: 99%

Oxidative phosphorylation is required for powering motility and development of the sleeping sickness parasite Trypanosoma brucei within the tsetse fly vector

Dewar

Casas-Sánchez

Dieme

et al. 2021

Preprint

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The single-celled parasite Trypanosoma brucei causes sleeping sickness in humans and nagana in livestock and is transmitted by hematophagous tsetse flies. Lifecycle progression from mammalian bloodstream form to tsetse midgut form and, subsequently, infective salivary gland form depends on complex developmental steps and migration within different fly tissues. As the parasite colonises the glucose-poor insect midgut, its ATP production is thought to depend on activation of mitochondrial amino acid catabolism via oxidative phosphorylation. This process involves respiratory chain complexes and the F1FO-ATP synthase, and it requires protein subunits of these complexes that are encoded in the parasite's mitochondrial DNA (kinetoplast or kDNA). Here we show that a progressive loss of kDNA-encoded functions correlates with an increasingly impaired ability of T. brucei to initiate and complete its development in the tsetse. First, parasites with a mutated F1FO-ATP synthase with a reduced capacity for oxidative phosphorylation can initiate differentiation from bloodstream to insect form, but they are unable to proliferate in vitro. Unexpectedly, these cells can still colonise the tsetse midgut. However, these parasites exhibit a motility defect and are severely impaired in colonising or migrating to subsequent tsetse tissues. Second, parasites with a fully disrupted F1FO-ATP synthase complex that is completely unable to produce ATP by oxidative phosphorylation can still differentiate to the first insect stage in vitro but die within a few days and cannot establish a midgut infection in vivo. Third, mutant parasites lacking kDNA entirely can initiate differentiation but die within 24 h. Together, these three scenarios show that efficient ATP production via oxidative phosphorylation is not essential for initial colonisation of the tsetse vector, but it is required to power trypanosome migration within the fly.

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Influence of DNA Complexing Compounds on the Kinetoplast of Trypanosomatids

Cited by 25 publications

References 145 publications

Trypanosoma evansi: Unique Concavities on the Surface Membrane of Pararosaniline-induced Akinetoplastic Clones as Revealed by Scanning Electron Microscopy.

Trypanosoma evansi: Unique Concavities on the Surface Membrane of Pararosaniline-induced Akinetoplastic Clones as Revealed by Scanning Electron Microscopy.

Workshop no. 6. Structure, function and evolution of kinetoplast DNA

Oxidative phosphorylation is required for powering motility and development of the sleeping sickness parasite Trypanosoma brucei within the tsetse fly vector

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